E
Early Childhood Tutor
▶ Itinerant Teacher
Early Diagnosis
Tony Charman
Centre for Research in Autism and Education,
Department of Psychology and Human,
Institute of Education, University of London,
London, UK
Definition
Although autism spectrum disorders can be
diagnosed at any age, the classification sys-
tems require onset prior to 3 years of age or
in early childhood. The term “early diagnosis”
refers to diagnosis in the second and third year
of life.
Historical Background
Notwithstanding progress in understanding of the
genetic and neurodevelopmental processes that
lead to autism spectrum disorders (ASD), clinical
diagnosis is reliant on the developmental and
behavioral presentation. Until the 1990s, it was
rare for children to receive a diagnosis of autism
F.R. Volkmar (ed.), Encyclopedia of Autism Spectrum Disorders,
DOI 10.1007/978-1-4419-1698-3, # Springer Science+Business Media New York 2013
until the age of 3 or 4 years, and sometimes
considerably later (Howlin & Asgharian, 1999).
This was despite the fact that the DSM and ICD
diagnostic systems (American Psychiatric
Association [APA], 2000; World Health Organi-
sation [WHO], 1993) require that the symptoms
be evident in the first 3 years of life, although in
the proposed modifications in DSM-5, this
requirement has been changed to “Symptoms
must be present in early childhood (but may not
become fully manifest until social demands
exceed limited capacities).” However, nowadays
many children are now first identified in the
toddler and preschool period (Charman &
Baird, 2002; Mandell, Novak, & Zubritsky,
2005; Manning et al., 2011), although others, in
particular those with average or above average
language and cognitive abilities, are not diag-
nosed until school age or older. Several factors
have driven this change, including efforts to
improve earlier identification with the recogni-
tion that earlier-delivered intervention may
improve outcomes and prevent “secondary”
neurodevelopmental disturbances (Dawson,
2008; Mundy, Sullivan, & Mastergeorge, 2009):
the development of prospective screening instru-
ments to identify possible cases of autism from
the first few years of life (Barbaro &
Dissanayake, 2009); and the use of the genetic
“high-risk” research design of prospectively
studying younger siblings of children with
a diagnosis of ASD from the first year of life
(Rogers, 2009; Yirmiya & Charman, 2010).
E 1026
Current Knowledge
One of the most significant challenges and con-
cerns of this new era of prospectively studying
children with autism spectrum disorders from the
age of 2 and 3 years concerns diagnosis. Given
the relatively lack of experience of applying the
diagnostic criteria to children of this age, even
among the relatively expert clinical teams
conducting such research programs, one critical
question was whether the diagnosis was possible,
accurate, and stable when applied to toddlers at
the age of 2 or 3? Over the past decade, a number
of research teams have followed up children first
seen at the age of 2 years into early, and more
recently middle, childhood and provided an
answer, to some extent, to this important
question.
A number of studies have examined the sta-
bility and accuracy of diagnosis, both in samples
of children referred for assessment at an early age
and from screening studies. Over the past decade,
these diagnostic outcome studies have followed
cohorts of children from initial diagnostic assess-
ments around the age of 2 years into the preschool
years and in several of the more recent studies
(Charman et al., 2005; Lord et al., 2006; Turner,
Stone, Pozdol, & Coonard, 2006) into the school
age years. The first series of studies (Cox et al.,
1999; Lord, 1995; Moore & Goodson, 2003;
Stone et al., 1999) all showed high stability of
diagnosis in particular for “core” autism, with
somewhat lower stability for broader autism
spectrum disorder (ASD) and pervasive
developmental disorder not otherwise specified
(PDD-NOS). The movement across the ASD/
PDD-NOS diagnostic category boundary was
somewhat different in the different studies, with
Stone et al. (1999) finding that 4 out of 12 chil-
dren who met broader ASD criteria at the initial
assessment did not meet criteria for an autism
spectrum disorder at follow-up, whereas Cox
et al. (1999) found that 7 from 31 children who
did not receive an autism spectrum diagnosis at
the initial assessment met criteria for broader
ASD at follow-up. Several of the early studies
(Cox et al., 1999; Lord, 1995; Stone et al., 1999)
concluded that for 2-year-olds, expert clinical
Early Diagnosis
judgment is more reliable than the standard diag-
nostic instruments. Several studies also found
that behaviors from the third symptom cluster
that defines autism – restricted and repetitive
behaviors and activities – were less evident at 2
years of age than at 3–5 years of age (Cox et al.,
1999; Moore & Goodson, 2003; Stone
et al., 1999).
The more recent studies differ in a number of
features, most notably in that some have consid-
erably larger sample sizes (N ¼ 172, Lord et al.
2006; N ¼ 89, Chawarska, Klin, Paul, Macari, &
Volkmar 2009; N ¼ 77, Kleinman et al. 2008)
and that the follow-up periods extend to age 7
years in the Charman et al. (2005) study and to
age 9 years in the Lord et al. (2006) and Turner
et al. (2006) studies. Broadly, the lessons are the
same – that the diagnosis of autism is highly
stable in these samples but that of broader ASD
is less so see Rondeau et al. (2011); for a review).
Lord et al. (2006) found that age 2 scores on
measures of repetitive and restricted behaviors
and activities predicted an autism diagnosis at
age 9 years. In some of these more recent studies,
there was greater movement from having an ASD
diagnosis at age 2 years to a non-spectrum diag-
nosis at age 4 (Kleinman et al., 2008; Turner &
Stone, 2007). While the authors report the factors
associated with these “good outcomes” – princi-
pally higher IQ and better language competency
– it is important to remain cautious regarding
predictors of poorer or better outcomes in chil-
dren diagnosed at such a young age.
Future Directions
For clinicians, the lesson is to accept that autism
is a developmental disorder and at a very young
age, there may be less certainty regarding the
pattern of behavior that a child is showing and
the likelihood of them continuing to meet diag-
nostic criteria into the future. Charman and Baird
(2002) discuss the importance of understanding
the diagnostic process as an iterative process to
be worked out between clinician teams and
parents over time and that concepts such as
a “working diagnosis” can be helpful. An
Early Diagnosis
important aspect of early diagnostic consultation
is an open and straightforward approach to the
negotiation of the diagnostic view with parents
over time. At the same time, clinical teams need
to be aware of the need to provide sufficient
certainty regarding the child’s condition
that they are not refused services following
assessment.
Clinical work is often concerned with those
children who do not clearly meet full criteria for
childhood autism but who have apparently milder
social problems or where there are mixed devel-
opmental difficulties. Clinical experience also
suggests that some children who show definite
features of autism earlier make remarkable devel-
opmental progress. Therefore, caution must be
used, especially under 3 years, for those children
with features of the broader autistic spectrum
who may attract a PDD diagnosis. Experienced
clinicians report that parents understand the
difficulties of certainty in developmental assess-
ment. Most appreciate honesty on professionals’
part about the difficulty of reaching a precise
prognosis on a very young child and can under-
stand a frank discussion about the possible
outcomes if accompanied by appropriate advice
and help for intervention. Understanding why
one’s child behaves as he or she does is half
way to doing something about it.
One other important clinical reminder is that
while the trajectory of early emerging impair-
ments in social and communication development
accompanied by rigid and repetitive behaviors
and interests characterizes many children on the
autism spectrum, there is a subgroup of particu-
larly verbal and able children who go on to
receive a diagnosis of autism (sometimes called
“high functioning autism”) or Asperger syn-
drome who may not receive a diagnosis in the
preschool years. There is also another group who
might meet diagnostic criteria for an autism spec-
trum disorder who do not receive an explicit
diagnosis – those individuals with moderate to
severe intellectual disability or those with an
already identified preexisting associated medical
condition. In a recent epidemiological study,
Baird et al. (2006) found that for cases meeting
research diagnostic criteria for an ASD following
1027 E
in-depth assessment, low IQ predicted those who
had not received a clinical diagnosis by local
clinical services by age 10 years.
One final caveat is that the studies summarized
have largely come from expert research clinical
centers specifically studying young cohorts of
children. In community settings in many coun-
tries, there is evidence including from recent
studies that for many children and their families,
a diagnosis is not confirmed until children are
E
well into the school age years and this has
implications for the training of community
practitioners (Wiggins, Baio, & Rice, 2006).
See Also
▶ Diagnosis and Classification
▶ Diagnostic Process
References and Readings
American Psychiatric Association. (2000). Diagnostic
and statistical manual of mental disorders (4th Ed. –
Text Revision) (DSM-IV-TR). Washington, DC:
Author.
Baird, G., Simonoff, E., Pickles, A., Chandler, S., Loucas,
T., Meldrum, D., et al. (2006). Prevalence of disorders
of the autism spectrum in a population cohort of chil-
dren in South Thames: The Special Needs and Autism
Project (SNAP). Lancet, 368, 210–215.
Barbaro, J., & Dissanayake, C. (2009). Autism spectrum
disorders in infancy and toddlerhood: A review of the
evidence on early signs, early identification tools, and
early diagnosis. Journal of Developmental and Behav-
ioral Pediatrics, 30, 447–459.
Charman, T., & Baird, G. (2002). Practitioner review:
Diagnosis of autism spectrum disorder in 2-and
3-year-old children. Journal of Child Psychology and
Psychiatry and Allied Disciplines, 43, 289–305.
Charman, T., Taylor, E., Drew, A., Cockerill, H., Brown,
J. A., & Baird, G. (2005). Outcome at 7 years of
children diagnosed with autism at age 2: Predictive
validity of assessments conducted at 2 and 3 years
of age and pattern of symptom change over time.
Journal of Child Psychology and Psychiatry, 46,
500–513.
Chawarska, K., Klin, A., Paul, R., Macari, S., & Volkmar,
F. (2009). A prospective study of toddlers with ASD:
Short-term diagnostic and cognitive outcomes. Jour-
nal of Child Psychology and Psychiatry, 50,
1235–1245.
E 1028
Cox, A., Klein, K., Charman, T., Baird, G., Baron-Cohen,
S., Swettenham, J., et al. (1999). Autism spectrum
disorders at 20 and 42 months of age: Stability of
clinical and ADI-R diagnosis. Journal of Child Psy-
chology and Psychiatry, 40, 719–732.
Dawson, G. (2008). Early behavioral intervention, brain
plasticity, and the prevention of autism spectrum disor-
der. Development and Psychopathology, 20, 775–803.
Howlin, P., & Asgharian, A. (1999). The diagnosis of
autism and Asperger syndrome: Findings from
a survey of 770 families. Developmental Medicine
and Child Neurology, 41, 834–839.
Johnson, C. P., Myers, S. M., & The American Academy of
Pediatrics Council on Children with Disabilities. (2007).
Identification and evaluation of children with autism
spectrum disorders. Pediatrics, 120, 1183–1215.
Kleinman, J. M., Ventola, P. E., Pandey, J., Verbalis,
A. D., Barton, M., Hodgson, S., et al. (2008). Diagnos-
tic stability in very young children with autism
spectrum disorders. Journal of Autism and Develop-
mental Disorders, 38, 606–615.
Lord, C. (1995). Follow-up of two-year-olds referred for
possible autism. Journal of Child Psychology and
Psychiatry and Allied Disciplines, 36, 1365–1382.
Lord, C., Risi, S., DiLavore, P. S., Shulman, C., Thurm,
A., & Pickles, A. (2006). Autism from 2 to 9 years of
age. Archives of General Psychiatry, 63, 694–701.
Mandell, D. S., Novak, M. M., & Zubritsky, C. D. (2005).
Factors associated with age of diagnosis among
children with autism spectrum disorders. Pediatrics,
116, 1480–1486.
Manning, S. E., Davin, C. A., Barfield, W. D., Kotelchuck,
M., Clements, K., Diop, H., et al. (2011). Early diag-
noses of autism spectrum disorders in Massachusetts
birth cohorts, 2001–2005. Pediatrics, 127, 1043–1051.
Moore, V., & Goodson, S. (2003). How well does early
diagnosis of autism stand the test of time? Follow-up
study of children assessed for autism at age 2 and devel-
opment of an early diagnostic service. Autism, 7, 47–63.
Mundy, P., Sullivan, L., & Mastergeorge, A. M. (2009).
A parallel and distributed- processing model of joint
attention, social cognition and autism. Autism
Research, 2, 2–21.
Rogers, S. J. (2009). What are infant siblings teaching us
about autism in infancy? Autism Research, 2, 125–137.
Rondeau, E., Klein, L. S., Masse, A., Bodeau, N., Cohen,
D., & Guile, J. M. (2011). Is pervasive developmental
disorder not otherwise specified less stable than autis-
tic disorder? A meta-analysis. Journal of Autism and
Developmental Disorders, 41, 1267–1276.
Stone, W. L., Lee, E. B., Ashford, L., Brissie, J.,
Hepburn, S. L., Coonrod, E. E., et al. (1999). Can
autism be diagnosed accurately in children under 3
years? Journal of Child Psychology and Psychiatry
and Allied Disciplines, 40, 219–226.
Turner, L. M., & Stone, W. L. (2007). Variability in
outcome for children with an ASD diagnosis at age 2.
Journal of Child Psychology and Psychiatry, 48,
793–802.
Early Intensive Behavioral Intervention (EIBI)
Turner, L. M., Stone, W. L., Pozdol, S. L., & Coonard,
E. E. (2006). Follow-up of children with autism spec-
trum disorders from age 2 to age 9. Autism, 10,
243–265.
Volkmar, F. R., State, M., & Klin, A. (2009). Autism and
autism spectrum disorders: Diagnostic issues for the
coming decade. Journal of Child Psychology and Psy-
chiatry, 50, 108–115.
Wiggins, L. D., Baio, J., & Rice, C. (2006). Examination
of the time between first evaluation and first autism
spectrum diagnosis in a population-based sample.
Journal of Developmental and Behavioral Pediatrics,
27, S79–S87.
World Health Organisation. (1993). Mental disorders:
A glossary and guide to their classification in accor-
dance with the 10th revision of the International Clas-
sification of Diseases: Research Diagnostic Criteria
(ICD-10). Geneva: Author.
Yirmiya, N., & Charman, T. (2010). The prodrome of
autism: Early behavioral and biological signs, regres-
sion, peri- and post-natal development and genetics.
Journal of Child Psychology and Psychiatry, 51,
432–458.
Early Intensive Behavioral
Intervention (EIBI)
Susan Hepburn
Department of Psychiatry & Pediatrics,
JFK Partners, University of Colorado at Denver,
Aurora, CO, USA
Definition
Early intensive behavioral intervention (EIBI) is
a treatment approach that is based upon the
principles of applied behavior analysis (ABA)
and the research of Ivar Lovaas and colleagues
at the UCLA Young Autism Project. The EIBI
approach has been extensively studied
and actively debated in the scientific literature,
popular media, and policy arena.
Historical Background
Developed by Lovaas and colleagues across
several years of research and development at the
University of California–Los Angeles, the EIBI
Early Intensive Behavioral Intervention (EIBI)
approach has been extensively studied and
actively debated in the scientific literature, popu-
lar media, and policy arena. Influenced by theo-
ries of learning and motivation, practitioners of
EIBI refer to it as “the science of teaching.”
Rationale or Underlying Theory
Applied behavior analysis is the overarching
philosophy underlying EIBI. Integrating princi-
ples from learning theory, operant conditioning,
behavioral economics, and motivational theory,
proponents of EIBI value the power of changing
aspects of the teaching context in order to
promote child gains. By providing systematic,
direct instruction in an intensive manner
(i.e., 30–40 h per week, 1:1 with an adult),
proponents of EIBI suggest that young children
with autism can improve significantly.
Treatment Participants
Early intensive behavioral intervention (EIBI) is
a treatment approach that is thought to benefit
children with autism who are younger than
5 years of age. Developers of the intervention
emphasize the importance of beginning when
a child is as young as possible, hopefully younger
than 3 1/2 years.
There is some evidence that children who are
more intellectually competent respond best to
EIBI.
Treatment Procedures
Based upon the principles of applied behavior
analysis (ABA), an EIBI program usually includes
these characteristics: (1) active engagement of the
child for 40 + h per week in (2) planful interven-
tion, (3) delivered primarily in direct, 1:1 child-
adult instruction (4) with specific individual goals,
(5) carefully operationalized instructional objec-
tives and procedures, and a (6) data collection
system to promote objective observation and
(7) analysis of a child’s behavioral responses to
1029 E
different aspects of instruction. (8) Teaching strat-
egies are then dynamically revised based upon this
analysis, (9) implemented consistently across
providers, and (10) evaluated again for effective-
ness by monitoring the child’s trajectory of skill
acquisition. The built-in evaluation system
enables families and providers to make dynamic
decisions about how and where to modify
approaches, as the child progresses and/or faces
new challenges. Young children participating in
E
this treatment usually spend 6–8 h per day
in treatment sessions, with breaks every 2–3 h.
Often, the sessions happen in the child’s home.
Efficacy Information
There is a debate between the proponents and
critics of the effectiveness research documenting
EIBI, as summarized below (see References and
Readings).
Proponents’ View
1. Meta-analytic methods (i.e., statistically
analyzing all available data across several dif-
ferent studies) and comprehensive scientific
reviews support the effectiveness of EIBI for
some, but not all, children (Eldevik et al.,
2011; Howlin, Magiati, & Charman, 2009;
Matson & Smith, 2007; Peters-Scheffer
et al., 2011; Reichow & Wolery, 2009).
2. Many of the teaching strategies used in EIBI
are evidence-based (National Standards
Project, 2010), including discrete trial train-
ing, frequent reinforcement, and ongoing
assessment of child behavior.
Critics’ Views of EIBI
1. It can be difficult to implement an intensive
treatment model for many families, both with
regard to time, family stress, and financial
resources (Gresham & MacMillan, 1998;
Schopler, Short & Mesibov, 1989).
2. Some of the studies that are in the literature
do not demonstrate a lot of improvement, and
it is difficult to know which children will
respond best to this particular model of
intervention.
E 1030
3. Some researchers are critical of features of the
studies which are frequently cited as demon-
strative of effectiveness of EIBI (i.e., Lovaas,
1987; McEachin et al., 1993; Smith et al.,
2000). For example, some early outcome stud-
ies reported a return to normal functioning for
a substantial number of children (Lovaas,
1987), which has been refuted by other scien-
tists (Shea, 2004). Some researchers have
expressed caution in interpreting the findings
for effectiveness of EIBI, in part due to the
ways the outcomes were measured and how
decisions about group membership were
made, issues of sample size, variability of
characteristics of children across studies, lack
of intervention fidelity across sites, and some
inconsistent findings in studies conducted at
replication sites (Bassett et al., 2000; Gresham
& MacMillan, 1997a, b; Howlin et al., 2009;
Myers et al., 2007; Spreckley & Boyd, 2008).
4. Developmentally oriented practitioners
suggest that the curricula are not sequenced/
implemented in a way that is consistent with
principles of effective early childhood
education.
5. Prioritizing 1:1 direct instruction with the
child usually means foregoing instruction in
group settings (i.e., preschool), and the child
may lack opportunities to learn social and
communication skills in real-life settings
with other children.
6. Some children become passive learners, coop-
erative in instructional sessions but not able to
spontaneously practice the targeted skill in
natural settings.
7. Parent and family involvement is not neces-
sarily a part of the intervention program.
Outcome Measurement
1. Many young children make significant gains
in overall developmental functioning with
this approach, with improvements in IQ
scores ranging from 15 to 25 points after 2
years of intensive intervention during early
childhood (see Fenske et al., 1985; Lovaas,
1987; McEachin et al., 1993; Sheinkopf &
Early Intensive Behavioral Intervention (EIBI)
Siegel, 1998; Smith, Groen & Wynn, 2000).
There is some evidence that children who
are more intellectually competent respond
best to EIBI.
2. Several studies examined school placement
and report that children receiving EIBI
were likely to be fully included in general
education classrooms at first grade (Sallows
& Graupner, 2005).
Qualifications of Treatment Providers
EIBI is most effective when delivered and
supervised by a team of well-trained profes-
sionals (Bibby et al., 2001; Smith et al., 2000).
EIBI teams tend to be multidisciplinary, with
team members who are certified behavior ana-
lysts, speech therapists, educators, occupational
therapists, and paraprofessionals.
See Also
▶ Applied Behavior Analysis
▶ Direct Instruction
▶ Lovaas Approach
▶ UCLA Young Autism Project
References and Readings
Scientific Studies Examining Effectiveness
Howard, J. S., Sparkman, C. R., Cohen, H. G., Green, G.,
& Stanislaw, H. (2005). A comparison of intensive
behavior analytic and eclectic treatments for young
children with autism. Research in Developmental
Disabilities, 26, 359–383.
Lovaas, O. I. (1987). Behavioral treatment and normal
educational and intellectual functioning in young
autistic children. Journal of Consulting and Clinical
Psychology, 55, 3–9.
Sallows, G. O., & Graupner, T. D. (2005). Intensive
behavioral treatment for children with autism: Four-
year outcome and predictors. American Journal on
Mental Retardation, 110, 417–438.
Critiques of EIBI
Shea, V. (2004).
Early Intervention
Publications That Review EIBI and Other Early
Intervention Programs
Harris, S. L., & Handleman, J. S. (2001). Preschool edu-
cation programs for children with autism (2nd ed.,
pp. 23–39). Austin, TX: Pro-Ed.
National Research Council, Committee on Educational
Interventions for Children with Autism. (2008). Edu-
cating children with autism. Washington, DC:
National Academy Press.
Vismara, L.A. & Rogers, S.J. (2007). Early intervention:
Teaching approaches with demonstrated success.
Autism Advocate, 48, Autism Society of America.
Books for Parents
Maurice, C., Green, G., & Luce, S. L. (1996). Behavioral
intervention for young children with autism: A manual
for parents and professionals. Austin, TX: Pro-Ed.
Websites
http://www.autismspeaks.org/whattodo/index.php
For a list of questions to ask about treatments: http://www.
nimh.nih.gov/health/publications/autism/treatment-
options.shtml
Early Intervention
Moira Lewis
Speech-Language Pathologist, Marcus Autism
Center Children’s Healthcare of Atlanta, Atlanta,
GA, USA
Synonyms
Birth-to-three; EI; Early intervention
Definition
Early intervention (EI) refers to publicly funded
programs available to infants and toddlers with
disabilities and their families, through the Indi-
viduals with Disabilities Education Act (IDEA),
first authorized by congress in 1986. EI programs
offer specialized health, educational, and thera-
peutic services designed to meet the needs of
children, from birth up until age 3, who have
a developmental delay or disability, and their
families. EI programs often have various names
among different states. For example, the
1031 E
statewide EI program in Connecticut is often
referred to by parents and professionals as
“Birth-to-three,” while those in Georgia use the
program name “Babies Can’t Wait.” EI programs
receive both federal and state funding, in order to
offer services to families free of charge.
To be eligible for services, children must be
less than 3 years of age and have a confirmed
disability or established developmental delay, as
defined by their state of residence, in one or more
E
of the following areas of development: cognitive,
communication, social-emotional, motor skills,
and/or adaptive skills.
Following developmental evaluation to deter-
mine eligibility, services are typically delivered
to children in their home, or within community
and center-based programs, or other natural envi-
ronments. EI service providers include special
educators, social workers, speech therapists,
physical therapists, occupational therapists,
nurses, psychologists, and nutrition specialists.
EI programming may also be provided to chil-
dren who are considered to be at risk of develop-
ing substantial delays if services are not provided.
The following are considered overarching
goals of EI: to reduce the likelihood of delays
among at-risk children, support improved out-
comes and independence among children with
developmental disabilities throughout the
lifespan, empower and educate families, and to
provide intervention to children, regardless of
race, ethnicity, or income.
See Also
▶ Early Diagnosis
▶ First Words Project
References and Readings
American Speech-Language-Hearing Association.
(2008). Roles and responsibilities of speech-language
pathologists in early intervention: Guidelines
(Guidelines). Retrieved from www.asha.org/policy
Matson, J. L., & Minshawi, N. F. (2006). Early interven-
tion for autism spectrum disorders: A critical analysis.
Oxford, UK: Elsevier.
E 1032
National Dissemination Center for Children with Disabil-
ities, Help for Babies (0–3) (n.d.). Overview of early
intervention. Retrieved from: http://www.nichcy.org/
babies/overview/Pages/default.aspx
National Dissemination Center for Children with
Disabilities (n.d.). State specific information.
Retrieved from: http://www.nichcy.org/Pages/
StateSpecificInfo.aspx
Early Language Milestone Scale
Moira Lewis
Speech-Language Pathologist, Marcus Autism
Center Children’s Healthcare of Atlanta,
Atlanta, GA, USA
Synonyms
Early language milestone scale-2; ELM scale-2
Description
The Early Language Milestone Scale-2 (ELM
Scale-2) was developed for use in pediatric clin-
ical settings as a brief screening of the language
abilities of children under the age of 3 years
(Coplan, 1993). Responses are obtained from
a combination of parental/caregiver report,
examiner observation, and direct testing. This
assessment has three sections: auditory expres-
sive, auditory receptive, and visual. It also
provides screening for speech intelligibility
(how understandable the child’s speech is) at
3–4 years of age. The instrument is composed of
43 items and takes approximately 10 min to
administer. The ELM Scale-2 is available in
English only.
Historical Background
The ELM Scale-2 was published in 1993,
authored by James Coplan, M.D.
Early Language Milestone Scale
Psychometric Data
The measure has a relatively small normed sam-
ple of under 200 children under 3 years of age
with no breakdown by age within the sample.
Eighty percent of the sample is classified as
white and 20% is classified as “nonwhite.” Eighty
percent of the sample is classified as middle-class
socioeconomic background and 20% from
“lower” socioeconomic background groups. The
manual reports higher inter-rather reliability, but
lower test-retest specificity. Concurrent validity
data reported supports the use of the ELMS-2 as
a screening instrument, to be completed prior
to a more thorough communication assessment,
if warranted. Although specificity is high,
suggesting the measure is valid for identifying
24-month-old children who have normal
language development, sensitivity is lower, so
that it may be less useful for identifying children
with the possibility of language delay.
Clinical Uses
This test is quick and easy to administer with little
training. Aside from standardized, comprehen-
sive language assessments administered by
trained speech-language pathologist, the ELM
Scale-2 can be administered by other medical
and healthcare practitioners in pediatric clinical
settings and early intervention settings.
The ELM Scale-2 contains scoring options, as
it may be administered using a “pass/fail” or
a point scoring method. The pass/fail method
yields a global pass or fail rating for the test as
a whole, whereas the point scoring yields percen-
tile values, standard scores, and age equivalents
for each area of language function mentioned
above. Its properties suggest it is a viable screen-
ing measure; however, due to the small and lim-
ited normative sample, standard scores provided
for the ELM Scale-2 must be used with caution.
See Also
▶ Expressive Language
▶ Receptive Language
Early Social-Communication Scales (ESCS) 1033 E
References and Readings Description

Coplan, J. (1993). Early language milestone scale-2. The Early Social Communication Scales is
Austin, TX: Pro-Ed.
a structured assessment designed to provide
Paul, R., & Lewis, M. (2007). Assessing communication
disorders. In A. Martin, F. Volkmar, & M. Lewis (Eds.), measures of individual differences in nonverbal
Child and adolescent psychiatry (pp. 371–376). communication skills in children with mental
New York: Guilford Press. ages between 8 and 30 months of age. The admin-
istration requires 15–25 min involving the
presentation of approximately 17 tasks which
provide opportunities for social communication.
E
Tasks include the presentation of object spectacle
Early Language Milestone Scale-2 toys (e.g., a wind-up toy), turn-taking tasks (e.g.,
ball play), social interaction (e.g., tickling), gaze
▶ Early Language Milestone Scale
following tasks, and opportunities to respond to
an invitation to play. The child is typically seated
across the table from the examiner, and may
be either seated in a chair or seated in their
Early Literacy parent’s lap.
The session is videotaped and from the record-
▶ Emergent Literacy ings, observers classify children’s behaviors into
the following mutually exclusive categories
of early social-communication: joint attention
behaviors (use of nonverbal behaviors to share
experiences), behavioral requests (use of nonver-
Early Multiword Utterances bal behavior to obtain objects or events), and
social interaction behaviors (ability to engage in
▶ Telegraphic Speech playful turn-taking behavior). These behaviors
are also classified based on whether or not they
are child-initiated bids or child responses to the
examiner.

Early Social Communication

Historical Background
▶ Preverbal Communication
The ESCS was first developed in 1982 and from
a Piagetian stage–based understanding of early
development, emphasizing the complexity of
a child’s social communicative skills within the
Early Social-Communication Scales
context of a child’s goals with a behavior (either
(ESCS)
communicative or interpersonal). In the previous
version, a set of 25 semi-structured situations
Amanda Steiner
were utilized to elicit social communication,
Yale Child Study Center, New Haven, CT, USA
with approximately 110 possible occurrences of
child behavior rated in terms of its complexity,
goal, and degree of initiation. The current
Synonyms abridged version of the ESCS was designed to
be utilized as a more practical research and
ESCS clinical tool.
E 1034
Psychometric Data
Several research studies have been conducted
exploring the performance of typically develop-
ing children and children with developmental
disabilities on the ESCS as well as the reliability
of the instrument. In addition, preliminary
normative information is available within the
ESCS manual (Mundy et al., 2003). In typical
populations, performance in responding to joint
attention on the ESCS between 14 and 17 months
was a significant predictor of subsequent recep-
tive language development (Mundy & Gomes,
1998). Research has been conducted on the
ESCS across several clinical populations, includ-
ing children with Down syndrome (Mundy,
Kasari, Sigman, & Ruskin, 1995; Mundy,
Sigman, Kasari, & Yirmiya, 1988) and also
infants at risk (Sheinkopf, Mundy, Claussen, &
Willoughby, 2004). In terms of ASD, research
suggests that children with ASD tended to
demonstrate the greatest deficits in joint attention
behaviors on the ESCS, although difficulties were
noted across all areas of nonverbal communica-
tion for children on the spectrum (Mundy,
Sigman, & Kasari, 1994). Moreover, children
with ASD displayed greater deficits in gestural
joint attention skills, and these skills significantly
predicted language development in children with
ASD (Mundy, Sigman, & Kasari, 1990).
Clinical Uses
The ESCS is largely utilized as a research tool (as
it requires detailed offline scoring); however, it
can also be used as a clinical tool by speech-
language pathologists, early childhood special-
ists, and psychologists, as well as other profes-
sionals trained to administer the assessment in
the context of a diagnostic or developmental
evaluation.
See Also
▶ Joint Attention
▶ Nonverbal Communication
Early Stanford-Binet, Fifth Edition (Early SB5)
References and Readings
Mundy, P., Delgado, C., Block, J., Venezia, M., Hogan,
A., & Seibert, J. (2003). A manual for the abridged
early social communication scales. Coral Gables, FL:
University of Miami.
Mundy, P., & Gomes, A. (1998). Individual differences in
joint attention skill development in the second year.
Infant Behavior and Development, 21, 469–482.
Mundy, P., Kasari, C., Sigman, M., & Ruskin, E. (1995).
Nonverbal communication and language development
in children with Down syndrome and children with
normal development. Journal of Speech and Hearing
Research, 38, 1–11.
Mundy, P., Sigman, M., & Kasari, C. (1990).
A longitudinal study of joint attention and language
development in autistic children. Journal of Autism
and Developmental Disorders, 20, 115–128.
Mundy, P., Sigman, M., & Kasari, C. (1994). Joint
attention, developmental level, and symptom presen-
tation in young children with autism. Development and
Psychopathology, 6, 389–401.
Mundy, P., Sigman, M., Kasari, C., & Yirmiya, N. (1988).
Nonverbal communication skills in Down syndrome
children. Child Development, 59, 235–249.
Sheinkopf, S., Mundy, P., Claussen, A., & Willoughby, J.
(2004). Infant joint attention skill and preschool
behavioral outcomes in at-risk children. Development
and Psychopathology, 16, 273–291.
Early Stanford-Binet, Fifth Edition
(Early SB5)
▶ Stanford-Binet Intelligence Scales and
Revised Versions
Early Start Denver Model
Sally J. Rogers
Department of Psychiatry and Behavioral
Sciences, UC Davis M.I.N.D. Institute,
Sacramento, CA, USA
Definition
The Early Start Denver Model (ESDM) is
a comprehensive early intervention for toddlers
with autism ages 12–48 months. The model
Early Start Denver Model
resulted from the collaboration of Sally Rogers
and Geraldine Dawson and their colleagues at the
University of Washington Autism Center, with
Rogers’ colleagues, especially Laurie Vismara, at
the University of California, Davis, and at JFK
Partners, University of Colorado Health Sciences
Center. The approach is manualized and
described in detail by Rogers and Dawson (2010).
The ESDM and the Denver Model (DM) that
preceded it were developed to target the core
deficits seen in toddlers and preschoolers with
autism: social orientation, attention, affect shar-
ing and attunement, imitation, joint attention,
language development, and functional and sym-
bolic play. The ESDM has an interactive commu-
nication- and relationship-based framework that
fosters active experiential learning by supporting
child spontaneity and initiative. It has
a developmental curriculum which incorporates
teaching techniques that have received empirical
support for improving skill acquisition.
The ESDM is based on a fusion of the Denver
Model, an affective and developmentally-based
intervention for children (ages 2–5) with autism
(Rogers, 2000); the nature of the teaching interac-
tions and the curricular priorities are influenced by
Stern’s model of infant interpersonal development
(Stern, 1985) and pivotal response training (PRT),
developed by Laura Schreibman and Robert and
Lynn Koegel (Koegel et al., 1989). PRT involves
a naturalistic application of applied behavior anal-
ysis (ABA) to develop language and social skills.
The main differences between ESDM and DM
involve (1) focus on toddlers ages 12–48 months in
the ESDM; (2) fusion of practices and principles of
PRT with those of the DM; (3) added concept and
explicit terminology from applied behavior analy-
sis; (4) more rigorous and defined measurement
practices; and (5) a well-defined curriculum appro-
priate for children 12–48 months of age.
The ESDM and DM have been tested in class-
room applications, in one-on-one delivery, in inten-
sive delivery of 15–20 hours a week, and via parent
delivery. The approach is flexible and designed to
be used (1) at home, embedded within typical play
and caretaking activities, and in child care and
preschool settings; (2) in 1:1 treatment sessions
including parent coaching provided by credentialed
1035 E
providers; and (3) in group programs that can pro-
vide individual support to a child.
Historical Background
Development of the Denver Model (DM) began
at the University of Colorado Health Sciences
Center in 1981, in response to demonstration
preschool funding from the US Department of
E
Education. The DM had a developmental and
pragmatic approach to language acquisition and
emphasis on learning through play and through
positive, lively relationships. An interdisciplin-
ary strategy, including a strong role of occupa-
tional therapy, positive behavior supports, and
a central role of parents, has persisted. The cur-
riculum tool was begun during this period and
enhanced and extended for toddlers in the ESDM.
The DM expanded into an approach suitable for
use as a 1:1 home-based program during the 1990s.
Replications in publically funded sites demon-
strated that the model could be implemented in
community settings and that child development
significantly accelerated with its use.
Significant enhancements of the model
occurred in the past 10 years, including more
rigorous definitions of delivery and measurement
and data collection procedures when the Univer-
sity of Washington tested the approach in
a randomized controlled trial with a focus on
toddlers (Dawson et al., 2010).
Rationale or Underlying Theory
Three theoretical models provide the foundations
for the ESDM curriculum and teaching practices.
These include Rogers and Pennington’s model of
interpersonal development in autism (Rogers &
Pennington, 1991), Dawson and colleagues’
model of autism as a disorder of social motivation
(Dawson et al., 2004), and the approach to learn-
ing defined by PRT (Schreibman & Pierce, 1993).
Rogers and Pennington (1991) hypothesized
a developmental model of autism that began with
biologically-based deficits in imitation abilities
and related impairments in emotional sharing
E 1036
and nonverbal communication in the first year of
life. The authors were influenced by Daniel
Stern’s 1985 model of interpersonal development
in infancy. This model presents a theory
concerning autism-specific impairments in three
developmentally critical behaviors – imitation,
emotion sharing, and joint attention. A main
focus of the ESDM is to address these critical
behaviors within affectively rich relationships
with responsive, sensitive others.
The ESDM has been influenced by research on
another core feature of autism: impaired social
motivation. Dawson and colleagues (Dawson
et al., 2004, 2005) have contributed to identifying
this characteristic in infants who will develop
autism, and they hypothesize that the biology of
autism involves a deficiency in social motivation
due to the infant’s lack of sensitivity to social
reward. This lack of sensitivity results in
a failure to have a normal preference and active
attention to social information, including others’
faces, voices, gestures, and speech. This failure,
combined with impairments in imitation, emo-
tional sharing, and joint attention, is an obstacle
to the child’s development of socio-emotional
and communicative skills. As a result, the child
with autism becomes increasingly removed from
the social world and all the learning experiences
that exist inside that world. The child falls farther
behind because he or she lacks the skills needed
to access the social learning environment.
Dawson and colleagues have suggested that this
lack of engagement not only alters the course of
behavioral development but also affects the way
neural systems, underlying the perception and
representation of social and linguistic informa-
tion, are developed and organized (Dawson,
2008). Several of the strategies utilized in the
ESDM are designed to increase the salience of
social rewards and enhance the child’s attention
and motivation for social interaction.
PRT involves a naturalistic use of applied
behavior analysis to develop language and social
skills. The approach is flexible and is designed to be
embedded within typical play and caretaking
activities at home and in child care and preschool
settings. PRT is an empirically supported practice,
given its documentation of enhanced child
Early Start Denver Model
motivation, spontaneity, and social initiation and
of improved language, maintenance and response
generalization, and for concomitant reductions in
unwanted behaviors. Child motivation is optimized
by the use of reinforcers related to the child’s goals
and responses and child choice, interspersing
acquired tasks with acquisition tasks, therapist rein-
forcement of attempts to perform the desired
behavior, and using activities that are highly moti-
vating to the child. Therapists take turns with the
child to share control of the interaction, to capture
child attention, and to model behavior that may not
be in the child’s repertoire.
These three orientations have in common the
view that autism impedes an infant’s interper-
sonal experiences. In so doing, it creates barriers
to social-communicative development, which
lead to greater impairments due to the loss of
social learning opportunities.
Goals and Objectives
Goals and Objectives
The goal of ESDM intervention is to increase child
social-communicative and relational learning. The
main intervention objectives are (1) to bring the
child into coordinated, interactive social relations
for most of his or her waking hours by supporting
all caregivers and therapists to embed ESDM tech-
niques into all daily activities; (2) to provide the
child with social learning tools involving imita-
tion, joint attention, language, and social play
through teaching inside all daily activities; and
(3) to embed a high frequency of specific dyadic
learning opportunities in each activity of daily life
and also into each intervention activity to “fill in”
the learning deficits that have resulted from the
past lack of social learning (Rogers, 2000). These
goals and objectives are accomplished with the
following ESDM guiding principles:
(a) A positive emotional exchange between chil-
dren and key adults. ESDM intervention
activities involve a series of play routines
which facilitate the child’s pleasure and
social engagement and create many opportu-
nities for shared affect and reciprocal
interactions.
Early Start Denver Model
(b) Joint activity routines (Ratner & Bruner,
1978) are the primary vehicle for teaching,
and the teaching episodes are carried out
inside this joint activity frame. The play
interactions are child-centered, in that chil-
dren’s choices and preferred activities and
materials are featured. The adult shares con-
trol of the play by selecting what objects are
available, what actions are modeled and
reinforced, and how activities are sequenced.
Joint activities involve objects and activities
that are found in natural environments for
children of this age. All developmental skills
are taught in this way, including the develop-
ment of a repertoire of sensory motor and
constructive, functional, and symbolic play.
(c) The ESDM is grounded in the science of
learning and uses teaching strategies consis-
tent with the principles of applied behavior
analysis. ABA has received empirical sup-
port, altering the symptoms associated with
both autism and general developmental
delays (Koegel, O’Dell, & Dunlap, 1988;
Lovaas, 1987). Core teaching techniques
from PRT that are emphasized in the model
include (1) obtaining child attention before
delivering an instruction or model; (2) using
a clear A-B-C format in teaching trials that
are embedded in play activities (the anteced-
ent stimulus precedes the behavior, which is
followed by a consequence); (3) reinforcing
target skills using intrinsic reinforcers where
they exist, pairing nonsocial reinforcers with
social attention, and delivering contingent
consequences; (4) using shaping, chaining,
prompting, fading, and error correction to
develop the antecedent-behavior link and to
shape a partial performance to a more accu-
rate performance.
(d) The language intervention approach comes
from the science of communication develop-
ment and recognizes that verbal language
develops from nonverbal communication
(Bates & Dick, 2002; Bruner, 1975). Both
verbal language and nonverbal communica-
tion coordinate people’s activities and allow
partners to share mental states: intentions,
desires, interests, thoughts, and feelings.
1037 E
In each intervention session, multiple and
varied communicative opportunities are pro-
vided and many communications, both ver-
bal and nonverbal, are elicited from the child.
The range of communicative functions is
developed so that a child not only requests
an activity but also protests, greets familiar
adults, shares attention, and comments, as
well as other functions. Children’s spontane-
ous communications exert much control over
E
interactions and activities, thus demonstrat-
ing the power of communication and assuring
its reinforcement.
(e) The ESDM views autism as disrupting devel-
opment in all domains (Goodman, 1989), and
it uses a multidisciplinary approach to
address specific domains. Children’s devel-
opmental skills are evaluated in each domain,
and intervention objectives are written for all
areas. Though developmental patterns in
autism have been understudied, research in
different domains has demonstrated that
young children with autism follow fairly nor-
mal trajectories of development even in their
affected areas (see Lifter, Sulzer-Azaroff,
Anderson, Coyle, & Cowdery, 1993 regard-
ing symbolic play; Tager-Flusberg et al.,
1990 regarding language development; and
Ungerer & Sigman, 1987 regarding early sen-
sory motor development). The curriculum
domain items were extracted from research
in early child development in multiple
domains: cognition, expressive and receptive
language, social-emotional development,
fine and gross motor development, self-care
skills, play, and imitation. The curriculum
was developed by a team of professionals
with expertise in developmental and clinical
psychology, applied behavior analysis, early
childhood special education, speech and lan-
guage pathology, and occupational therapy.
Developmental and clinical psychologists
contribute to the sequence of acquisition and
the normative strategies for interaction, cog-
nitive development, play, and imitation.
Applied behavior analysts contribute empiri-
cally derived strategies for effective teaching
and use of functional assessment and analysis
E 1038
to develop approaches for unwanted behav-
iors and effective teaching practices. Early
childhood special education contributes
expertise on cognition and play and pre-
academic development. Speech and language
pathology informs the sequence of speech
development, the varied functions of commu-
nication, and augmentative and alternative
communication approaches. Occupational
therapy informs the sequence and content of
motor and self-care skills, personal indepen-
dence, the use of activities to build develop-
mental skills, and optimization of arousal and
sensory responsivity to facilitate attention
and engagement in learning. Developmental
and behavioral pediatrics contributes knowl-
edge of the health concerns of individual
children which can interfere with children’s
ability to benefit from the intervention.
(f) The ESDM team provides oversight and con-
sultation regarding treatment design and
delivery to the parent and primary therapist
for each child. At this time, ESDM is primar-
ily delivered by parents and trained therapists
providing 1:1 teaching, though it can also be
used in group situations, and several research
studies are currently in progress concerning
efficacy of group delivery. Direct delivery of
the intervention is generally directed by one
professional, the team leader, or primary ther-
apist, working with parents and therapy assis-
tants in a generalist model, with the
multidisciplinary team supporting that pri-
mary provider. The generalist delivery
approach is used to keep the intervention con-
sistent across treatment sessions and as eco-
nomical as possible. It also models what
parents need to do: address all the child’s
needs. The full team is available as consul-
tants to the primary therapist and family.
When ESDM is delivered in a group pre-
school setting, the classroom teacher takes
the generalist role. The team leader must be
credentialed in his or her profession and cer-
tified as an ESDM therapist. The team leader
is responsible for a variety of tasks: working
with the parents to learn ESDM at home and
to assess children’s strengths and needs;
Early Start Denver Model
administering the Curriculum Checklist quar-
terly and writing 3-month objectives and
breaking them down into teaching steps;
delivering the intervention and supporting
the parents to do so; training and supervising
any noncredentialed person who is helping to
deliver ESDM; coordinating care with other
professionals; and keeping and analyzing
daily data and adapting the intervention plan
as needed to foster rapid child progress.
(g) Parent learn to deliver ESDM at home from
their team leader, since the embedding of
ESDM techniques throughout daily care and
play routines is fundamental to the model and
necessary for optimal progress. A manual for
parents is published by Rogers, Dawson, and
Vismara, An Early Start for Your Child with
Autism: Using Everyday Activities to Help
Kids Connect, Communicate, and Learn
(2012, Guilford Press).
Treatment Participants
The approach is developed for young children
with autism, ages 12–48 months, and develop-
mental quotients over 35 and has been demon-
strated to be effective for children with a wide
range of skill levels. However, it has only been
tested with ambulatory children who have func-
tional hand use and are interested in toys and
other objects. It has not been tested with children
who have additional diagnoses like Down syn-
drome or fragile X. In all trials of ESDM, parents
have learned to use the methods at home. Effec-
tiveness when parents have not learned to use the
method and are not supported on a weekly basis
has not been tested.
Treatment Procedures
Each child’s learning plan is defined by short-term
objectives that represent what is to be learned over
a 12-week period and activities carried out daily to
teach the objectives. The objectives are derived
from a curriculum assessment carried out each
12 weeks using the ESDM Curriculum Checklist
Early Start Denver Model
(Rogers & Dawson, 2010). The ESDM Curricu-
lum Checklist covers the following domains:
receptive communication, expressive communica-
tion, social interaction, imitation skills, cognitive
skills, play skills, fine motor skills, gross
motor skills, independence/behavior, and joint
attention. Each objective is broken down into
5–6 teaching steps that lay out the build-up of
the skill. A daily data sheet allows the therapist
to teach skills and track progress in very small
steps.
Fourteen aspects of the teaching process are
quantified in the ESDM fidelity tool. A primary
characteristic involves child-initiated activities in
which adults embed instruction into play and
other daily functional activities, since this kind
of teaching has demonstrated gains in spontane-
ity, motivation, maintenance, and generalization.
Adults provide children with choices of materials
and activities to support learning of the targeted
objectives and to maximize attention and moti-
vation, while considering the child’s preferences,
age, developmental skills, and learning style.
Joint activity routines (Ratner & Bruner,
1978) are the vehicle for teaching. A joint activity
routine involves a four-part play activity between
child and adult that allows for an activity to
be begun, developed, elaborated, and completed.
Objectives from two or more different develop-
mental domains are addressed in each
2–5-minutes joint activity routine. Learning
opportunities occur approximately every 10–15
seconds during these activity routines. Transi-
tions between activities are responsive to chil-
dren’s need for change and are accomplished in
a fashion that fosters child independence, moti-
vation, and choice. Adult emotion is expected to
be warm, positive, and playful. Adults and chil-
dren interact reciprocally with objects and in
communication exchanges, taking turns and shar-
ing leader-follower roles.
Another key aspect of the teaching process
involves adult language. Adults use natural lan-
guage fit to the child’s ongoing activity and syntac-
tically constructed using the “one up” rule, which
specifies that the adult’s language should involve
sentence length that is roughly one word longer
than the child’s typical sentence. Adults are to
1039 E
narrate, comment, and label actions, objects, and
emotions; to model appropriate gestures and
speech; and to expand child utterances rather than
to question children or tell them what to say.
Children’s communication begins with gestural
development and multiple pragmatic intents, with
a focus on phonetic development, development of
intentional vocalization, and reciprocal and mean-
ingful vocal exchanges.
Adult-child interactions are playful and follow
E
children’s interests and motivations, addressing
short-term objectives from multiple domains.
Adults are expected to provide clear learning
opportunities, at a rate of several per minute.
A systematic decision process (response to
intervention [RTI]) is used in ESDM to “tailor
the treatment,” by systematically altering teaching
procedures if children are not progressing rapidly.
This decision tree (Rogers & Dawson, 2010) is
highly articulated and allows for a “toolbox” of
empirically-based teaching practices for young
children with autism to be used if needed, but it
prescribes how, when, and for how long, to alter
the basic ESDM teaching processes. While the
basic ESDM teaching approach favors naturalistic
teaching, warm and emotionally positive relation-
ships, varied activities, intrinsic reinforcers, and
shared control, no empirically supported teaching
approach is “off limits”. However, the quality of
relationship and communication principles of
ESDM is embedded regardless of what specific
teaching practices are being used.
Parents are an integral part of ESDM, and their
priorities, values, and child-rearing practices are
incorporated into quarterly child objectives, teach-
ing practices, and assessment of progress (Vismara,
Colombi, & Rogers, 2009a). Parents learn to incor-
porate the ESDM approach into caretaking and
family routines as well as play activities. The trans-
mission process involves a coaching relationship
between provider and parents. The goal of parent
coaching is to promote the child’s social-
communication and cognitive development and to
promote parent-child communication and play, to
foster parents’ feelings of competence and confi-
dence in their interactions with their child, and to
maximize child learning opportunities (Vismara,
Young, Stahmer, Griffith, & Rogers, 2009b).
E 1040
Efficacy Information
DM effects as a group preschool intervention were
first examined in a series of papers examining
pre-post test data (Rogers & DiLalla, 1991; Rogers
& Lewis, 1989). Significant accelerations in devel-
opmental rates of young children with autism were
found in cognition, language, reduction in autism
symptoms, symbolic play, and social engagement.
As a group, the children with autism doubled their
developmental rates while in active treatment. Four
independent replications of the model (Rogers
et al., 2006) demonstrated significant accelerations
of developmental rates within 6 months of imple-
mentation. These studies suggested that the DM has
the capacity to affect development in many areas.
The first study of the DM as an individually
delivered intervention used a single-subject
design which randomized minimally verbal
preschoolers to either the DM or the PROMPT
treatment (Rogers et al., 2006). PROMPT is
a method for treating apraxia of speech devel-
oped by Deborah Hayden (formerly Chumpelik)
and her colleagues in the early 1980s. The tech-
nique was originally developed for adults suffer-
ing apraxia of speech secondary to brain injury
(Chumpelik, 1984). PROMPT involves physical
stimulation of the speech motor system during
intentional communicative vocalization or
verbalization. The DM delivery involved 1 hour
of individual treatment and parent training
weekly and daily 1-hour home parent practice
sessions for 12 weeks. Eighty percent of children
in both approaches acquired functional speech at
a frequency of 10–200 words per hour
(Rogers et al., 2006).
The most important outcome study of ESDM
used a randomized controlled design with 48 tod-
dlers with autism, ages 18–30 months (Dawson
et al., 2010). The ESDM group received 15 hours
per week of individual home treatment over a
24-month period, as well as 4 hours per month of
parent coaching. The comparison group received
a variety of community interventions for the same
period of time. Over a 24-month period, the ESDM
group demonstrated large and highly significant
increases compared to the community intervention
group in overall IQ gains, receptive and expressive
Early Start Denver Model
language gains, and adaptive behavior functioning.
These differences were not likely due to the number
of intervention hours delivered, since the two
groups’ intervention hours were very similar. Fol-
low-up studies of these children will determine the
trajectory of their development five years after this
study. A multisite replication of this study involv-
ing 100 12–24-month-olds is ongoing.
Outcome Measurement
Child learning objectives in all core developmen-
tal areas are written every 12 weeks. Child pro-
gress is monitored after every 15 minutes of
treatment on “daily data sheets” developed from
the child’s short-term objectives. Measurable
progress is expected on every objective within
a 1–2-week period and mastery of all objectives
is assessed every 12 weeks. New objectives are
written and broken down into small teachable
steps, and new data sheets are developed at
these 12-week intervals. Annual progress is mea-
sured through a battery of standardized tests,
involving development, adaptive behavior,
vocabulary and gesture use, and the Autism Diag-
nostic Observation Schedule (ADOS; Lord,
Rutter, DiLavore, & Risi, 1999) to measure the
number and severity of autism symptoms.
Qualifications of Treatment Providers
ESDM treatment providers have completed mul-
tiple levels of training and have received certifica-
tion as ESDM therapists. Those who coach
families to use ESDM at home have also been
certified as ESDM parent coaches, and those who
train others to use ESDM are certified as ESDM
trainers. Training is available at multiple sites in
the USA and abroad, and those seeking training
can find information on the ESDM website. All
ESDM published studies were carried out by
trained and credentialed therapists and staff. Pro-
fessionals from a wide number of disciplines may
be trained as ESDM therapists. Those professions
include occupational therapy, physical therapy,
speech and language pathology, early childhood
Early Start Denver Model
education, early childhood special education,
clinical child psychology, school psychology,
and other professions that include background
in early childhood development as part of the
graduate curriculum. Those without a professional
credential cannot be certified as an ESDM
therapist, though they may work under the training
and supervision of an ESDM-credentialed
therapist.
The ESDM was developed to be provided by
a team of childhood professionals with training
and experience in early autism intervention from
a variety of disciplines. The team leader is
credentialed in their profession and as an ESDM
provider and is responsible for a variety of tasks:
working with the parent to assess the child’s
needs and strengths; developing short-term
objectives and breaking them down into teaching
steps; delivering the intervention and supporting
the parent to do so; training and supervising any
nonlicensed persons who are helping deliver
ESDM; and keeping and analyzing data to assure
child progress or to adapt the intervention
methods to improve progress.
Parents learn to deliver ESDM at home from
their team leader, since the embedding of ESDM
techniques in play and caretaking routines is nec-
essary for optimal progress. Materials are avail-
able to help parents adopt the techniques, and
a manual is currently being published (Rogers,
Dawson, & Vismara, 2012).
For children who are receiving many hours of
ESDM weekly, well-trained paraprofessionals
may deliver the intervention under the ongoing
supervision of the team leader. Paraprofessionals
learn to deliver the model at appropriate levels of
fidelity of intervention under the supervision and
guidance of trained ESDM professionals. Fidelity
should be checked frequently when multiple
adults are delivering ESDM. Team meetings
should occur at least every 2 weeks to review
child progress, discuss the intervention plan,
and assure intervention consistency.
While printed ESDM materials are available
to the public, it is usually necessary to attend
specific training to master the ESDM. Those
wanting to learn ESDM can access training mate-
rials through the MIND Institute website.
1041 E
Information about training workshops in various
cities and countries is also posted.
http://www.ucdmc.ucdavis.edu/mindinstitute/
research/esdm/certification.html
See Also
▶ ABA
▶ Imitation E
▶ Joint Attention
▶ Occupational Therapy (OT)
References and Readings
Bates, E., & Dick, F. (2002). Language, gesture, and the
developing brain. Developmental Psychobiology, 40(3),
293–310.
Bruner, J. (1975). The ontogenesis of speech acts. Journal
of Child Language, 2, 1–19.
Chumpelik, D. (1984). The PROMPT system of therapy:
Theoretical framework and applications for developmen-
tal apraxia of speech. Seminars in Speech and Language,
5, 139–156.
Dawson, G. (2008). Early behavioral intervention, brain
plasticity, and the prevention of Autism spectrum disor-
der. Development and Psychopathology, 20, 775–803.
Dawson, G., Rogers, S., Munson, J., Smith, M., Jamie, W.,
Greenson, J., et al. (2010). Randomized controlled trial
of the early start denver model: A developmental behav-
ioral intervention for toddlers with Autism: Effects on
IQ, adaptive behavior, and autism diagnosis. Pediatrics.
doi:10.1542/peds.2009-0958.
Dawson, G., Toth, K., Abbott, R., Osterling, J., Munson, J.,
Estes, A., & Liaw, J. (2004). Early social attention
impairments in Autism: Social orienting, joint attention,
and attention to distress. Developmental Psychology,
40(2), 271–283.
Dawson, G., Webb, S. J., & McPartland, J. (2005). Under-
standing the nature of face processing impairment in
autism: Insights from behavioral and electrophysio-
logical studies. Developmental Neuropsychology,
27(3), 403–424.
Goodman, R. (1989). Infantile Autism: A syndrome of
multiple primary deficits. Journal of Autism and
Developmental Disorders, 19(3), 409–424.
Koegel, L. K., Koegel, R. L., Hurley, C., & Frea, W. D.
(1992). Improving social skills and disruptive behavior
in children with Autism through self-management.
Journal of Applied Behavior Analysis, 25, 341–353.
Koegel, R. L., O’Dell, M. C., & Dunlap, G. (1988). Pro-
ducing speech use in nonverbal Autistic children by
reinforcing attempts. Journal of Autism and Develop-
mental Disorders, 18, 525–538.
E 1042
Koegel, R. L., Schreibman, L., Good, A., Cerniglia, L.,
Murphy, C., & Koegel, L. (1989). How to teach pivotal
behaviors to children with Autism: A training manual.
Santa Barbara, CA: University of California.
Lifter, K., Sulzer-Azaroff, B., Anderson, S. R., Coyle, J. T.,
& Cowdery, G. E. (1993). Teaching play activities to
preschool children with disabilities: The importance of
developmental considerations. Journal of Early Inter-
vention, 17, 139–159.
Lord, C., Rutter, M., DiLavore, P., & Risi, S. (1999).
Autism diagnostic observation schedule: Manual.
Los Angeles, CA: Western Psychological Services.
Lovaas, O. I. (1987). Behavioral treatment and normal
education and intellectual functioning in young Autis-
tic children. Journal of Consulting and Clinical Psy-
chology, 55, 3–9.
Ratner, N., & Bruner, J. (1978). Games, social exchange,
and the acquisition of language. Journal of Child
Language, 5, 391–402.
Rogers, S. J. (2000). Interventions that facilitate sociali-
zation for children with Autism. Journal of Autism and
Developmental Disorders, 30(5), 399–410.
Rogers, S. J. & Dawson, G. (2010). Early Start Denver
Model for young children with autiss: Promoting
language, learning, and engagement. NY: Guilford
Press.
Rogers, S. J., & Dawson, G. (2010). Early Start Denver
Model curriculum checklist for young children with
Autism. New York: Guilford.
Rogers, S. J., & DiLalla, D. L. (1991). A comparative
study of the effects of a developmentally based pre-
school curriculum on young children with Autism
and young children with other disorders of behavior
and development. Topics in Early Childhood Special
Education, 11(2), 29–47.
Rogers, S. J., Hall, T., Osaki, D., Reaven, J., & Herbison, J.
(2000). The Denver model: A comprehensive, inte-
grated, educational approach to young children with
Autism and their families. In S. Harris & J. Handleman
(Eds.), Preschool education programs for children with
Autism (2nd ed.). Austin, TX: Pro-Ed.
Rogers, S. J., Hayden, D., Hepburn, S., Charlifue-Smith,
R., Hall, T., & Hayes, A. (2006). Teaching young
nonverbal children with Autism useful speech:
A pilot study of the Denver Model and PROMPT
interventions. Journal of Autism and Developmental
Disorders, 36(8), 1007–1024.
Rogers, S. J., & Lewis, H. (1989). An effective day
treatment model for young children with pervasive
developmental disorders. Journal of the American
Academy of Child and Adolescent Psychiatry, 28,
207–214.
Rogers, S. J., & Pennington, B. F. (1991). A theoretical
approach to the deficits in infantile Autism. Develop-
ment and Psychopathology, 3(2), 137–163.
Rogers, S. J., Dawson, G, & Vismara, L. A. (2012). An
early start for your child with autism; Using everyday
activities to help kids connect, communicate, and
learn. NY: Guilford Press.
Eating Disorders
Schreibman, L., & Pierce, K. (1993). Achieving greater
generalization of treatment effects in children with
autism: Pivotal response training and self-manage-
ment. Clinical Psychology, 46, 184–191.
Stern, D. N. (1985). The interpersonal world of the infant:
A view from psychoanalysis and developmental psy-
chology. New York: Basic Books.
Tager-Flusberg, H., Calkins, S., Nolin, T., Baumberger,
T., Anderson, M., & Chadwick-Dias, A. (1990).
A longitudinal study of language acquisition in Autis-
tic and down syndrome children. Journal of Autism
and Developmental Disorders, 20(1), 1–21.
Ungerer, J. A., & Sigman, M. (1987). Categorization
skills and receptive language development in Autistic
children. Journal of Autism and Developmental
Disorders, 17(1), 3–16.
Vismara, L. A., Colombi, C., & Rogers, S. J. (2009a).
Can 1 hour per week of therapy lead to lasting changes
in young children with Autism? Autism: an Interna-
tional Journal, 13(1), 93–115.
Vismara, L. A., Young, G. S., Stahmer, A. C., Griffith,
E. M., & Rogers, S. J. (2009b). Dissemination of
evidence-based practice: Can we train therapists from
a distance? Journal of Autism and Developmental Dis-
abilities, 39(12), 1636–1651.
Eating Disorders
Annemarie van Elburg
Child and Adolescent Psychiatry, Rintveld center
for Eating Disorders, Altrecht Mental Health
Institute, University Medical Center Utrecht,
Utrecht, The Netherlands
Synonyms
Anorexia; Bulimia nervosa; Pica; Rumination
disorder
Short Description or Definition
Eating disorders like anorexia and bulimia
nervosa (AN/BN) are complex psychosomatic
disorders of unknown etiology, primarily affect-
ing adolescent girls and young women. They are
characterized by aberrant patterns of eating
behavior and weight regulation which in AN
result in weight loss and endocrine abnormalities
Eating Disorders
such as amenorrhea, disturbances in attitude
and perception about weight and shape, and an
intense fear of gaining weight. Patients are
classified AN according to the Diagnostic and
Statistic Manual 4th edition (DSM-IV, American
Psychiatric Association, 1994) when they are
incapable to maintain a body weight above
a minimal normal level (BMI < 17.5 kg/m2 for
adults), demonstrate an intense fear of becoming
fat, have disturbed perceptions of body shape and
size, and (after menarche) show amenorrhea.
Two subgroups are classified, the restricting
type in which weight loss is the result of dietary
restriction and the binge/purge type in which
periods of binging or purging and dietary restric-
tion coexist. When compared to other psychiatric
disorders, AN has the highest mortality rate:
10–15%. BN shares many features with AN but
for the weight loss.
Accompanying symptoms, such as perfection-
ism, obsessive-compulsive behavior, and social
anxiety, are observed in many but not all patients.
This characteristic cluster of personality and
temperamental traits often persists after recovery
and has been described preceding the onset of
disease as well. In addition, a large proportion
of AN patients displays abnormally high physical
activity levels and over exercises, although
estimations vary from 31% to 80% because of
definition difference.
Although the etiology of AN is as yet unclear,
a combination of cultural, social, psychological,
genetic, and biological factors is implicated:
“Genes load the gun, environment pulls the
trigger” (Bulik & Tozzi, 2004).
Other problems sometimes observed include
pica (eating of nonnutritive substances) and rumi-
nation (repeated regurgitation and rechewing of
food).
Categorization
The combination of eating disorders with
autism spectrum disorders is uncommon and
little researched. Most studies focus on disturbed
eating behavior in autistic children. Some studies
find that the behaviors themselves also occur in
1043 E
normally developing children, but much less
often. Normally developing children seem to
outgrow these behaviors while children with
a disorder in the autistic spectrum do not.
Two-thirds of parents of children with autistic
spectrum disorder describe picky eating in their
children. The most frequently described eating
disturbances are food neophobia and selective
eating; other disturbances such as pica and
rumination seem to be more common in autism
E
associated with mental retardation.
Problems with eating – including particular
food refusal, food fads, pica, hoarding, overeat-
ing, and various degrees of anorectic behaviors,
including complete food refusal and compulsive
ordering of food on the plate – are extremely
common in autism. Pica and rumination may
also be seen.
Epidemiology
The total incidence of AN in the Netherlands
is relatively stable. In the period of 1995–1999,
the age and sex adjusted incidence rate was
7.7/100,000. Interestingly, the incidence in
female 15–19-year-olds (as well as 10–14-year-
olds) almost doubled when compared to 10 years
before, indicating that the onset of the disease is
currently taking place at a younger age (Van Son,
2006). Average prevalence rates of AN in Europe
appear stable at 0.29% (Hoek & van Hoeken,
2003).
In a controlled study of representative cases of
anorexia nervosa, 18% had an autism spectrum
disorder (4% autistic disorder, 6% Asperger
syndrome, and 8% atypical autism), both at the
time of onset of the eating disorder (around
15 years of age) and 5 and 10 years later.
Natural History, Prognostic Factors,
and Outcomes
Recovery of anorexia nervosa in general takes
a long time; it has been reported that stable phys-
ical recovery is reached after on average 4.7 years
and psychosocial recovery after 6.6 years. Final
E 1044
outcome figures of AN leave room for improve-
ment. According to Steinhausen (2002), 20.8%
(0–79%) of AN patients remain chronically ill,
and 5.3% (0–22%) die as a consequence of star-
vation or by suicide. Chances for recovery range
from 0% to 92%, averaging at 46.5%. Data in
younger patient groups are more optimistic,
reaching about 60% for complete recovery.
Clinical Expression and
Pathophysiology
A large number of studies indicate that there may
be a propensity for underweight or comorbid
eating disorders. One-fourth of male cases with
autism of Asperger syndrome had a BMI in the
5th percentile or below, though no eating disorder
diagnoses were justified. No association was
found between autistic behavior and BMI, but
there was a small effect of hyperactivity.
Disturbed Eating Behaviors in ASD
Rumination, the repetitive regurgitation of
recently ingested food into the mouth with sub-
sequent spitting or remastication and swallowing,
has been described in adolescents and adults with
autism. It can lead to tooth erosion caused by
gastric acid, as well as malnutrition and esopha-
geal abnormalities.
Pica, or eating inedible nonfood substances,
seems to be a problem especially in institutional-
ized cases of mental retardation associated with
autism. When present, it is potentially dangerous
and difficult to treat. Pica may result in gastroin-
testinal problems or poisoning with heavy metals.
Overeating.
Eating disturbances in Asperger, teenage
boys: selective eating and hyperactivity resulting
in low body weight. In adults with ASD and
normal intelligence, health reasons are often
given for special diets.
Psychogenic polydipsia (excessive water
intake) presents a problem in autism with mental
retardation.
Food neophobia is the avoidance of all new
foods. This has been linked to selective eating but
should be treated separately.
Eating Disorders
Selective eating (eating only ten foods or
fewer, sometimes food of a special color, texture,
or brand, avoidance or refusal of new foods)
Proposed Underlying Mechanisms in
Disturbed Eating Behaviors in ASD
Sensory abnormalities: Hyper/hyposensitivity
to auditory, visual, tactile stimuli and to smell
and taste may play a large part in mealtime
behaviors.
Interests: Restricted and intense ideas and
interests, for example, having strict ideas
about the appropriate amount of food required
without paying attention to feeling of hunger
or satiety, fixating on ideas of which food are
healthy etc.
Routines: Ritualized eating routines.
Social interaction and other skills involved
in dining: Eating with other people is an ordeal
for many persons with autism because of doing
several tasks simultaneously, leading to unusual
table manners in some cases.
Motor functioning: Motor problems are
common in ASD, which can make the use of
knife and fork difficult.
Gastrointestinal problems: A high rate of
gastrointestinal symptoms is reported in children
with ASD compared to peers, in most cases
without known medical causes.
Anorexia nervosa: It is suggested that ASD
and AN share some features, namely, obsessive-
ness, insistence on sameness, and social impair-
ment. It is suggested that a subgroup of AN
has a cognitive style very similar to ASD.
Gender issues: AN and Asperger are both
considered to be specific to one gender; perhaps
if the criteria of AN would be reconsidered with
the male population in mind, and the Asperger
criteria would include more behaviors and atti-
tudes more appropriate to females, much more
overlap would occur.
Evaluation and Differential Diagnosis
Evaluation and assessment vary depending on the
nature of the eating problem. In all cases,
a careful search for possible contributory factors
Echolalia
(environmental, associated medical conditions,
and so forth) is indicated. Weight loss and eating
problems can be observed in various disorders
(e.g., depression), and sometimes unusual beliers
about food or eating are seen in other psychiatric
conditions (e.g., schizophrenia). Diagnosis can
be more complicated in individuals with autism
and with cognitive disability.
Treatment
Treatments vary depending on the specific of the
situation and the nature of the difficulty. Some
syndromes of intellectual disability are associ-
ated with eating problems. For pica and rumina-
tion disorder, various behavioral procedures have
been used. In younger children, it is important to
be sure that other medical problems or environ-
mental factors do not complicate the situation. In
anorexia nervosa and bulimia nervosa, treatment
is topically multifaceted with outpatient treat-
ment preferred if possible. Pharmacological
treatments may be combined with cognitive
behavior therapy approaches depending on the
specific situation.
See Also
▶ Asperger Syndrome
▶ Cognitive Flexibility
▶ Extreme Male Brain (EMB) Theory
▶ Gender Differences
▶ Pica
▶ Rumination
▶ Weak Central Coherence
References and Readings
Bölte, S., Özkara, N., & Poutska, F. (2002). Autism
spectrum disorders and low body weight: Is there
really a systematic association? International Journal
of Eating Disorders, 31, 349–351.
Råstam, M. (2008). Eating disturbances in autism
spectrum disorders with focus on adolescent and
adult years. Clinical Neuropsychiatry, 5, 31–42.
1045 E
Schreck, K. A., Williams, K., & Smith, A. F. (2004).
A comparison of eating behaviors between children
with and without autism. Journal of Autism and
Developmental Disorders, 34, 433–434.
Volkmar, F. R., & Martin, A. (2011). Essentials of child
and adolescent psychiatry. Philadelphia: Lippincott,
Williams, and Wilkins.
Zucker, N. L., Losh, M., Bulik, C. M., LaBar, K. S.,
Piven, J., & Pelphry, K. A. (2007). Anorexia nervosa
and autism spectrum disorders: Guided investigation
of social cognitive endophenotypes. Psychological
Bulletin, 133, 976–1006.
E
Echolalia
Moira Lewis
Speech-Language Pathologist, Marcus Autism
Center Children’s Healthcare of Atlanta,
Atlanta, GA, USA
Synonyms
Delayed echolalia; Imitative speech; Immediate
echolalia; Scripting
Definition
Echolalia, either immediate or delayed, is the
repetition of sounds, words, phrases, or larger
chunks of language. It is a repetitive pattern of
language that does not necessarily contain mean-
ing, nor is it directed to others for a specific
purpose. Echolalia can be seen in individuals
with various developmental disorders, including
autism, Tourette’s syndrome, aphasia, and
schizophrenia.
Typical children who are developing language
may demonstrate echoed speech between
the ages of 12–30 months of age. Lovaas
(1981) reported that in typically developing
children, echolalia peaks at approximately
30 months. This pattern tends to fade as a child’s
vocabulary and variety of language forms
develop. For children with autism, however, the
pattern can persist beyond 30 months and their
E 1046
repetitive talk may often be related to areas of
special interest, media, or other environmental
factors. Children may echo language used by
people in their environment, or language heard
within TV or songs.
Research (Prizant & Duchan, 1981) has
shown that children and adults with autism
may use echolalia for a variety of communicative
purposes, such as a way to process language
and improve their comprehension, as a means
to initiate a conversation, or to form a reply.
Echolalia is also thought to be a way for some
children to cope with and “tune out” stressful
situations.
Immediate echolalia is the repetition of a word
or phrase directly following its utterance by
another. For example, a child may repeat
a question mother has just asked (Mother:
“Do you want juice?” Child replies, “Do you
want juice?”). Delayed echolalia is the repetition
of words and phrases heard at some previous
time, for example, a child may repeat an
announcement heard at school the previous
day (“Today we will be having a fire drill”).
As spontaneous language improves in children
with autism, echolalia tends to decrease, as it
does among typically developing children.
See Also
▶ Movie Talk
References and Readings
Paul, R. (2007). Special considerations for special
populations. In R. Paul (Ed.), Language disorders
from infancy to adolescence (3rd ed., p. 138).
St. Louis, MO: Mosby Elsevier.
Prizant, B., & Duchan, J. (1981). The functions of imme-
diate echolalia in autistic children. Journal of Speech
and Hearing Disorders, 46, 241–249.
Tager-Flusberg, H., Paul, R., & Lord, C. (2005). Language
and communication in autism. In F. R.
Volkmar, A. Klin, R. Paul, & D. J. Cohen (Eds.),
Handbook of autism and pervasive developmental
disorders (Vol. 1, pp. 346–347). Hoboken, NJ: Wiley.
Ecological Inventory
Ecological Inventory
Frances L. Kohl
Department of Special Education, University of
Maryland, College Park, MD, USA
Definition
An approach to identify functional, age-
appropriate curriculum content a student needs
in specific environments within the following
curriculum domains: personal management,
community, vocational, leisure, and school. The
process involves five phases: (1) identify the cur-
riculum domains, (2) identify current and future
natural environments within each curriculum
domain, (3) identify the subenvironments within
the natural environments, (4) inventory the rele-
vant tasks within each subenvironment, and
(5) analyze each task into component skills
needed to perform the task from start to finish.
References and Readings
Brown, L., Branston, M. B., Hamre-Nietupski, S.,
Pumpian, I., Certo, N., & Gruenewald, L. (1979).
A strategy for developing chronological age appropri-
ate and functional curricular content for severely
handicapped adolescents and young adults. Journal
of Special Education, l3(l), 8l–90.
Ecological Model of Autism
Jeffrey Danforth
Department of Psychology, Eastern Connecticut
State University, Willimantic, CT, USA
Definition
The ecological model of autism studies the behav-
ior of individuals with autism within the context
of many levels of environmental influence and
assumes bidirectional influences between (a) the
Ecological Model of Autism
person and these environmental influences and
(b) the many environmental levels. Context refers
to the wide range of system levels that influence
individuals with autism, including the immediate
responses of caregivers and family, school,
local community, as well as broader cultural,
economic, and political practices. Some variables
have a direct immediate impact, and some more
distal variables have an indirect impact. With
the ecological model, the appropriate unit of
study is the interaction of the environment and
individual, the organism-environment system;
“autism is not a static condition existing within
a person, but a developmental process that can
only be understood as taking place through the
interaction of person and environment” (Loveland,
2001, p. 22). An essential element of the ecological
model of autism “is that every level of the
ecological system is interconnected and thus can
influence all the other subsystems. These influences
are reciprocal rather than unidirectional” (Weiss,
Kreider, Lopez, & Chatman-Nelson, 2010, p. xxv).
Ecological models attempt to explain not
only the immediate impact of caretaker/client
interaction on the behavior of the individual with
autism but also the impact of social and economic
policies and the impact of those variables on one
another.
Historical Background
The ecological model of autism is a component of
the broader interactional model that assumes many
variables interconnect to produce an outcome. The
transactional model is one type of interactional
model used to study development. The primary
assumption is that development is the outcome
of dynamic interactions between the individual
and many layers of the environment. The context
of the environment ranges from variables
near the individual to those that are quiet distant
(Wicks-Nelson & Israel, 2009). One type of
transactional model is the ecological model.
The comprehensive ecological systems theory
emphasizes the importance of the context
in understanding a person’s behavior
(Bronfenbrenner, 1979; Gibson, 1979). Early
1047 E
behavioral models emphasize contextual variables
such as discriminative stimuli and setting events,
but the ecological model of autism analyzes
a broader range of environmental variables,
from microsystems that include physical space,
lighting, and noise in the teaching environment
to broader cultural and historical events and the
interactions between these variables.
E
Current Knowledge
The ecological approach to treatment of autism
requires a multidisciplinary treatment team to
tailor services to the specific needs of the individ-
ual and their caretakers, so treatment is not lim-
ited to the individual and their family.
Intervention extends to any ecological or contex-
tual variable that affects the individual with
autism.
The ecological theory of autism may be con-
ceptualized as a multidimensional series of con-
centric circles having the individual with autism
in the middle (Zigler & Stevenson, 1993). Many
investigators consider the critical autistic feature
the inability of the individual to understand what
others think or feel, a weakness in theory of mind.
Broader developmental characteristics include
observable operant behavior (both desirable and
undesirable), cognition, neurological conditions,
emotional behavior and mood, social behavior,
communication skills, motor behavior, medical
conditions, and sensory deficits. Molecular
behavior includes the form of the response, dura-
tion, latency between antecedent and behavior,
the time between responses, and the intensity of
the response. The individual’s personal goals,
preferences, and strengths are important consid-
erations. The ultimate criterion “emphasizes that
assessment efforts and intervention objectives
specifically target behavior that will be functional
for the individual with a disability in real envi-
ronments” (Powers, 2005, p. 818).
The microsystem is the first level of the envi-
ronment. This includes the minute-by-minute and
day-to-day interactions between the individual
with autism and caregivers (parents and
teachers), peers, and siblings as well as the daily
E 1048
settings and physical structure of home, school,
and community. Within these systems, it is criti-
cal to recognize the bidirectional effects of
behavior; caretakers influence people with
autism, but the stress of autistic behavior also
influences caretakers, and stressful caretaker
reactions can in turn affect the autistic behavior.
For example, in response to unusual social and
emotional behavior, caretakers of children with
autism are more directive and may even smile
less toward the children. Loveland (2001) con-
tends the socially inappropriate behavior of indi-
viduals with autism is a product of both
neurobiological impairment and the abnormal
reactions of significant others to the unusual
social behavior. Furthermore, the abnormal feed-
back of others may affect neurological develop-
ment (e.g., synaptic pruning) in the young child
whose behavior then becomes more atypical,
with the cycle revolving. At this level, the eco-
logical unit of analysis may also examine coer-
cive processes (Binnendyk et al., 2009; Patterson,
1982). Such analyses may evaluate whether inap-
propriate behavior is the outcome of positive
reinforcement by attention, negative reinforce-
ment by caretaker acquiescence, or exacerbated
by repeated commands or reprimands for trivial
behavior.
The determination of target behavior strengths
and weaknesses selected for treatment is an
important component, as practitioners must also
consider whether the selected targets are mean-
ingful to the family, day-to-day caretakers, and
the community (Kazdin, 1977). Behavior analy-
sis of the microsystem would include operational
definitions of selected target behaviors, distal
setting events, antecedents that immediately pre-
cede the behavior (discriminative stimuli), and
consequences that immediately follow the behav-
ior (reinforcers and punishers). Ecological valid-
ity, or ecological assessment (Powers, 1997),
identifies whether the selected prosocial target
behaviors are functional in the person’s day-to-
day environment. For generalization of behavior
across time and settings, selected target behaviors
must be naturally functional (i.e., reinforced by
the natural community) within the microsystem,
and care is taken to identify obstacles in the
Ecological Model of Autism
natural environment that may punish the selected
behavior.
The physical structure of home, school, and
community takes into account characteristics of
the general setting such as large crowds, noise,
and predictable schedules versus chaotic routines
that may influence autistic behavior. For exam-
ple, in the context of challenges presented to
individuals with autism in the form of schedules
and routines, Binnendyk et al. (2009) conceptu-
alize the essential unit of analysis as the quality of
parent-child interactions embedded within rou-
tines of everyday life. The quality of family inter-
actions within these routines may have
a “profound” impact on the child’s development.
Family-selected routines that have served as the
basis for routine-specific treatment plans include
bathroom routines, restaurant routines, dining at
home, dining at a restaurant and fast food estab-
lishments, grocery shopping, family television
time, and bedtime.
Other units of analysis go beyond the behavior
of the individual person and require myriad
sources of data from larger social systems. The
next level of the environment is the mesosystem,
representing the interactions across the individ-
ual’s microsystem. Variables that influence the
individual with autism include parents’ marital
strain, extended family relationships, the recipro-
cal relationships between parents and teachers,
parents and siblings, teacher and school, etc. For
example, interpersonal conflict between parents
and teachers or parents and siblings may have an
effect on the behavior of the individual with
autism, and if this were determined to be the
case, an ecological approach will consider that
conflict a variable that needs to be addressed as
part of treatment. Sometimes, the highly sophis-
ticated practices of treatment workers contrast
with parent training intellectually limited family
members at home. If these contrasting styles pre-
vent adequate application of services in the home
setting, then an ecological approach will consider
that disconnect a variable that needs to be
addressed as part of treatment.
Contexts that influence the child indirectly
compose the exosystem of the ecological system.
The exosystem influences the child indirectly by
Ecological Model of Autism
effecting institutions and people in the individ-
ual’s microsystem. For example, a parent may
lose a job or be transferred to employment in
another state. The stress of parental unemploy-
ment or moving to another state with concomitant
schedule and routine changes may influence the
behavior of the individual with autism, especially
an individual whose repertoire includes resis-
tance to change or well-established rituals. Struc-
tural changes within social service agencies that
provide counseling and family support may lead
to new treatment workers who are required to
relearn details of the family’s goals and objec-
tives and establish new relationships, all of which
can affect the individual with autism. Other
exosystems that do not include the person with
autism but can influence them include parent
social networks, socioeconomic status of the
family and neighborhood, the availability of
mental health services in the community, the
availability of professional training in empiri-
cally validated practices for service providers,
the availability of materials and human resources
required to meet the needs of the child (Lovaas,
2003), and the availability of follow-up care and
respite as needed.
In recognition of the growing diversity of the
family unit, an ecological analysis also includes
a subjective understanding of a family’s values
and beliefs. This allows treatment plans to con-
sider culturally sensitive interventions when col-
laborating with families, sometimes referred to as
cultural competence (Lynch & Hanson, 2004).
The broadest level of influence composed of
the culture’s values, the economy, political
trends, and social policy is the macrosystem.
Resources for the family and school, tolerance
of individual differences, and general opportuni-
ties afforded individuals with autism are greatly
influenced by the macrosystem. State and federal
law has mandated a number of recent social pol-
icy trends. In 1990, the US Congress added the
word “autism” to laws that guarantee special
education services. The Individuals with Disabil-
ities Education Act, the federal law pertaining to
special education, was reauthorized in 1997
(National Dissemination Center for Children
with Disabilities), and both of these acts have
1049 E
resulted in more educational/treatment services
to children with autism and more inclusion in less
segregated (and less restrictive) general school
settings. At the same time, economic conditions
in the 2010s may lead to reduced local school
budgets and reduced educational services.
Many states in the USA have passed laws
requiring state-regulated group health plans to
include coverage for autism, and federal law pro-
hibits insurance companies from refusing to issue
E
or renew coverage for children because of
preexisting conditions including autism. The out-
come for families of children with autism
includes monetary saving and less emotional
stress, with children eligible for a wide array of
services.
The chronosystem signifies time both within
the lifetime of the individual of interest and the
historical context within which the person lives
(Weiss et al., 2010). Over the course of time, the
child and family’s growth and learning can affect
each of the above-described systems. Further-
more, the historical context within which the
person lives influences the services available to
that person. Compared with individuals living
prior to 1980, much has changed for individuals
with autism. One critical difference is how the
definition of autism presented in the American
Psychiatric Association’s Diagnostic and Statis-
tical Manual of Mental Disorders (DSM, Ameri-
can Psychiatric Association [APA], 1980, 1994,
2000) has changed. Although Kanner identified
autism in the 1940s, it was not until 1980 that
criteria for autism were defined in the DSM.
Since then, the phrasing to describe autism has
become far less restrictive. The 1980 DSM
required six mandatory criteria with phrasing
that limited the number of people diagnosed
with autism (e.g., “A pervasive lack of respon-
siveness to other people” in the 1980 DSM is
replaced by “Lack of spontaneous seeking to
share. . . achievements with other people”). In
conjunction with the 1994 inclusion of
Asperger’s disorder in the DSM, the acknowledg-
ment that autism can exist among people across
the entire range of intelligence, and recent efforts
to take advantage of neural plasticity by identify-
ing and providing comprehensive treatment
E 1050
among the youngest children with autism, the
number of people on the autism spectrum eligible
for services has expanded greatly. Perhaps three
fourths of those diagnosed with autism are
accounted for by those diagnosed with milder
variants (Chakrabarti & Fombonne, 2001), and
only 35 years ago, many of these people would
not have been eligible for services.
Ultimately, ecologically sensitive interven-
tions synthesize data from multidisciplinary
sources to develop a holistic intervention that
addresses the individual with autism, their care-
takers, the physical structure of important set-
tings, and cultural variables.
See Also
▶ Advocacy
▶ Classroom Structure
▶ Clinical Assessment
▶ Ecological Inventory
▶ Ecological Validity
▶ Family Therapy
▶ Functional Ecological Approach
References and Readings
American Psychiatric Association. (1980). Diagnostic
and statistical manual of mental disorders (3rd ed.).
Washington, DC: Author.
American Psychiatric Association. (1994). Diagnostic
and statistical manual of mental disorders (3rd ed.
Rev.). Washington, DC: Author.
American Psychiatric Association. (2000). Diagnostic
and statistical manual of mental disorders (4th ed.
Text Rev.). Washington, DC: Author.
Binnendyk, L., Fossett, B., Cheremshynski, C.,
Lohrmann, S., Elkinson, L., & Miller, L. (2009).
Toward an ecological unit of analysis in behavioral
assessment and intervention with families of children
with developmental disabilities. In W. Sailor, G.
Dunlap, G. Sugai, & R. Horner (Eds.), Handbook of
positive behavior support. New York: Springer.
Bronfenbrenner, U. (1979). Contexts of childrearing:
Problems and prospects. American Psychologist, 34,
844–850.
Chakrabarti, S., & Fombonne, E. (2001). Pervasive devel-
opmental disorders in preschool children. Journal of
the American Medical Association, 285, 3093–3099.
Ecological Validity
Gibson, J. J. (1979). The ecological approach to VISUAL
perception. Boston: Houghton-Mifflin.
Kazdin, A. E. (1977). Assessing the clinical or applied
importance of behavior change through social valida-
tion. Behavior Modification, 1, 427–451.
Lovaas, O. I. (2003). Teaching individuals with develop-
mental delays. Austin, TX: Pro-Ed.
Loveland, K. A. (2001). Toward an ecological theory of
autism. In J. A. Burack, T. Charman, N. Yirmiya, &
P. R. Zelazo (Eds.), The development of autism: Per-
spectives from theory and research. Mahwah, NJ:
Lawrence Erlbaum.
Lynch, E. W., & Hanson, M. J. (2004). Developing cross-
cultural competence: A guide for working with chil-
dren and their families (3rd ed.). Baltimore: Brookes.
National Dissemination Center for Children with Disabil-
ities. Retrieved from http://nichcy.org/laws/idea
Patterson, G. R. (1982). A social learning approach (Coer-
cive family process, Vol. 3). Eugene, OR: Castalia.
Powers, M. D. (1997). Behavioral assessment of autism.
In D. J. Cohen & F. R. Volkmar (Eds.), Handbook of
autism and pervasive developmental disorders
(2nd ed., pp. 448–459). New York: Wiley.
Powers, M. D. (2005). Behavioral assessment of individ-
uals with autism: A functional ecological approach. In
F. R. Volkmar, R. Paul, A. Klin, & D. Cohen (Eds.),
Handbook of autism and pervasive developmental dis-
orders, assessment, interventions, and policy (Vol. 2,
pp. 817–830). New York: Wiley.
Weiss, H. B., Kreider, H., Lopez, M. E., & Chatman-
Nelson, C. (2010). Preparing educators to engage
families: Case studies using an ecological systems
framework. Los Angeles: Sage.
Wicks-Nelson, R., & Israel, A. C. (2009). Abnormal child
and adolescent psychology. Upper Saddle River, NJ:
Pearson/Prentice Hall.
Zigler, E. F., & Stevenson, M. F. (1993). Children in
a changing world: Development and social issues.
Pacific Grove, CA: Brookes/Cole.
Ecological Validity
Erin Rotheram-Fuller
School Psychology, Department of
Psychological Studies in Education,
College of Education Temple University,
Philadelphia, PA, USA
Synonyms
External validity
Edinburgh Handedness Inventory
Definition
Ecological validity is the degree to which exper-
imental measures (i.e., settings, treatment agents,
materials, behaviors) occur naturally and are
representative of events that occur in everyday
life or in the settings in which the skill or behavior
is expected to be performed (Brewer, 2000;
Schlosser, 2003). The results of an ecologically
valid assessment are predictive of appropriate
behavior in a free environment (Franzen, 2000).
Ecological validity is important for descriptive or
demonstrative research (Brewer, 2000) and is an
aspect of external validity that is closely related
to, but not to be confused with, social validity
(Schlosser, 2003).
See Also
▶ External Validity
References and Readings
Brewer, M. B. (2000). Research design and issues of
validity. In H. T. Reis & C. M. Judd (Eds.), Handbook
of research methods in social and personality psychol-
ogy (pp. 3–16). Cambridge, UK: Cambridge Univer-
sity Press.
Franzen, M. D. (2000). Validity as applied to neuropsy-
chological assessment. In Reliability and validity in
neuropsychological assessment (pp. 33–54).
New York: Springer.
Sbordone, R. J., & Long, C. J. (Eds.). (1996). Ecological
validity of neuropsychological testing. Boca Raton:
CRC Press.
Schlosser, R. W. (2003). Validity. In R. W. Schlosser (Ed.),
The efficacy of augmentative and alternative communi-
cation (pp. 27–41). San Diego, CA: Academic Press.
Edinburgh Handedness Inventory
Janine Robinson
CLASS, Cambridgeshire & Peterborough NHS
Foundation Trust, Cambridge, UK
Synonyms
EHI
1051 E
Description
The Edinburgh Handedness Inventory (Oldfield,
1971) is a measurement scale which is employed
to establish hand dominance. The 20-item inven-
tory contains a list of instructions to be carried out
by the individual being assessed. Items are rated
by direct observation of the individual’s behavior
or by self-report of everyday behavior. Oldfield
developed a second, shorter version, namely,
E
a 10-item inventory, and it is this form which
has been used most often.
This brief quantitative measure has proved to
be of use in neuropsychological, general, clinical,
and research fields. However, where the question
of establishing laterality is critical, such as in
research, the author has reported that this scale
used on its own is not sufficient to determine
cerebral laterality and is effectively best
employed as a screening measure. Given its sim-
plicity and brevity, it would be particularly useful
where large populations are being assessed. The
measure benefits from properties which provide
a useful standard of comparison in the neuropsy-
chological field. The EHI is the most widely used
instrument to measure handedness, and this
appears to have increased in recent years (Fazio,
Coenen & Denney, 2011).
Oldfield (1971) strongly urges clinicians and
researchers to follow the instructions closely in
order to ensure limitation of misinterpretation
and to ensure the form is completed properly.
However, Fazio et al. (2011) found that the orig-
inal instructions were in fact problematic and
only 47.3% of individuals in their study were
unable to follow the instructions completely. By
contrast, 88.2% of these individuals could suc-
cessfully follow the instructions on a different
measure with Likert-style presentation. The
authors note that the level of education and the
handedness of the participants significantly
predicted their ability to adhere to the instructions
which had clear implications for the use of the
Edinburgh Handedness Inventory.
Where individuals are being required to com-
plete the form (rather than being observed in a
clinical setting), they are presented with a typed
sheet and instructed to provide information
E 1052
regarding age and sex. The original inventory
asks whether they have ever had a tendency to
left-handedness.
The individual is then presented with a list of
ten items to score. They are instructed to consider
their hand preference for each activity, indicating
with one plus (þ) if the preference is for the left
or right hand. If they are indifferent, a plus is
placed in both L and R columns. “Where the
preference is so strong that you would never try
to use the other hand unless absolutely forced to,
put ++” (Oldfield, 1971). Since some tasks
require two hands (e.g., striking a match), they
are asked to indicate the hand preference for the
key object, e.g., the match. All items are scored
unless the individual has no experience of a task
or object at all. A laterality quotient (LQ) is
obtained by
ðR  LÞ=ðR þ LÞ  100
where R ¼ number of ticks in the right column
and L ¼ number of ticks in the left column.
Interpretation of results:
Left-handed < 40
Ambidextrous 40 to +40
Right-handed > +40
While the core instrument has remained in
use, various authors appear to have made adjust-
ments to the instructions and presentation of the
form. In addition, some authors have added fur-
ther questions, e.g., holding a computer mouse
(Cohen, 2008; Dragovic, 2004b), holding a cup
for drinking, and using a key to unlock a door
(Cohen, 2008). Williams (1986) proposed
a revision of the EHI resulting in changes in
number of items tested – reducing these from
ten to seven – and consistent with Dragovic’s
suggestion (2004b), adding the item computer
mouse. He argues that two items (opening a box
and using a broom) have been discarded since
new factor-analytic studies have found these
items to be low outliers when loaded onto the
“handedness” factor. The computer mouse is
viewed as a significantly “unimanual activity in
today’s world” (Williams, 1986).
The EHI (revised) proposes the adoption of
a Likert-style format, thus reducing the wording
Edinburgh Handedness Inventory
in the instructions to “Please mark the box that
best describes which hand you use for the activity
in question.” For each item, the respondent hence
selects from five possible options, namely,
always left, usually left, no preference, usually
right, and always right. The procedure for arriv-
ing at the laterality quotient (LQ) is by necessity
adjusted and can be used to identify those
individuals who are mixed-handed (LQ between
+50 and 50). Scoring is as follows: “50”
always left, “25” usually left, “0” no preference,
“25” usually right, and “50” always right.
Scores on the eight rows are summed to pro-
vide a score LQ* of 400 to +400. If the LQ*
score is then divided by 4, an LQ of 100 to +100
is then achieved, i.e., complete left-handedness to
complete right-handedness as per the original EHI.
With the revised scoring method, 200 to + 200
becomes mixed-handedness. Williams describes
a clinical observation that the mixed-handedness
group may further divide into two, namely, clumsy
or coordinated. He anticipates that the clumsy
group may have an LQ* score of 200 to 1
and the coordinated group an LQ* of 0–200.
Historical Background
When first published in 1971, the Edinburgh
Handedness Inventory was initially named the
Edinburgh Inventory (Oldfield). Previous assess-
ment of handedness relied on either (a) observa-
tion of the individual carrying out tasks
(seminovel) with left or right hands separately
or (b) posing a number of questions about
day-to-day activities and the hand use in these.
In the former, the individual’s performance may
be rated on time and/or error, enabling the calcu-
lation of an index of handedness.
The EHI has been used extensively in research
(Boucher, 1977; Dragovic 2004a, b; Cohen, 2008;
Escalante-Mead, Minshew, & Sweeney, 2003;
Fazio et al., 2011; Williams, 1991). Oldfield
developed a 20-item and a 10-item version of
the EHI. When the 10-item version was
compared to Annett’s 12-item scale (1970),
Williams found that, owing to the instructions,
the EHI produced more “either hand” responses
Edinburgh Handedness Inventory
when usually the “left hand” would be the
response (1991). He suggested that where neuro-
psychological researchers were looking to detect
any degree of left-handedness, the questionnaire
by Annett might be preferable.
While the EHI has remained a well-used
instrument to establish handedness, it has been
adapted by a number of authors primarily
adjusting the presentation of the recording system
and simplifying the instructions which have been
deemed too complicated and potentially confus-
ing for testees (Dragovic, 2004b; Fazio, Coenen,
& Denney, 2011; Cohen, 2008).
Lateralization in autism has been of interest
to scientists for many years, and the EHI has
been employed in studies researching cerebral
dominance and language development in
individuals with autistic conditions (Boucher,
1977; Froehlich et al., 2011; Williams, 1986,
1991).
Psychometric Data
The Edinburgh Handedness Inventory has been
refined since the original 20-item questionnaire in
1971. Oldfield discarded those items found to be
redundant or inappropriate given the purpose of
devising a measure that would have universal
application. He conducted a study of the
20-item inventory on 1,100 students. Analysis
of items on the basis of sex, socioeconomic, and
cultural factors resulted in ten items being
discarded, leaving the inventory in its current
form. On analysis of 1,027 responses (360
males and 667 females) where a score <0 denotes
left-handedness, 10% of males and 5.92% females
scored <0 (chi-squared ¼ 6.21, p < 0.02).
The authors noted the difficulties conducting
statistical analyses on the data owing to the nature
of the frequency distribution (a U form with the
left side only containing about 10% of the total
population). Treating the sections separately with
the LQ cut at zero, percentage cumulative curves
could be represented as the “right-handed” and
“left-handed” sections, respectively. While the
“right-handed” section could be represented in
decile values, the “left-handed” section was less
1053 E
regular. The author notes that larger numbers will
be needed in future studies to establish larger
frequency values for the left-handed group.
Hence, decile values remain provisional.
In a study of hand preference in the parents of
autistic children, a similar pattern of results was
found with 5.9% males and 0% females using the
left hand more than the right (Boucher, 1977). In
Oldfield’s student sample, 10% of those who
predominantly used their right hand showed
E
a very marked (LQ ¼ 95–100) or almost exclu-
sive preference. In Boucher’s study, 69.1% of
males and females who preferred the right hand
used this almost exclusively. “Pure” right-
handedness was significantly different between
the groups at the p <.001 level on Guilford’s
test of the difference between two proportions.
These unexpected results were nonetheless con-
founded by concerns regarding the reliability of
the EHI and the possibility that some participants
did not fully follow the instructions. Evaluation
of handedness in the autistic children of these
parents, on the other hand, indicated
a persistent, but slightly increased tendency of
children with autism to use the left hand.
McMeekan and Lishman’s study (1975) com-
pared the EHI (10-item) with the 12-item Annett
questionnaire. The test-retest reliability results
were unexpectedly moderate (0.80), but Williams
notes (1991) a number of potentially significant
methodological factors which most likely affected
the results. On retesting with the EHI, participants
often changed the classification from strong to
weak. Williams does state that the EHI has one
particular difficulty in the procedure employed for
deriving the laterality quotient (LQ). Employing
the equation, (R  L)/(R + L), it is possible to
achieve an LQ score of 100 in two ways: if there
are 10–20 ticks in the R column, but none in the
L column. In other words, there is no ability to
discriminate between degrees of right-handed-
ness. The issue of weighting of inventory items
is also of some concern with no justification for
equal weighting of some items and double
weighting of items scored with two ticks. Wil-
liams (1991) notes that Annett’s designation of
“primary” and “secondary” items facilitates
more sophisticated statistical discrimination.
E 1054
Clinical Uses
The Edinburgh Handedness Inventory (Oldfield,
1971) is used to assess hand dominance in every-
day activities. The measure may be rated by an
observer or by the individual’s self-reporting.
The author viewed the latter as less reliable
since individuals tend to overestimate the number
of tasks carried out using the dominant hand.
Nonetheless, for ease of use, clinicians and
researchers predominantly employ
a questionnaire-based assessment of handedness
over performance-based measures (Williams,
1991). Such questionnaires have demonstrated
themselves to be highly correlated with behav-
ioral measures (Chapman & Chapman, 1987).
Establishing hand preference may shed light
on how the brain matures. Laterality has been
demonstrated to be of importance in the autistic
spectrum conditions, language, mathematical,
and musical ability.
For instance, in a study of early language
disturbance and lateral preference (on the Edin-
burgh Handedness Inventory), researchers found
that individuals with autism who had early lan-
guage disturbance displayed more atypical cere-
bral dominance than normal controls and
individuals with autism who had had normal lan-
guage development (Escalante-Mead et al.,
2003). Results indicated that there was not in
fact a greater incidence of left-handedness in
autism, but rather a disturbance in the develop-
mental process of establishing lateral dominance.
An atypical pattern or delay in establishing cere-
bral dominance may have implications for lan-
guage development in autism.
The Edinburgh Handedness Inventory remains
a valuable tool in clinical neuropsychology.
References and Readings
Boucher, J. (1977). Hand preference in autistic children
and their parents. Journal of Autism and Childhood
Schizophrenia, 7(2), 177–187.
Chapman, L. J. & Chapman, J. P. (1987). The measure-
ment of handedness. Brain and Cognition, 6, 175–183.
Cohen, M. S. (2008). Handedness questionnaire.
Retrieved from www.brainmapping.org
Education
Dragovic, M. (2004a). Categorization and validation of
handedness using latent class analysis. Acta Neuropsy-
chiatrica, 16, 212–218.
Dragovic, M. (2004b). Towards an improved measure of
the Edinburgh handedness inventory: A one factor
congeneric measurement model using confirmatory
factor analysis. Laterality, 9, 411–419.
Escalante-Mead, P. R., Minshew, N. J., & Sweeney, J. A.
(2003). Abnormal brain lateralization in high-
functioning autism. Journal of Autism and Develop-
mental Disorders, 33(5), 539–543.
Fazio, R., Coenen, C., & Denney, R. L. (2011). The
original instructions for the Edinburgh Handedness
Inventory are misunderstood by a majority of partici-
pants. Laterality: Asymmetries of Body, Brain and
Cognition, 9, 1–8.
Froehlich A., Anderson, J. S., Lange N., Zielinski, B. A.,
Dubray M. B., Nielsen J. A., et al. (2011). Relationship
between handedness and language lateralization in
autism. International Meeting for Autism Research,
San Diego, CA.
McMeekan, E. R. L. & Lishman, W. A. (1975). Retest
reliabilities and inter-relationship of the Annett hand
preference questionnaire and the Edinburgh Handed-
ness Inventory. British Journal of Psychology, 66,
53–59.
Oldfield, R. C. (1971). The assessment and analysis of
handedness: The Edinburgh inventory. Neuropsy-
chologia, 9, 97–113.
Soper, H. V., Satz, P., Orsini, D. L., Rolando, R. H., Zvi,
J. C., & Schulman, M. (1986). Handedness patterns in
autism suggest subtypes. Journal of Autism and Devel-
opmental Disorders, 16(2), 155–167.
Williams, S. M. (1986). Factor analysis of the Edinburgh
handedness inventory. Cortex, 22, 325–326.
Williams, S. M. (1991). Handedness inventories: Edinburgh
versus Annett. Neuropsychology, 5(1), 43–48.
Education
Marjorie H. Charlop1, Catherine A.
Miltenberger2 and Alissa L. Greenberg2
1
Department of Psychology, Claremont
McKenna College, Claremont, CA, USA
2
Claremont Graduate University, Claremont,
CA, USA
Definition
Autism is characterized by communicative,
social, and behavioral impairments. These issues
can make it difficult for children with autism to
Education
succeed in traditional educational settings
(Mesibov & Shea 1996; Noland, Cason, &
Lincoln, 2007). However, many children can
progress and even excel with the proper support.
To ensure that children with autism have access
to this support, federal legislation requires that
public schools provide eligible children with
autism with “special education and related
services designed to meet their unique needs”
(Steedman, 2007, p. 147). In other words, schools
are required to provide each eligible student with
autism an education that is designed to meet his
or her individual needs and that allows him or her
to progress. Because students with autism have
different strengths and needs, their educational
programs may look very different. Researchers
and professionals have used research, legislation,
and professional experience to develop autism
program quality indicators (Crimmins, Durand,
Theurer-Kaufman, & Everett, 2001; New Jersey
State Department of Education, 2004). These
indicators include comprehensive student assess-
ment, assessment-based and detailed individual-
ized education plans (IEPs), ongoing progress
monitoring, individualized and appropriate cur-
ricula and instructional methods and activities,
procedures for assessing and replacing challeng-
ing behaviors, qualified and appropriate school
personnel, and high levels of family involvement
(please see Current Knowledge for more
information).
Historical Background
In the past, students with autism and other
disabilities were often denied access to a public
education. It was not until the 1960s and 1970s
that the states and Congress passed legislation
intended to protect children with disabilities’
right to a free and appropriate public education
(Yell, Rogers, & Rogers, 1998). Unfortunately,
many children with disabilities continued to
receive no or inappropriate educational services
after these legislative changes (Steedman, 2007).
In an effort to better serve children with
disabilities, the federal government enacted the
Education for All Handicapped Children Act of
1055 E
1975 (EAHCA; Yell et al., 1998). This act was
designed to provide all children with disabilities
with more extensive educational rights. In 1990,
this act was amended and renamed the Individ-
uals with Disabilities Education Act (IDEA).
IDEA continues to undergo revisions designed
to better protect the rights and facilitate the suc-
cess of children with disabilities. It was most
recently amended in 2004. IDEA 2004 promises
all children an appropriate education, but there
E
continues to be debate concerning the extent and
quality of services that schools are required to
supply. Further, many schools report that they
lack the funds and resources required to provide
students with appropriate services (Block &
Block, 2007; please see Current Knowledge for
more information).
Current Knowledge
The Individuals with Disabilities Education Act
(IDEA) of 2004 requires school districts to
provide eligible individuals with autism and
other disabilities ages 3–21 with a free and
appropriate education. This education should be
designed around the students’ individual
strengths and deficits. Each student’s program
should include the special education and other
services the student needs to make progress and
should be delivered in the least restrictive envi-
ronment possible. The program should target the
skills that the student needs to achieve indepen-
dent functioning, continue his or her education,
and succeed in the workforce. Each of these main
components is briefly described below.
Individualized and appropriate education.
Although children with autism share common
areas of deficit, there is considerable variation in
individual students’ abilities and impairments.
Because of this heterogeneity, no single educa-
tional program will benefit all students with
autism. IDEA recognizes this and requires that
each student receive an education designed to
build upon his or her strengths and address his
or her deficits. Each student’s educational
program must be detailed in an individual
education plan (IEP). This plan should be
E 1056
developed by a multidisciplinary team including
school personnel, relevant professionals (e.g., an
autism specialist, speech and language
pathologist, or occupational therapist), and the
student’s parents. The IEP should describe
the student’s current abilities, his or her goals
for the next year, and the specific services and
accommodations that the child will receive to
facilitate his or her progress. The IEP team must
meet to review and update the IEP at least once
a year. Parents or school staff can request
additional IEP meetings any time that they feel
the plan is not meeting the student’s needs.
Special education and other services. IDEA
requires that eligible students with autism receive
the special education and related services that
they need to benefit from their educational pro-
gram. Special education refers to any curricular
or instructional modifications that the child needs
to progress. Related services refer to any
additional support that will help the child to
succeed. For children with autism, speech ther-
apy, occupational therapy, and transportation to
and from school are common related services
(Steedman, 2007). When developing these
special education and other services, the schools
are required to use evidence-based practices as
much as possible (Steedman, 2007). In other
words, the school should use instructional prac-
tices or interventions that have received empiri-
cal support. Using educational strategies that
have been found to benefit at least some children
with autism is believed to increase the likelihood
that this intervention will benefit the current
student with autism (Morris & Mather, 2008).
Considerable debate remains over the extent and
quality of services that schools are required to
provide. The Supreme Court ruled that schools
may not deny a child services based on their cost.
However, the Supreme Court has also declared
that schools do not have to offer children with
disabilities the best education possible. Instead,
services must allow children to “benefit” from
their education (Steedman, 2007).
Least restrictive environment. IDEA states
that each student’s educational program
should be implemented in the least restrictive
environment possible. Whenever possible, the
Education
student’s special education and other services
should be delivered in general education
classrooms with typically developing peers.
However, the IEP team must determine which
type of placement best facilitates the academic,
social, and behavioral progress of the student.
Placement options include inclusion, special
education, and mainstreaming. Inclusion is the
least restrictive environment possible. Inclusion
is generally defined as placement in a general
education classroom with neurotypical peers,
with additional services delivered as needed
(Mesibov & Shea, 1996). These services can be
provided within the general education classroom
(i.e., push-in services) or outside of the classroom
(i.e., pull-out services). Advocates of inclusion
argue that this environment provides students
with autism more rigorous academic instruction
and increased access to appropriate peer models
and interactions. However, others contend that
general education classrooms do not meet the
special learning needs of students with autism.
Placement in a special education classroom is
considered a more restrictive environment.
Special education classrooms are populated by
students with disabilities. Special education
classrooms tend to contain fewer students and
have a higher adult to child ratio. Teachers
typically tailor their instruction to the special
needs of their students. These classrooms may
provide a more supportive environment for the
students but are often believed to be less academ-
ically rigorous and provide fewer opportunities
for typical peer models and interactions. Students
with autism may also be mainstreamed, spending
part of their day in a special education classroom
and part of their day in a general education
classroom (Mesibov & Shea, 1996). This
placement allows children to receive more
individualized special education instruction
while also exposing them to typical curricula and
peer models. However, the extent to which simply
exposing children with autism to neurotypical
peers leads to the desired benefits is unclear.
Program quality indicators
As previously noted, it is not possible to develop
a single “best” program for students with autism.
Education
However, researchers and professionals have
used existing research and their professional
experience to develop a number of program
quality indicators or components of effective
programs. Several of these components are
described below; however, this list is not exhaus-
tive. For full lists and comprehensive descrip-
tions of program quality indicators, please see
New York’s autism program quality indicators
(Crimmins et al., 2001), New Jersey’s autism
program quality indicators (New Jersey State
Department of Education, 2004), and the cited
references.
Child assessment. Assessments allow educa-
tors to identify the strengths and deficits of
children with autism. Assessments should be
comprehensive, with measures of the child’s
social and language skills, academic skills,
adaptive and maladaptive behaviors, and
cognitive abilities across settings. The selected
assessments should provide information that can
be used to inform the student’s educational
program (Crimmins et al., 2001).
Individualized education programs. The IEP
should state the student’s current level of func-
tioning across communicative, social, academic,
and developmental domains in school, home, and
community settings. This information should be
used to formulate new, measurable goals that will
facilitate the child’s success and independence
across skill domains and environments. The IEP
should specify the special education and related
services that will be used to promote student
progress (Steedman, 2007). These may include
parent services or training that will help the
parents facilitate child progress in home and
community settings. These services and accom-
modations should be detailed so that all parties
(e.g., parents, school staff) understand their
roles and responsibilities (New Jersey State
Department of Education, 2004).
Progress monitoring. Effective programs
should include ongoing and systematic measure-
ment of individual student progress towards set
IEP goals. This information should be used to
make appropriate educational decisions. When
a student meets a set goal, the educational team
should develop new goals to further facilitate
1057 E
child progress. When a student does not progress
towards meeting a goal, the educational team
should consider adjusting the method or intensity
of the student’s current program to better meet his
or her needs (Crimmins et al., 2001; New Jersey
State Department of Education, 2004).
Curriculum. Each student’s educational
program should focus on the skills that he or she
needs to achieve independent functioning,
continue his or her education, and succeed in
E
the workforce. Therefore, educational programs
should address a wide range of skills, including
communication and social skills, adaptive skills,
academic skills, and, for older students,
vocational skills. The specific content of each
student’s educational program should be based
on his or her current functioning level and be
adjusted as needed. Whenever appropriate, the
curriculum should integrate age-appropriate
state standards (New Jersey State Department of
Education, 2004; Noland et al., 2007).
Instructional methods and activities.
Whenever possible, instructional methods and
activities should be research-based. Methods
and activities should be adapted to the strengths
of the child with autism. Skills should be targeted
within appropriate instructional formats
(e.g., individual, small-group, or large-group
instruction). When appropriate, skills should be
targeted via naturally occurring opportunities
and reinforcers. Programs should include compo-
nents designed to promote independent skill use,
generalization across people and settings, and
maintenance (Crimmins et al., 2001; New Jersey
State Department of Education, 2004).
Challenging behaviors. Children with autism
often demonstrate stereotypic, disruptive, or
self-injurious behaviors (Lopez,Hill, Shaw, &
Gabriels, 2007). Programs should have a process
for systematically assessing the function of these
behaviors (e.g., functional assessments). This
information should be used to develop a plan to
eliminate the challenging behaviors and replace
them with more adaptive behaviors (Crimmins
et al., 2001; New Jersey State Department of
Education, 2004).
School personnel. School staff (e.g., teachers,
other service providers, paraprofessionals)
E 1058
should be educated on the needs and strengths of
students with autism, effective educational prac-
tices, methods of individualizing educational
programs to meet each student’s needs, and
behavior management and naturalistic teaching
strategies. All staff should attend professional
development workshops. Paraprofessionals, who
tend to have less knowledge and experience,
should receive continuous supervision and
instruction from classroom teachers and other
personnel. The program should have enough
personnel (teachers, aides, therapists, etc.) to
meet the needs of the students. Personnel should
be familiar with each student’s IEP and be aware
of their role in its implementation (Crimmins
et al., 2001; New Jersey State Department of
Education, 2004; Noland et al., 2007).
Family involvement. Legally, schools are
required to include parents in the development
of the student’s educational program. Involving
parents and family members in the development,
implementation, and revision of the student’s
program is believed to increase program effec-
tiveness. Therefore, the school should make an
effort to inform or refer parents to information on
available services and their student’s program
and progress. Parents should also be given sup-
port and training that allows them to better meet
their student’s needs in home and community
settings. Student’s programs should be developed
with consideration of the family’s beliefs and
values (Crimmins et al., 2001; New Jersey State
Department of Education, 2004).
Sample schedule and activities
A sample special education classroom sched-
ule, activity descriptions, and recommenda-
tions are provided below. The activities can be
adjusted to meet the individual needs of each
student.
Consulting activity schedules. Activity sched-
ules are a great way to prepare the student for the
day’s activities and transitions and to increase
independence (McClannahan & Krantz, 1997).
Each classroom should have a clearly visible
general schedule, and each student should have
an individual schedule detailing his or her
Education
specific activities for the day. Depending on the
student’s level of functioning, a schedule could
be a written list or pictures.
Opening Circle. Opening circle is a good time
to target communication skills and attending in
a large-group setting. Opening circle activities
may include reviewing the day’s general sched-
ule, singing songs, or sharing about a given topic
(e.g., what students did over the weekend or
favorite ice cream flavor).
Individual work time. Individual work time
should focus on each student’s IEP goals. The
following steps should be taken to maximize on-
task behavior and correct responding.
Structuring the Work Environment. Individ-
uals with autism benefit from a structured work
environment (Schopler, Brehm, Kinsbourne, &
Reichler, 1971). Structuring the work environ-
ment may include a work area with minimal
distractions, clearly presenting the demand,
visual instructions, and immediately reinforcing
a correct response with praise, tokens, or tangible
reinforcers (Mesibov, Schopler, & Hearsey,
1994).
Brief Stimulus Assessment Task. To ensure
that each student is motivated, a brief stimulus
assessment should be conducted at the beginning
of each work session to identify items that can be
used as reinforcers. In a brief stimulus assessment
task, students are presented with a number of
potential reinforcers and the first three items
they choose are considered the preferred items.
These items should then be used during the fol-
lowing work session (Roane, Vollmer, Ringdahl,
& Marcus, 1998).
Varying Maintenance and Acquisition Tasks.
During individual work time, the one-to-one aide
should present the student with a mix of mainte-
nance and acquisition tasks (Dunlap, 1984;
Dunlap & Koegel, 1980). For example, if
a student is learning expressive language and
categories but has already mastered receptive
body parts, a work session should include trials
on all three tasks.
Using an Appropriate Level of Prompting. As
students acquire a given task, they will need
different levels of prompting or support.
Education
Teachers and aides should give the student the
minimal prompt necessary to help them succeed
at the given task.
Using a Variety of Preferred Reinforcers. To
make sure that the student stays motivated and
does not grow bored with their reinforcer, the
student should be reinforced with different
preferred items throughout the session (Egel,
1981; Fisher, Bowman, & Hagopian, 1992).
Incorporating Naturalistic Teaching Opportu-
nities. The classroom provides a number of
opportunities for naturalistic teaching strategies,
such as incidental learning. Preferred toys may be
placed on high shelves or in clear, hard to open
bins so that the student must ask for them. Using
naturalistic teaching strategies in the classroom
promotes generalization and spontaneous use
(Delprato, 2001).
Lunch Time. Meals are ideal times to provide
natural learning opportunities. For example,
instead of automatically providing a student
with his or her food, the teacher or aide may
wait for the student to request that the food be
passed to them.
Small-Group Time. Small-group time is the
perfect time to practice communication and
social skills in a fun, motivating environment.
Teachers or classroom aides can facilitate peer
interactions during a variety of desired activities.
These activities may include board or card
games, arts and crafts, or conversations about
preferred topics.
Physical Education/Outside Play. Physical
activity has been shown to decrease stereotypic
and disruptive behavior in individuals with
autism (Levinson & Reid, 1993). Having students
with autism participate in small-group or
team games also provides additional opportuni-
ties to facilitate communicative and social inter-
actions. During outside play, students may
participate in activities such as kickball, tag, or
relay races.
Closing Circle. Closing circle is a good time to
practice communication skills and attending in
a large-group setting. Closing circle activities
may include reviewing the day’s activities, ask-
ing students to share their favorite part of the day,
1059 E
or having students share a favorite item from
home with the rest of the group.
Token Systems. Tokens can be used to rein-
force correct responding and appropriate behav-
ior throughout the day (Tarbox, Ghezzi, &
Wilson, 2006). Using objects of obsession (e.g.,
a favorite TV character) as the tokens may be
especially effective (Charlop-Christy & Haymes,
1998). At the end of the day, students should be
given the opportunity to spend any tokens they
E
have earned on preferred items. If students
choose, they should be allowed to save their
tokens until they have earned enough for
a bigger item.
Future Directions
Over the past several decades, there have been
tremendous gains in the education of students
with autism (Yell et al., 1998). However, the
education of children with autism is far from
perfect. While IDEA guarantees children with
autism and other disabilities an appropriate edu-
cation, its implementation is often less than ideal
(Block & Block, 2007). Schools report that they
lack the funds and resources required to meet the
extensive and diverse needs of the increasingly
large population of students with autism and
other disabilities.
One way to address these issues is to continue
to research effective educational practices
for children with autism. IDEA recognizes
the importance of research-based practices
(Steedman, 2007), but the necessary body of
research is yet to develop. Although many strat-
egies have been shown to be effective when
working with children with autism in tightly
controlled settings, much less is known about
the outcomes of these strategies when
implemented at school. There is a particular
need for research addressing effective educa-
tional interventions for older and more impaired
students with autism (Noland et al., 2007).
Researching interventions and identifying effec-
tive practices will provide educational teams
with information that can be used to develop
E 1060
efficient and effective educational programs
(Morris & Mather, 2008).
See Also
▶ Individuals with Disabilities Education Act
(IDEA)
▶ Special Education
References and Readings
Block, A. W., & Block, S. R. (2007). Family resources
during the school-age years. In R. L. Gabriel & D. E.
Hill (Eds.), Growing up with autism (pp. 164–182).
New York: The Guilford Press.
Charlop-Christy, M. H., & Haymes, L. K. (1998). Using
objects as tokens reinforcers for children with autism.
Journal of Autism and Development Disorders, 28,
189–198.
Charlop-Christy, M. H., & Kelso, S. E. (2003). Teaching
children with autism conversational speech using a cue
card/written script program. Education and Treatment
of Children, 26, 108–127.
Crimmins, D. B., Durand, V. M., Theurer-Kaufman, K., &
Everett, J. (2001). Autism program quality indicators:
A self review and quality improvement guide for
schools and programs serving students with autism
spectrum disorders. Retrieved May 12, 2011, from
http://www.p12.nysed.gov/specialed/autism/apqi.htm
Delprato, D. J. (2001). Comparisons of discrete-trial and
normalized behavioral language intervention for
young children with autism. Journal of Autism and
Developmental Disorders, 31, 315–325.
Dunlap, G. (1984). The influence of task variation and
maintenance tasks on the learning and affect of autistic
children. Journal of Experimental Child Psychology,
37, 41–64.
Dunlap, G., & Koegel, R. L. (1980). Motivating autistic
children through stimulus variation. Journal of
Applied Behavior Analysis, 13, 619–627.
Egel, A. L. (1981). Reinforcer variation: Implications for
motivating developmentally disabled children. Jour-
nal of Apllied Behavior Analysis, 14, 3–12.
Fisher, W. P., Bowman, C. C., Hagopian, L. P. (1992). A
comparsion of two approaches for identifying rein-
forcers for persons with severe and profound
disabilities. Journal of Applied Behavior Analysis,
25, 491–498.
Levinson, L. J., & Reid, G. (1993). The effects of exercise
intensity in the stereotypic behaviors of individuals
with autism. Adapted Physical Activity Quarterly, 10,
255–268.
Lopez, B. R., Hill, D. E., Shaw, S., & Gabriels, R. L.
(2007). School consultation and interventions for
Education as Therapy
middle school and high school students with autism.
In R. L. Gabriel & D. E. Hill (Eds.), Growing up with
autism (pp. 247–271). New York: The Guilford Press.
McClannahan, L. E., & Krantz, P. J. (1997). In search of
solutions to prompt dependence: Teaching children
with autism to use photographic activity schedules.
In D. M. Baer & E. M. Pinkston (Eds.), Environment
and behavior (pp. 271–278). Boulder, CO: Westview
Press.
Mesibov, G. B., Schopler, E., & Hearsey, K. A. (1994).
Structured teaching. In E. Schopler & G. B. Mesibov
(Eds.), Behavioral issues in autism. New York:
Plenum Press.
Mesibov, G. B., & Shea, V. (1996). Full inclusion of
students with autism. Journal of Autism and
Developmental Disorders, 26(3), 337–346.
Morris, R. J., & Mather, N. (2008). Evidence-based inter-
ventions for students with learning and behavioural
challenges. New York: Routledge.
New Jersey State Department of Education. (2004).
Autism program quality indicators: A self-review and
quality improvement guide for programs serving
young students with autism spectrum disorder.
Retrieved May 12, 2011, from http://celebratethe-
children.org/old/Documents/Indicators.pdf
Noland, R., Cason, N., & Lincoln, A. (2007). Building
a foundation for successful school transitions and edu-
cational placement. In R. L. Gabriel & D. E. Hill
(Eds.), Growing up with autism (pp. 205–227).
New York: The Guilford Press.
Roane, H. S., Vollmer, T. R., Ringdahl, J. E., & Marcus,
B. A. (1998). Evaluation of brief stimulus assessment.
Journal of Applied Behavior Analysis, 31, 605–620.
Sansosti, F. J., Powell-Smith, K. A., & Cowan, R. J.
(2007). High-functioning autism/Asperger syndrome
in schools. New York: The Guilford Press.
Schopler, E., Brehm, S., Kinsbourne, M., & Reichler, R. J.
(1971). The effect of treatment structure on
development in autistic children. Archives of General
Psychiatry, 24, 415–421.
Steedman, W. (2007). Advocating for services: Legal
issues confronting parents and guardians. In R. L.
Gabriel & D. E. Hill (Eds.), Growing up with autism
(pp. 145–163). New York: The Guilford Press.
Tarbox, R. S., Ghezzi, P. M., & Wilson, G. (2006). The
effects of token reinforcement on attending in a young
child with autism. Behavioral Interventions, 21(3),
155–164.
Yell, M. L., Rogers, D., & Rogers, E. L. (1998). The legal
history of special education: What a long, strange
trip it’s been! Remedial and Special Education, 19,
219–228.
Education as Therapy
▶ Educational Therapy
Educational Interventions
Education for All Handicapped
Children Act of 1975 (PL94-14L)
Pamela Brucker
Special Education and Reading,
Southern Connecticut State University,
New Haven, CT, USA
Synonyms
PL94-142
Definition
P.L.94-142, passed in 1975, was the public law
that ensured that all children with disabilities
would receive a free and appropriate education.
It was the first law to mandate special education
in all states. It has been reauthorized several
times, most recently in 2004 as the Individuals
with Disabilities Education Act (IDEA).
See Also
▶ Individuals with Disabilities Education Act
(IDEA)
▶ Legal education rights
References and Readings
IDEA Partnerships. www.fape.org
Nation Dissemination Center for Children with Disabil-
ities. www.nichcy.org
Turnbull, A, Wehmeyer, M. L., & Turnbull, R. (2009).
Exceptional lives: Special education in today’s
schools. Prentice-Hall, pp. 8–21.
U.S. Department of Education, Office of Special Educa-
tion Programs. www ed.gov.osep
Vaughn, S., Bos, C., & Schumm, J. S. (2010). Teaching
exceptional, diverse, and at-risk students. Prentice-
Hall, pp. 2–17.
Educational Assistant
▶ Para-educator
1061 E
Educational Interventions
Michelle Lestrud
The Gengras Center, University of Saint Joseph,
West Hartford, CT, USA
Definition
E
The role of education for all children is to provide
the experiences needed to learn skills that will
lead to “personal independence and social
responsibility” (National Research Council
[NRC], 2001, p. 40). Educational interventions
provide students with the support needed to
acquire the skills being taught by the educational
system and should address functional skills, aca-
demic, cognitive, behavioral, and social skills
that directly affect the child’s ability access an
education. For students with autism spectrum
disorders, the interventions often address some
of the core deficits in the areas of communication,
social skills, and behavioral differences. The
interventions should be aimed at skills that need
to be acquired or that need to be performed more
often to lead to successful results. For children
with autism, these educational interventions must
be specific and targeted to address the deficits and
lead to generalization and maintenance.
Educational interventions vary widely
depending on the needs and age of the student,
resources available, background of the team
members, philosophy of the program, parental
requests and beliefs, and student progress. In
addition, the interventions used are based on
the child’s profile which should include thor-
ough assessments and reports detailing
strengths, weaknesses, learning style, prefer-
ences, past successes, etc., and should lead to
the most successful outcome. Data to monitor
and assess the interventions should be reviewed
a regular basis to determine effectiveness and to
link progress or lack of progress specifically to
the intervention. Prescribed interventions
change over time as new research is conducted,
as new theories are developed, and as new tech-
nology is designed.
E 1062
See Also
▶ Academic Supports
▶ Activity-Based Instruction
▶ Early Intervention
▶ Education
References and Readings
Carter, E. W., Sisco, L. G., Yun-Ching, C., & Stanton-
Chapman, T. L. (2010). Peer interactions of students
with intellectual disabilities and/or autism: A map of
the intervention literature. Research & Practice for
Persons with Severe Disabilities, 35(3/4), 63–79.
Hume, K., Loftin, R., & Lantz, J. (2009). Increasing inde-
pendence in autism spectrum disorders: A review of
three focused interventions. Journal of Autism and
Developmental Disorders, 39, 1329–1338.
Lynch, S. L., & Irvine, A. N. (2009). Inclusive education
and best practice for children with autism spectrum
disorder: An integrated approach. International Jour-
nal of Inclusive Education, 13(8), 845–859.
National Research Council. (2001). Educating children
with autism. Committee on Educational interventions
for Children with Autism (Catherine Lord and James
P. McGee, Eds.). Division of Behavioral and Social
Sciences and Education. Washington, DC: National
Academy Press.
Odom, S. L., Collet-Klingenberg, L., Rogers, S. J., &
Hatton, D. D. (2010). Evidence-based practices in
interventions for children and youth with autism
spectrum disorders. Preventing School Failure,
54(4), 275–282.
Sherer, M. R., & Schreibman, L. (2005). Individual
behavioral profiles and predictors of treatment
effectiveness for children with autism. Journal of
Consulting and Clinical Psychology, 73(3), 525–538.
Educational Psychology
Arlette Cassidy
Psychologist, The Gengras Center, University of
Saint Joseph, West Hartford, CT, USA
Definition
Educational psychology is the study of the rela-
tionship between learning and our physical and
social environments. Educational psychologists
study the psychological processes involved in
learning and develop strategies for enhancing
Educational Psychology
the learning process. Educational development
focuses on the cognitive development, and what
a teacher can do impacts the development of the
child. It teaches about how children learn and how
they can be taught for them to be successful. Edu-
cational psychologists “study what people think
and do as they teach and learn a particular curric-
ulum in a particular environment where education
and training are intended to take place.” Two fun-
damental assumptions that underlie formal educa-
tional systems are that students (a) retain
knowledge and skills they acquire in school and
(b) can apply them in situations outside the class-
room. Aspirations of the discipline rested on the
application of the scientific methods of observa-
tion and experimentation to educational questions.
Ultimately, the goal of those working in the field of
educational psychology is to understand the pro-
cesses and conditions under which human beings,
both in childhood and throughout their lifespan,
learn to become mature human beings who fulfill
their individual potential, live in service to their
community, and exercise loving stewardship over
the environment.
It is likely that educational psychologists will
continue to contribute to education as they learn
more about the brain and how learning occurs;
the development of intellect, affect, personality,
character, and motivation; ways of assessing
learning; and the creation of multifaceted learn-
ing environments.
The Journal of Educational Psychology is
a peer-reviewed academic journal that was
established in 1910 and covers educational
psychology. It is published by the American
Psychological Association.
See Also
▶ School Psychologist
References and Readings
Alexander, P. A. (1996). The past, present, and future of
knowledge research: A reexamination of the role of
knowledge in learning and instruction. Educational
Psychologist, 31, 89–92.
Educational Therapy
Berliner, D. C. (1993). The 100-year journey of educa-
tional psychology: From interest, to disdain, to respect
for practice. In T. K. Fagan & G. R. Vanden-Bos
(Eds.), Exploring applied psychology: Origins and
critical analyses. Washington, DC: American Psycho-
logical Association.
Mayer, R. E. (1992). Cognition and instruction: Their his-
toric meeting within educational psychology. Journal of
Educational Psychology, 84, 405–412.
Woolfolk Hoy, A. (2001). Educational psychology (8th ed.).
Boston: Allyn and Bacon.
Zimmerman, B. J., & Schunk, D. H. (Eds.). (2002). Educa-
tional psychology: A century of contributions. Mahwah,
NJ: Erlbaum.
Educational Psychotherapy
▶ Educational Therapy
Educational Testing
Michele Goyette-Ewing
Yale Child Study Center, New Haven, CT, USA
Synonyms
Academic testing; Achievement testing
Definition
Educational testing refers to the formal assessment
of academic achievement. This can take the form of
group or individually administered tests which to
formally evaluate performance in the areas of read-
ing, decoding, and comprehension; writing, spell-
ing, mathematics, computation, and problem
solving; and, on occasion, other subject areas such
as science. Test scores compare the individual’s
performance to age-based or grade-based norma-
tive groups. These scores are frequently used as part
of the assessment academic progress and in the
diagnosis and monitoring of specific learning dis-
abilities or learning disorders. Commonly used
individually administered educational testing
1063 E
instruments include the Wechsler Individual
Achievement Test 3rd Edition, the Woodcock-
Johnson Achievement Battery, and the Kaufman
Achievement Battery for Children Edition II.
The Achievement Test Desk Reference: A
Guide to Learning Disability Identification by
Dawn P. Flanagan, Samuel O. Ortiz, Vincent C.
Alfonso, and Jennifer T. Mascolo (Jun 30, 2006).
E
References and Readings
Flanagan, D. P., Ortiz, S. O., Alfonso, V. C., & Mascolo,
J. T. (2006). The achievement test desk reference:
A guide to learning disability identification. Hoboken,
NJ: Wiley.
Educational Therapy
Rita Jordan
School of Education, The University of
Birmingham, Birmingham, UK
Synonyms
Education as therapy; Educational psychother-
apy; Therapeutic education
Definition
Educational therapy (also known as educational
psychotherapy) has roots in early psychoanalyti-
cal models of child development but is now more
concerned with remediation of learning and emo-
tional difficulties based on neuropsychological
models. In the UK, there is a master’s qualifica-
tion in educational psychotherapy but no official
role for educational therapists (ETs) within the
educational system and most work is undertaken
privately. In the USA, the work of ETs is also
private but certified by professional organizations
such as the Association of Educational Therapists
(AET). The focus of the work of ETs is on those
with specific learning difficulties (such as
E 1064
dyslexia) and emotional and behavioral difficul-
ties, rather than ASD. Their goal is to improve
academic success (Ficksman & Adelizzi, 2010)
by addressing psychological factors that may be
impeding learning. The AET approves training
courses in educational therapy, which are at
postgraduate to master’s level. Entry
requirements include qualified teacher status,
educational psychology, or qualified therapist
status with some experience of special education.
Other routes may be approved by the AET. ETs
may work with individuals within the autism
spectrum, but the efficacy of such work has not
been established. They focus on changing, or
building, underlying psychological processes
which are involved in auditory processing,
reading, or on positively influencing self-esteem
and optimism, which are known to be related to
academic success. Evidence of efficacy, even in
cases without an ASD, is largely based on
case study or pre-post designs (Maslow &
Ungerleider, 2007), which are not scientifically
robust.
Jordan (2005) used the term “educational ther-
apy” to refer to aspects of special education in
autism spectrum disorders (ASD) that address the
core symptoms; it is included as a concept in
specialist autism training for professionals in the
UK and features in the UK and European guide-
lines for good practice in ASD. It is intended to be
an adjunct to academic education, but individuals
with ASD will also need compensatory tech-
niques to help them access the culturally valued
skills, knowledge, and understanding to which
everyone is entitled (i.e., the usual curriculum).
Educational therapy is intended to characterize
the work of all who educate and care for those on
the spectrum; it is not confined to therapists. It is
based on the recognition that explicit specialist
education can help remediate many problems in
ASD, but specific attempts to do so require eval-
uation. Golan et al. (2010) (a matched controlled
study without random allocation to groups) and
Herrera et al. (2008) (a small case study) are
typical of evaluations in this area, where there is
still need for more robust scientific evaluation.
Neither “education as therapy,” as used by
Jordan, nor the work of ETs is meant to replace
Effexor
the entitlement of children with ASD to a full and
broad education. Therapists, including ETs, may
have a role in ASD in addressing specific diffi-
culties or in meeting emotional and mental health
needs. ETs may also address some of the comor-
bid specific learning difficulties that may accom-
pany ASD. However, such roles are aids to
development and to access educational entitle-
ment, rather than alternatives to education. Like-
wise, Jordan’s view of educational therapy
expresses the need to extend education in ASD
to include specific teaching of aspects of
development that occur naturally in those not on
the autism spectrum, not to limit education to
those aspects.
See Also
▶ Cognitive Behavioral Therapy (CBT)
▶ Cognitive Enhancement Therapy
References and Readings
Ficksman, M., & Adelizzi, J. U. (Eds.). (2010). The clinical
practice of educational therapy. London: Taylor &
Francis.
Golan, O., Ashwin, E., Granader, Y., McClintock, S., Day,
K., Leggett, V., et al. (2010). Enhancing emotional
recognition in children with autism spectrum condi-
tions: An intervention using animated vehicles with
real emotional faces. Journal of Autism and Develop-
mental Disorders, 40, 269–279.
Herrera, G., Alcantua, F., Jordan, R., Blanquer, A., Labajo,
G., & De Pablo, C. (2008). Development of symbolic
play through the use of virtual reality tools in children
with autistic spectrum disorders: Two case studies.
Autism: The International Journal of Research & Prac-
tice, 12(2), 143–158.
Jordan, R. R. (2005). Managing autism and Asperger’s
syndrome in current educational provision. Paediatric
Rehabilitation, 8, 104–112.
Maslow, P., & Ungerleider, D. (2007). The efficacy of
educational therapy Pt.2. The Educational Therapist,
28(3), 16–21.
Effexor
▶ Venlafaxine
Ego Development
Effexor XR
▶ Venlafaxine
Efficacy
▶ Self-advocacy
Efficiency (Behavioral Assessment)
Jessica Rohrer
The Center for Children with Special Needs,
Glastonbury, CT, USA
Definition
Efficiency refers to the principle that responses
which require less effort and produce more rein-
forcement will occur more frequently than
responses that require more effort and produce
the same or less reinforcement. Responses that
take less effort and produce a similar level of
reinforcement as more effortful responses are
considered to be more efficient. To increase the
likelihood that a desired behavior will occur,
the environment or other antecedents can be
manipulated to increase the efficiency of the
response (decrease the response effort), therefore
making the response more likely. To decrease the
likelihood that an undesirable behavior will
occur, the efficiency of that response should be
decreased (increase response effort), therefore
making it more likely that the individual
will engage in competing behaviors that require
less effort.
See Also
▶ Response Effort
1065 E
References and Readings
Miltonberger, R. G. (2004). Behavior modification princi-
ples and procedures (3rd ed.). Belmont, CA:
Wadsworth/Thomson Learning.
Effort (Behavioral Assessment)
E
Jessica Rohrer
The Center for Children with Special Needs,
Glastonbury, CT, USA
Synonyms
Response effort
Definition
Response effort is the amount of effort that
a person must put forth to successfully com-
plete a specific behavior. The amount of effort
required to complete the behavior has an
impact on the frequency at which that behav-
ior will be emitted. If two responses result in
fairly equal reinforcement, the behavior that
requires less response effort is more likely to
occur than the behavior that requires more
response effort.
References and Readings
Miltonberger, R. G. (2004). Behavior modification
principles and procedures (3rd ed.). Belmont, CA:
Wadsworth/Thomson Learning.
Retrieved from http://www.olemiss.k12.in.us/intervention/
behavior/respeffort.pdf
Ego Development
▶ Identity Development
E 1066
EHI
▶ Edinburgh Handedness Inventory
EI
▶ Early Intervention
Eisenberg, Leon
Fred R. Volkmar
Director – Child Study Center, Irving B. Harris
Professor of Child Psychiatry, Pediatrics and
Psychology, School of Medicine,
Yale University, New Haven, CT, USA
Name and Degrees
Leon Eisenberg received both his B.A. and M.D.
degrees from the University of Pennsylvania. He
completed an internship at Mt. Sinai before
teaching briefly at the University of Pennsylva-
nia. Following work as a psychiatrist in the
U.S. Army, he became a resident at Sheppard
Pratt hospital before beginning child psychiatry
training at Johns Hopkins.
Major Appointments (Institution,
Location, Dates)
Johns Hopkins University: Baltimore, MD,
1953–1967, Instructor, Associate Professor,
and Professor and Chief of Child Psychiatry.
Harvard University, Cambridge, MA,
1967–1993, Professor of Psychiatry, Chair
Department of Social Medicine and
Health Policy, Maude and Lillian Presley
Professor of Social Medicine, Emeritus status
in 1993.
EHI
Major Honors and Awards
Leon Eisenberg was the recipient of numerous
honorary degrees and awards; some of the
major awards include the Richmond award
from the American Academy of Pediatrics,
the Thomas W. Salmon Medal from the New
York Academy of Medicine, and Juan José
López Ibor Award from the World Congress
of Psychiatry. In addition, several awards have
been named in his honor. In 2009, the Leon
Eisenberg Chair of Child Psychiatry at
Children’s Hospital Boston was named in his
honor.
Landmark Clinical, Scientific, and
Professional Contributions
Dr. Eisenberg conducted the first follow-up study
(with Leo Kanner) of children with autism. Other
accomplishments included his role in the first
randomized control study of psychopharmacol-
ogy in children and the first randomized con-
trolled trial of stimulants in adolescents and of
brief psychotherapy. He had long-standing inter-
ests in the social brain and in social medicine
including an active role in working with Physi-
cians for Human Rights.
Short Biography
A child psychiatrist and medical educator,
Dr. Eisenberg was an original contributor to
a series of innovations in the field of child psychi-
atry. These included, in collaboration with his
mentor Leo Kanner, M.D., some of the first fol-
low-up studies of children with autism, in devel-
opment of randomized clinical trials (RCTs),
evidence-based medicine, and social medicine
and international advocacy including for human
rights.
Dr. Eisenberg followed Leo Kanner as the
leader of child psychiatry at Johns Hopkins until
his retirement there in 1967. At that time, he moved
to Harvard University where he assumed leadership
of the child psychiatry program. In 1974, he was
Electroencephalogram (EEG)
appointed the Maude and Lillian Presley Professor
of Psychiatry and, in 1980, became chair of the
Department of Social Medicine and Health Policy
until his retirement in 1993 when he became emer-
itus. He remained an active researcher and advocate
until shortly before his death.
1067 E
Kanner, L., & Eisenberg, L. (1958). Child psychiatry;
mental deficiency. American Journal of Psychiatry,
114, 609–615.
Rutter, M., Lebovici, S., Eisenberg, L., Sneznevskij,
A. V., Sadoun, R., Brooke, E., et al. (1969).
A triaxial classification of mental disorders in child-
hood. Journal of Child Psychology and Psychiatry, 10,
41–61.

See Also
Elated, Euphoric and Grandiose E
▶ Kanner, Leo
▶ Mania

References and Readings

Elective Mutism
Conners, C. K., Rothschild, G., Eisenberg, L., Schwartz,
L. S., & Robinson, E. (1969). Dextroamphetamine sul-
fate in children with learning disorders. Archives of Gen- ▶ Selective Mutism
eral Psychiatry, 21, 182–190.
Eisenberg, L. (1956). The autistic child in adolescence.
American Journal of Psychiatry, 112, 607–612.
Reprinted in Alexander et al. (Eds.). (1959). Psycho- Electroencephalogram (EEG)
pathology. Cambridge: Harvard University Press.
Eisenberg, L. (1957a). The fathers of autistic children.
American Journal of Orthopsychiatry, 27, 715–724. Benjamin Aaronson
Eisenberg, L. (1957b). The course of childhood schizo- Psychiatry and Behavioral Sciences, UW Autism
phrenia. Archives of Neurology and Psychiatry, 78, Center, University of Washington, Seattle,
69–83.
WA, USA
Eisenberg, L. (1957c). Progress in neuropsychiatry. Jour-
nal of Pediatrics, 51, 334–349.
Eisenberg, L. (1957d). Psychiatric implications of brain
damage in children. Psychiatric Quarterly, 31, 72–92. Synonyms
Eisenberg, L. (1968). The social development of human
intelligence. Harvard Medical Alumni Bulletin, 43, 2–7;
Reprinted in Freemen, H. (Ed.). (1969). Progress in Electroencephalography
mental health. Churchill.
Eisenberg, L. (1998). Nature, niche and nurture: The role
of social experience in transforming genotype into
phenotype. Academic Psychiatry, 22, 213–222.
Definition
Eisenberg, L. (2004). Social psychiatry and the human
genome: Contextualizing heritability. British Journal An electroencephalogram is a graphical represen-
of Psychiatry, 184, 101–103. tation of the brain’s electrical activity. In human
Glaser, K., & Eisenberg, L. (1956). Maternal deprivation.
assessment, electrodes are placed at various loca-
Pediatrics, 18, 626–642.
Kanner, L., & Eisenberg, L. (1956a). Child psychiatry; tions on the scalp. As neurons in the brain fire,
mental deficiency. American Journal of Psychiatry, these electrodes capture the resulting voltage,
112, 531–534. which is then amplified and recorded. This elec-
Kanner, L., & Eisenberg, L. (1956b). Early infantile
trical activity oscillates quite rapidly. The num-
autism 1943–1955. American Journal of Orthopsychi-
atry, 26, 55–65. Reprinted in: Alexander et al. (Eds.). ber of oscillations over a phase of time can be
Op. cit. Reprinted in Psychiatric Research Report measured and are termed “frequency.” Variations
1957 (April), American Psychiatric Association, in frequency have been historically quantified in
pp. 55–65.
terms of oscillations per 1-s period as hertz (Hz).
Kanner, L., & Eisenberg, L. (1957). Child psychiatry:
Mental deficiency. American Journal of Psychiatry, Common categorizations of frequencies include
113, 617. alpha (8–13 Hz), beta (13–30 Hz), gamma
E 1068
(30–600 Hz), delta (4 Hz), theta (4–8 Hz), and
mu (8–13 Hz).
A subtype of electroencephalography
examines changes in brain activity time-locked
to particular events, termed event-related poten-
tials (ERPs). ERPs are generally assessed in
small windows of time, in the tens and hundreds
of milliseconds.
See Also
▶ Electroencephalography
▶ Event-Related Potential
▶ Evoked Potentials
▶ Mu Rhythm
References and Readings
Andreassi, J. L. (2007a). Psychophysiology: Human
behavior & physiological response (5th ed.). Mahwah,
NJ: Lawrence Erlbaum Associates.
Andreassi, J. L. (2007b). The nervous system and mea-
surement of its activity. In J. T. Cacioppo, L. G.
Tassinary, & G. G. Berntson (Eds.), Handbook of
psychophysiology (3rd ed., pp. 85–119). Cambridge,
UK: Cambridge University Press.
Herrmann, C. S., Grigutsch, M., & Busch, N. (2005). EEG
oscillations and wavelet analysis. In T. C. Handy (Ed.),
Event-related potentials: A methods handbook
(pp. 229–259). Cambridge, MA: MIT Press.
Electroencephalography
Benjamin Aaronson
Psychiatry and Behavioral Sciences, UW Autism
Center, University of Washington, Seattle,
WA, USA
Synonyms
Electroencephalogram (EEG)
Definition
Electroencephalography (EEG) is the recording
of brain’s electrical activity. In human
Electroencephalography
assessment, electrodes are placed at various loca-
tions on the scalp. As neurons in the brain fire,
these electrodes capture the resulting voltage,
which is then amplified and recorded. This elec-
trical activity oscillates quite rapidly. The num-
ber of oscillations over a phase of time can be
measured and are termed “frequency.” Variations
in frequency have been historically quantified in
terms of oscillations per 1-s period as hertz (Hz).
Common categorizations of frequencies include
alpha (8–13 Hz), beta (13–30 Hz), gamma
(30–600 Hz), delta (4 Hz), theta (4–8 Hz), and
mu (8–13 Hz).
A subtype of electroencephalography
examines changes in brain activity time-locked
to particular events, termed event-related poten-
tials (ERPs). ERPs are generally assessed in
small windows of time, in the tens and hundreds
of milliseconds.
See Also
▶ Electroencephalogram (EEG)
▶ Event-Related Potential
▶ Evoked Potentials
▶ Mu Rhythm
References and Readings
Andreassi, J. L. (2007a). Psychophysiology: Human
behavior & physiological response (5th ed.). Mahwah,
NJ: Lawrence Erlbaum Associates.
Andreassi, J. L. (2007b). The nervous system and
measurement of its activity. In J. T. Cacioppo, L. G.
Tassinary, & G. G. Berntson (Eds.), Handbook of
psychophysiology (3rd ed., pp. 85–119). Cambridge,
UK: Cambridge University Press.
Herrmann, C. S., Grigutsch, M., & Busch, N. (2005). EEG
oscillations and wavelet analysis. In T. C. Handy (Ed.),
Event-related potentials: A methods handbook
(pp. 229–259). Cambridge, MA: MIT Press.
Electron Transport Chain Disorders
▶ Mitochondrial Deficits/Disorders
Elementary and Secondary Education Act (No Child Left Behind)
Electrophysiology
▶ Neurophysiology
Elementary and Secondary
Education Act (No Child Left Behind)
Kristin Ruedel
Department of Special Education, University of
Maryland Washington State University,
Richland, WA, USA
Definition
The No Child Left Behind (NCLB) Act of 2001
is the most recent reauthorization of the Elemen-
tary and Secondary Education Act (ESEA). It
was signed into law on January 8, 2002, and
received an overwhelming bipartisan majority
in both the House and the Senate. NCLB repre-
sents the most significant expansion of the fed-
eral government into education in our history as
it has dramatically increased federal mandates
and requirements on states, school districts, and
public schools. The Obama administration
released its blueprint for revising the Elemen-
tary and Secondary Education Act (ESEA) on
March 13, 2010.
The primary goals of NCLB are to increase
achievement of all students in American public
schools; reduce the achievement gap based on
race, ethnicity, language, socioeconomic status,
and disability; and ensure that students in every
public school achieve important learning goals
while being educated in safe classrooms by
well-prepared teachers.
NCLB is based on the following key
principles:
1. Accountability for results: By the 2005–2006
school year, each state must test students
annually in grades 3 through 8 in reading and
math and students in grades 10–12 at least
once in reading and math. Every student will
1069 E
be assessed according to each state’s standard
for proficiency in reading/language arts, math,
and science by the end of the 2013–2014
school year. Student test scores must be
made accessible to parents and communities.
Test score data must be disaggregated by
identified subgroups such as race/ethnicity,
socioeconomic status, and disability.
Schools that do not demonstrate “adequate
yearly progress” (AYP) in student proficiency
E
levels at large and within each of the
subgroups must provide students with supple-
mental services such as free tutoring or after-
school assistance.
2. Parental choice: Schools must provide parents
with a report about the overall achievement of
students in the school their child attends, the
qualifications of their child’s teacher, and
school safety. Parents of children in schools
that are not making AYP for at least two con-
secutive years have the option of transferring
their child to an alternate school within the
school district. Parents also have the right to
transfer their student if the school their child is
attending is considered persistently dangerous
or if their child has been a victim of a violent
crime.
3. Teacher quality: Each state must develop
a plan to ensure that all teachers of core aca-
demic subjects will be highly qualified by the
end of the 2005–2006 school year. Highly
qualified means that each teacher has full cer-
tification and a bachelor’s degree and has
passed a state-administered test on core aca-
demic subject knowledge.
4. Scientifically based methods of teaching:
There is an emphasis on the use of scientifi-
cally based methods of teaching under NCLB.
Schools that fail to meet adequate student
achievement goals are required to use scien-
tifically based instructional methods in order
to remain open.
5. Local flexibility: NCLB grants states and
school districts with unprecedented flexibil-
ity in how they use federal education funds
under NCLB in order to permit school
districts to respond to specific local
problems.
E 1070
References and Readings
ESEA reauthorization: A blueprint for reform. U.S.
Department of Education. Retrieved June 6, 2011,
from http://www2.ed.gov/policy/elsec/leg/blueprint/
index.html
Overview and introduction to the No Child Left Behind
Act. U.S. Department of Education. Retrieved June 7,
2001, from http://www2.ed.gov/nclb/landing.jhtml
The No Child Left Behind Act of 2001. U.S. Department of
Education. Retrieved June 6, 2011, from http://
www2ed.gov/policy/elsec/leg/esea02/index.html
Yell, M. L., & Drasgow, E. (2005). No child left behind
act: A guide for professionals. Upper Saddle River,
NJ: Merrill/Prentice Hall.
Elevated, Expansive, or Irritable
Mood
▶ Mania
Elgar, Sybil
Adam Feinstein
Autism Cymru and Looking Up, London, UK
Major Appointments (Institution,
Location, Dates)
Sybil Elgar was a pioneer in the education and
care of both children and adults with autism
both in the United Kingdom and internation-
ally. As Lorna Wing has written, Elgar was
“the UK’s first autism-specific teacher and an
inspiration to those who knew her, at a time
when autism was still ill-defined and widely
misunderstood.” In 1964, Sybil Elgar and the
newly formed Society for Autistic Children
(now the National Autistic Society) managed
to purchase premises to open the world’s first
residential school for children with autism, in
Ealing, West London. Elgar was a pioneer
twice over, as she also founded Somerset
Court, the first residential community for
adults with autism, in Brent Knoll, Somerset,
in 1974.
Elevated, Expansive, or Irritable Mood
Major Honors and Awards
Sybil Elgar was a founding member of the British
National Autistic Society. She was awarded
member of the Order of the British Empire
(MBE) in 1975.
Landmark Clinical, Scientific, and
Professional Contributions
There is some evidence to suggest that the
structured approach which forms the basis of
TEACCH – one of the main educational
approaches to autism used worldwide today –
was inspired, at least in part, by Sybil Elgar’s
pioneering work in the United Kingdom.
Dr Eric Schopler, who founded TEACCH in
North Carolina in the 1970s, visited the Sybil
Elgar School in the United Kingdom in the
previous decade and was very impressed by
what he saw.
Short Biography
Sybil Lilian Elgar was born in Willesden, North
West London, on June 10, 1914. After leaving
school, she became a town clerk’s assistant
before getting a job as a school secretary. She
had no money to go to college, and staying at
home to be with her then widowed and unwell
mother, she took a Montessori teaching diploma
as a correspondence course. Her interest in
helping children was first sparked during her
Montessori training when a visit to a hospital in
London for “severely emotionally disturbed
children” in 1958 left her deeply shocked. Elgar
revisited the hospital in 1960 and, seeing that
nothing had changed, decided to set up her own
school, initially in the basement of her home.
She developed a structured approach to teaching,
giving her pupils clear and simple instructions
and visual aids to ensure they understood what
was required of them. Her methods ran counter
to mainstream educational thought at the
time. However, all the children in her class
made substantial progress. Demand for her
Eligibility (for Services Under IDEA/ADA, etc.)
teaching rapidly grew, and in 1964, Elgar bought
the premises to open the world’s first residential
school for children with autism, in Ealing, West
London. She also founded Somerset Court, the
first residential community for adults with
autism, in Brent Knoll, Somerset, in 1974. Elgar
died on January 8, 2007, at the age of 92.
References and Readings
Feinstein, A. (2010). A history of autism: Conversations
with the pioneers. Oxford, England: Wiley-Blackwell.
Eligibility (for Services Under
IDEA/ADA, etc.)
John W. Thomas
Quinnipiac University School of Law, Hamden,
CT, USA
Definition
“Eligibility” in the context of this encyclopedia
refers to qualification to receive reimbursement
for or benefits from a variety of private and public
programs.
Historical Background
Eligibility issues regarding ASD patients may
present in private health care insurance, public
health care insurance, education, disability bene-
fits, and antidiscrimination contexts.
Current Knowledge
Private Health Care Insurance
Treatment for ASD can be costly, with annual
expenses exceeding $50,000 (NCSL) and mean
lifetime care expenses totaling $3.2 million
(Ganz, 2006). As a result, eligibility for private
health insurance coverage for ASD-related
1071 E
treatment can be important to people with ASD
and their families.
Insurance coverage is especially difficult to
obtain for behavioral therapies such as Applied
Behavioral Analysis therapy (ABA). Kaiser
Permanente, for example, classifies ABA therapy
as educational rather than clinical treatment and,
thus, denies insurance reimbursement for its cost
(Reinke, 2008).
In response to insurance company reluctance
E
to cover treatment for ASD, state legislatures
have begun to address the issue. At this writing,
the legislatures of 35 states and the District of
Columbia have enacted laws mandating some
types of insurance coverage for the treatment of
ASD. Statutes in 23 of those states – Arizona,
Colorado, Connecticut, Florida, Illinois, Indiana,
Iowa, Kansas, Kentucky, Louisiana, Maine, Mas-
sachusetts, Missouri, Montana, Nevada, New
Hampshire, New Jersey, New Mexico, Pennsyl-
vania, South Carolina, Texas, Vermont, and Wis-
consin – make specific reference to treatment for
ASD or autism. The remaining dozen mandate
coverage for mental health conditions that may
include ASD. The types of coverage mandated
under these laws vary from diagnostic testing to
a variety of therapies and treatment options.
Some laws prohibit insurers from setting pre-
mium or coinsurance rates based solely on an
ASD diagnosis.
State laws, however, are not applicable to all
insurance policies. The federal Employee Retire-
ment Income Security Act (ERISA) exempts self-
funded, employer-provided health insurance
plans from state coverage mandates (ERISA).
As a result, in 2009, the United States Congress
considered enacting the Autism Treatment
Acceleration Act. But, the bill failed to pass
either in the house of representatives or the
senate. As of this writing, there is no federal
mandate that insurers cover treatments or
therapies for ASD.
Public Health Insurance: Medicaid
Conventional Medicaid Eligibility
Medicaid is a national health care program
funded jointly by the federal and state govern-
ments. Adopted in 49 states and the District of
E 1072
Columbia and represented in the fiftieth state,
Arizona, by a similar program, Medicaid pro-
vides services to the poor. Eligibility is largely
limited to those with incomes no higher than the
federal poverty level, with slightly higher
incomes allowed for women, children, and other
groups. Those who meet the income and
other resource prerequisites qualify for a wide
range of health care benefits, including treatment
for ASD.
Services available to those with ASD vary by
state. Medicaid insurers in some states cover
a wide range of services, including Applied
Behavioral Analysis (ABA). In other states,
insurers are more reluctant to cover ABA and
other treatment modalities for ASD. In 2003, the
Centers for Medicare and Medicaid Services
issued a directive that characterized ABA as
habilitative rather than rehabilitative and, thus,
not mandatory coverage. In response, many
state Medicaid agencies have ceased providing
reimbursement for ABA (Mauch, Pfefferle,
Booker, Pustell, & Levin, 2011).
Medicaid “Waiver” Eligibility
All 49 states, the District of Columbia, and Ari-
zona also participate in the Medicaid waiver pro-
gram. Under these programs, parental financial
resource limitations are “waived” for certain ser-
vices for people under the age of 21 with devel-
opmental disabilities or long-term illnesses.
These waiver programs cover home- and com-
munity-based services (HCBS). A person qual-
ifies for HCBS services if he or she otherwise
“would require the level of care provided in
a hospital or a nursing facility or intermediate
care facility for the mentally retarded” (42 U.S.
C. } 1396n(c)).
Thirty states have ASD-specific waiver pro-
grams that delineate the specific services (Autism
NOW). Connecticut’s waiver, for example,
covers “residential habilitation, personal sup-
ports, respite, clinical behavioral supports,
supported employment, job coaching, commu-
nity transition services, life skills coaching, com-
munity transition services or short term crisis
stabilization to remain in their own home, family
home or other community home.”
Eligibility (for Services Under IDEA/ADA, etc.)
Patient Protection and Accountable Care Act
(PPACA)
By 2014, the PPACA, which congress enacted in
2010, will expand the Medicaid program to cover
nearly all people with incomes up to 133% of the
federal poverty level. The PPACA will also pre-
clude Medicaid from considering in an eligibility
determination resources other than income.
Disability Benefits
The Federal Social Security Program offers two
types of disability benefits for which children
with ASD may qualify.
Supplemental Security Income (SSI)
The SSI program provides monthly payments to
children from birth to age 18. Children whose
parents’ income and other financial resources
are within the statutory limits are eligible for
benefits if they are not “engaged in substantial
gainful activity” and are diagnosed with an
impairment that meets SSI’s disability definition
for children. Listed impairments include “mental
disorders,” which encompasses ASD.
At SSI’s enactment in 1973, the Social Secu-
rity Administration (SSA) required for eligibility
for benefits that a child’s impairment be “compa-
rable in severity” to an impairment that would
qualify an adult for benefits. In 1996, congress
modified the standard by enacting the Personal
Responsibility and Work Opportunity Reconcili-
ation Act of 1996 (PRA). This Act replaced the
“comparable severity” standard with a test to
determine whether a child suffers a “marked
and severe functional limitation.” Eligibility for
benefits requires two findings. First, the child’s
impairment must be “medically determinable.”
Second, the impairment must “meet, medically
equal, or functionally equal” a listed impairment
(20 CFR }416.92 and }416.926a).
SSA regulations establish six “domains” to
determine functional equivalence to a listed
impairment: “acquiring and using information,”
“attending and completing tasks,” “interacting
and relating with others,” “moving about and
manipulating objects,” “caring for yourself,”
and “health and physical well-being.” A child
must exhibit a “marked” limitation in at least
Eligibility (for Services Under IDEA/ADA, etc.)
two of these categories or an “extreme” limitation
in one. Factors relevant to these determinations
include “the child’s age; the effects of treatment
and/or medication; the effect of structured set-
tings; the need for assistive devices or adapta-
tions; school functioning, including attendance;
time spent in therapy; the effects of chronic ill-
ness; and the combined effects of multiple
impairments.” An “extreme” limitation exists
when the impairment or impairments “very seri-
ously” interfere with the ability to initiate, sus-
tain, or complete activities independently. This
status is consistent with a score three standard
deviations below the mean on an applicable stan-
dardized test. A “marked” limitation exists when
the impairment or impairments “seriously” inter-
fere with those same skills. This status is consis-
tent with a score of at least two but fewer than
three standard deviations below the mean on an
applicable standardized test.
The first step for determining eligibility for
SSI benefits based on ASD, the “medically deter-
minable” inquiry, requires a finding of deficien-
cies in “reciprocal social interaction and in verbal
and nonverbal communication and imaginative
activity, and a markedly restricted repertoire of
activities and interests” (Ruskell). The second
step typically finds “functional equivalence” to
the “mental disorders” listing and resolves not on
a finding of “extreme” limitation in a single
domain but on a “marked” limitation in two
domains, most commonly in “attending and com-
pleting tasks,” “interacting and relating with
others,” “caring for yourself,” and “health and
physical well-being.”
Finally, the ASD limitation must have existed
for at least 12 months.
Social Security Disability Insurance (SSDI)
SSDI provides benefits to adults who have
a disability that began before they reached the
age of 22 years. Because they are based on
the Social Security earning record of the
beneficiary’s parents, the social Security Admin-
istration considers SSDI to be a “child’s” benefit.
A disabled adult is entitled to SSDI benefits if one
of his or her parents is currently receiving Social
Security retirement or disability benefits or died
1073 E
after working long enough to qualify for some
form of Social Security benefit. In addition,
a “child” is eligible for SSDI benefits if he or
she received dependent benefits on a parent’s
Social Security earnings record prior to reaching
the age of 18.
SSDI eligibility differs from SSI eligibility in
that the recipient must meet the impairment def-
inition for adults. The adult disability impair-
ments include “autistic disorder and other
E
pervasive developmental disorders.”
Finally the “child” must not be engaged any
substantial work.
Education: The Individuals with Disabilities
Education Act (IDEA)
IDEA is a federal law that mandates the avail-
ability of a Free Appropriate Public Education
(FAPE) for all eligible children with disabilities.
IDEA defines “disability” as a person “(1) with
mental retardation, hearing impairments . . .
speech or language impairments, visual impair-
ments . . . serious emotional disturbance . . .
orthopedic impairments, autism, traumatic brain
injury, other health impairments, or specific
learning disabilities . . . (2) who needs special
education and related services because of his or
her disability or disabilities” (IDEA } 802,
emphasis supplied). Thus, children with ASD
are eligible for IDEA-related services.
IDEA’s regulations define autism as “a devel-
opmental disability significantly affecting verbal
and nonverbal communication and social interac-
tion, generally evident before age three that
adversely affects a child’s educational perfor-
mance. Other characteristics often associated
with autism are engagement in repetitive activi-
ties and stereotyped movements, resistance to
environmental change or change in daily rou-
tines, and unusual responses to sensory
experiences.”
A child with ASD is not eligible for IDEA-
related services if the “child’s educational perfor-
mance is adversely affected primarily because
the child has an emotional disturbance.” An
“emotional disturbance” is “a condition
exhibiting one or more of the following charac-
teristics over a long period of time and to
E 1074
a marked degree that adversely affects a child’s
educational performance”:
• “An inability to learn that cannot be explained
by intellectual, sensory, or health factors”
• “An inability to build or maintain satisfactory
interpersonal relationships with peers and
teachers”
• “Inappropriate types of behavior or feelings
under normal circumstances”
• “A general pervasive mood of unhappiness or
depression”
• “A tendency to develop physical symptoms or
fears associated with personal or school
problems”
IDEA’s regulations also classify schizophre-
nia as an emotional disturbance.
For those children diagnosed with ASD and not
an emotional disturbance, Part C of the IDEA,
Infants and Toddlers with Disabilities, provides
for developmental services for children from birth
to 3 years of age. Part B, Assistance for Education
of All Children with Disabilities, mandates educa-
tional services for children from ages 3 to 21. The
educational requirements of Part B include an indi-
vidualized education program (IEP) for each child
and demand the placement of each child in the
least restrictive environment (LRE) possible.
An “appropriate” education must address
a child’s specific educational needs. Determining
what is appropriate entails several steps. The
responsible state actor must conduct an individu-
alized assessment to ascertain a student’s
strengths and weaknesses. Next, an IEP team,
comprising representative of the school district,
a teacher, the child’s parents, and, if appropriate,
the child, must identify appropriate goals and
objectives for the student and construct an IEP
designed to aid the student in meeting the goals
and objectives. Finally, the IEP team is charged
with identifying the aids and services necessary
for the child to succeed in the IEP.
These services consist of “transportation and
such developmental, corrective, and other sup-
portive services as are required to assist a child
with a disability to benefit from special educa-
tion.” Specifically, they may include:
• Audiology
• Counseling services
Eligibility (for Services Under IDEA/ADA, etc.)
• Early identification and assessment of disabil-
ities in children
• Medical services for diagnosis or evaluation
• Occupational therapy
• Parent counseling and training
• Physical therapy
• Psychological services
• Recreation
• Rehabilitation counseling
• School health services
• Social work services
• Speech pathology
• Transportation
An IEP must include:
• “A statement of the child’s present levels of
academic achievement and functional”
• “A statement of measurable annual goals
including academic and functional”
• “A description of how the child’s progress
toward meeting the annual goals will be
measured”
• “A statement of the special education and
related services and supplementary aids and
services . . . to be provided”
• “An explanation of the extent, if any, to which
the child will not participate with nondisabled
children in the regular class and in extracur-
ricular and other nonacademic activities”
• “A statement of any individual appropriate
accommodations that are necessary to mea-
sure the academic achievement and functional
performance of the child”
• “The projected date for the beginning of the
services and program modifications and the
anticipated frequency, location, and duration
of those services and modifications”
• “Beginning not later than the first IEP to be
in effect when the child is 16 and updated
annually thereafter: appropriate measurable
postsecondary goals”
IDEA conditions state receipt of federal
funding on meeting its minimum requirements.
States may not provide fewer services but may
provide greater services.
The needs of children vary, and, as a result, chil-
dren with ASD will be eligible for varying IEPs and
services. Their needs and the services to which they
are entitled will also likely change over time.
Eligibility (for Services Under IDEA/ADA, etc.)
Antidiscrimination: The Americans with
Disabilities Act (ADA)
The ADA prohibits discrimination on the basis of
disability in employment, state and local govern-
mental services, public accommodations, trans-
portation, and telecommunications. A person is
“disabled” if he or she has a physical or mental
impairment that substantially limits one or more
major life activities, has a history or record of
impairment, or is perceived by others as having
an impairment.
The ADA does not enumerate the impairments
that are “substantially limiting,” leaving that
question to the regulators and courts. In the
decade and a half following the ADA’s enact-
ment in 1990, the federal courts, including the
United States Supreme Court, issued a number of
decisions construing the statutory phrase very
narrowly. This resulted in the denial of many
ADA claims, including claims of those with
ASD. In response, congress enacted the Ameri-
cans with Disabilities Act Amendments Act of
2008 (ADAAA). The ADAAA’s central feature
was a command that “the definition of disability
in this Act shall be construed in favor of broad
coverage of individuals under this Act, to the
maximum extent permitted under the terms of
the Act.”
Specifically, the ADAAA expanded the defi-
nition of “major life activities” by articulating
a non-exhaustive list of the activities: “caring
for oneself, performing manual tasks, seeing,
hearing, eating, sleeping, walking, standing,
lifting, bending, speaking, breathing, learning,
reading, concentrating, thinking, communicat-
ing, and working.” In addition, the Act included
“major bodily functions” within “major life
activities” and presented a non-exhaustive list of
these functions: “functions of the immune sys-
tem, normal cell growth, digestive, bowel, blad-
der, neurological, brain, respiratory, circulatory,
endocrine, and reproductive functions.”
The ADAAA also mandated that, with the
exception of eyeglasses and contact lenses, the
determination that impairment substantially
limits a major life activity “be made without
regard to the ameliorative effects of mitigating
measures” such as medication and other
1075 E
“assistive technology.” Most importantly for peo-
ple with ASD, the determination must be made
without regard to “learned behavioral or adaptive
neurological modifications.” A temporary
impairment, or one that is “episodic or in remis-
sion” qualifies as a disability even when inactive
“if it would substantially limit a major life activ-
ity when active.” Examples would include
posttraumatic stress disorder, epilepsy, or cancer.
On May 24, 2011, new regulations designed to
E
implement the ADAAA and issued by the Equal
Employment Opportunity Commission (EEOC),
the agency charged with enforcing the ADA,
went into effect. Echoing the ADAAA, the regu-
lations provide that “[t]he definition of disability
. . . shall be construed broadly, to the maximum
extent permitted by the terms of the ADA.” More
importantly, the regulations announce that the
ADAAA shifts the focus of an ADA claim from
whether a disability exists to “whether discrimi-
nation occurred.” Furthermore, the regulations
provide that the question whether an individual
is “substantially limited” in a major life activity
“should not demand extensive analysis” and
“usually will not require scientific, medical, or
statistical analysis.”
Most importantly for those with ASD, the
regulations provide the first explicit recognition
that autism constitutes an ADA-recognized
impairment. Indeed, Section 1630.2(j) (3) (iii)
provides that “in virtually all cases,” a number
of conditions, including autism, meet the defini-
tion of disability. According to the EEOC,
“autism substantially limits brain function” and
thus “will, at a minimum, substantially limit . . .
major life activities.”
As a result of the ADAAA and its accompa-
nying regulations, those diagnosed with ASD are
assured eligibility for remedies should they expe-
rience discrimination in employment, govern-
mental services, public transportation, public
accommodations, or in telecommunications. In
the employment context, the ADA prohibits dis-
crimination in recruitment, hiring, promotions,
training, pay, social activities, and other employ-
ment-related privileges. Governmental services
include public education, employment, transpor-
tation, recreation, health care, social services,
E 1076
courts, voting, and town meetings. Public trans-
portation includes city busses, subways, trains,
and the like. Public accommodations include
businesses and nonprofit service providers that
are open to the public. These enterprises include
privately operated educational facilities, trans-
portation services, and commercial facilities
such as restaurants, retail stores, hotels, movie
theaters, private schools, convention centers,
doctors’ offices, homeless shelters, transportation
depots, zoos, funeral homes, day care centers, and
recreation facilities including sports stadiums and
fitness clubs.
Accommodations accorded those with ASD
vary according to a person’s impairments and
the context. In the educational context (also cov-
ered by the Individuals with Disabilities Educa-
tion Act (IDEA)), accommodations include
special education teachers, teacher aides, more
frequent feedback from teachers, and help with
learning strategies or study skills. Other accom-
modations include the use of technological aids
such as calculators, computer software, and
audiobooks.
In the employment context, ASD-related
accommodations include the articulation of
clear job expectations, mandates that superiors
and colleagues communicate in a direct manner,
minimization of multitask assignments, and the
use of instructional visuals.
Future Directions
Eligibility for private and public health insurance
will be subject in the future to the fortunes of the
Patient Protection and Affordable Care Act
(PPACA). Eligibility for social security, educa-
tional, and antidiscrimination benefits will be
subject to the priorities and directions of federal
and state legislatures.
See Also
▶ Individuals with Disabilities Education Act
(IDEA)
▶ PL94-142
Eligibility (for Services Under IDEA/ADA, etc.)
References and Readings
20C.F.R. (2012). Ch. III, Pt. 404, Sbpt. P., Appen. 1,
}12.10.
29 Code of Federal Regulations (2012). }1630.2.
Administration, S. S. (2009). SSR 09-1p: Title XVI:
Determining childhood disability under the functional
equivalence rule – the “whole child” approach. Fed-
eral Register, 74(30), 7527. http://www.ssa.gov/
OP_Home/rulings/ssi/02/SSR2009-01-ssi-02.html.
Americans with Disabilities act (2008). 42. U.S.C.
}}12101 et seq.
Autism Now. http://autismnow.org/funding-and-public-
policy/funding-and-public-policy-introduction/
Autism Treatment Acceleration Act of 2009, S. 819, H.R.
2413 (2008).
Barner, A. (2009). Unlocking access to insurance cover-
age for autism treatment. Journal of Law, Economics
& Policy, 6, 107–135.
Bates, M. W. (1994). Free appropriate public education
under the individuals with disabilities education act:
Requirements, issues, and suggestions. Brigham
Young University Education and Law Journal,
215–222.
Breslin, M. A. (2009). No child left behind and the inher-
ent conflict with the individuals with disabilities edu-
cation act: Leaving special education students further
behind. Albany Government Law Review, 2, 653–676.
Caruso, D. (2010). Autism in the U.S.: Social movement
and legal change. American Journal of Law & Medi-
cine, 36, 483–539.
Department of Social Services, Department of Develop-
mental Services, Notice of Intent to Seek Three Med-
icaid Waivers for Individuals with Autism Spectrum
Disorders Who Do Not Also Have a Diagnosis of
Mental Retardation. (2011). Retrieved July 5, 2012,
from http://www.ct.gov/dds/cwp/view.asp?
a¼2730&Q¼476378
Employee Retirement Income Security Act (ERISA)
(2012). 29 USC }1001, et. Seq.
Ganz, M. (2006). The costs of autism. In S. Moldin &
J. Rubenstein (Eds.), Understanding autism: From
basic neuroscience to treatment. New York: CRC
Press.
Hinson, C. (2009). A supreme paradox: Autism spectrum
disorder and Rowley misapplication of judicial relic to
an unprecedented social epidemic. Florida A &
M University Law Review, 5, 87–105.
Holland, C. D. (2010). Autism, insurance, and the IDEA:
Providing a comprehensive legal framework. Cornell
Law Review, 95, 1253–1282.
IDEA Regulations (2010). } 300.8 Child with a disability.
Individuals with Disabilities Education Act (IDEA)
(2006). 20 U.S.C. }} 1400, et seq.
Mauch, D., Pfefferle, S., Booker, C., Pustell, M., & Levin,
J. (2011). Report on state services to individuals with
autism spectrum disorders (ASD), Centers for Medi-
care & Medicaid Services (CMS) ASD Services Pro-
ject 2011. Cambridge, MA: ABT Associates.
Embedded Figures Test (EFT) 1077 E
National Conference of State Legislators. (2010). Insurance
coverage for autism. Washington, DC: NCSL Press.
Patient Protection and Affordable Care Act (2012). Pub.
L. No. 111–148, } 2001(a)(1), 124 Stat. 272–75.
Regulations to Implement the Equal Employment
Provisions of the Americans With Disabilities
Act, as Amended. (2011). Retrieved July 5, 2012, from
http://www.federalregister.gov/articles/2011/03/25/2011-
6056/regulations-to-implement-the-equal-employment-
provisions-of-the-americans-with-disabilities-act-as#p-
326
Reinke, T. (2008). States increasingly mandate special
autism services. Managed Care, 17(8), 35–36. E
Ruskell, R. C. (2010). Social Security Disability Claims
Handbook. }2:33.
Social Security Act of 1965 (2012). 42 U.S.C. }} 1396-
1396W-5.
Social Security Administration. (2008). Disability
Evaluation Under Social Security, }12.00 Mental Dis-
orders – Adult. Retrieved July 5, 2012, from http://
www.ssa.gov/disability/professionals/bluebook/12.00-
MentalDisorders-Adult.htm

ELM Scale-2

▶ Early Language Milestone Scale

Embedded Figures Test (EFT), Fig. 1 The partici-
pant’s task is to find the simple shape within the complex
and camoflaging gestalt
ELS

▶ Test of Early Language Skill dependence – independence” (e.g., Witkin &

ELS Checklist
▶ Test of Early Language Skill
Embedded Figures Test (EFT)
Francesca Happé
MRC Social, Genetic and Developmental
Psychiatry Centre at the Institute of Psychiatry,
King’s College London, London, UK
Description
The Embedded Figures Test (EFT) was designed
by Witkin in 1971 to assess his concept of “field
Goodenough, 1981). Good performance on the
EFT was taken as a marker of field independence,
the ability to disembed information from context
or surrounding gestalt. The test requires the par-
ticipant to spot a simple form within a more com-
plex figure; the color and form of the latter create
a gestalt within which the part is hidden (see
Fig. 1). In the Children’s EFT, the complex figure
is also meaningful (e.g., a pram, within which the
triangle to be found is hidden in the hood).
Group-administered and short versions are also
available.
People with ASD are often extremely good at
the EFT, as first demonstrated by Shah and Frith
(1983). Fast and accurate performance on this test
is thought to reflect the ability to see parts within
wholes, to ignore the distracting effect of the
gestalt, and to focus on details. Indeed, superior
performance on the EFT (compared to age- and
E 1078
Embedded Figures Test (EFT), Fig. 2 In the children’s
version of this task, the complex figure within which the
target is hidden, is identifiable, adding meaning to
the gestalt-to-be-ignored
IQ-matched comparison group) was one of the
first demonstrations of so-called weak central
coherence in ASD and remains one of the best
replicated findings (see Happé & Frith, 2006 for
review) (Fig. 2).
Historical Background
Witkin (1916–1979) was a founder of the notion
of cognitive and learning styles. He proposed the
idea that personality could be measured in part
by how people perceived their environment. In
particular, he attempted to create objective tests
(in contrast to questionnaire methods), such as
the Rod-and-Frame test, to measure individual
differences in reliance on external versus inter-
nal frames of reference. The Embedded
Figures Test was created by Witkin as a more
portable and convenient test designed to mea-
sure these same facets of field dependence or
independence.
Shah and Frith (1983) were the first to use the
Embedded Figures Test with individuals with
autism, showing superiority compared to
Emergent Literacy
matched comparison groups. This was one of
the key findings that led Uta Frith to propose
her theory of “weak central coherence” in autism.
See Also
▶ Executive Function (EF)
▶ Global Versus Local Processing
▶ Theory of Mind
References and Readings
Happé, F., & Frith, U. (2006). The weak coherence
account: Detail-focused cognitive style in autism spec-
trum disorders. Journal of Autism and Developmental
Disorders, 36, 5–25.
Shah, A., & Frith, U. (1983). An islet of ability in autistic
children: A research note. Journal of Child Psychology
and Psychiatry, 24, 613–620.
Witkin, H. A., & Goodenough, D. R. (1981). Cognitive
styles: Essence and origins. New York: International
University Press.
Witkin, H. A., Oltman, P. K., Raskin, E., & Karp, S.
(1971). A manual for the embedded figures test.
California: Consulting Psychologists Press.
Emergent Literacy
Dawn Vogler-Elias
Communication Sciences and Disorders,
Nazareth College, Rochester, NY, USA
Synonyms
Early literacy; Preliteracy
Definition
Emergent literacy refers to the many literacy-rich
activities children participate in prior to formal
Emotion
reading and writing instruction from birth
to about 5 years of age. Specifically, emergent
literacy has been defined as “the reading and
writing behaviors of young children before they
become readers and writers in the conventional
sense” (Justice, 2006, p. 3). Examples of
emergent literacy activities include engaging in
shared storybook reading, pretending to write or
draw, incorporating literacy themes into play, and
engaging in oral wordplay such as rhyming.
Shared storybook reading is arguably the most
common emergent literacy activity for many
children. Parents read to children who are very
young before they can verbally participate.
Parents often engage in scaffolding or supportive
behaviors during emergent literacy activities.
Through scaffolding, parents adapt the experi-
ence to match the child’s growing abilities, thus
supporting the child’s participation. For typically
developing children, emergent literacy instruc-
tion is most effective when it is targeted authen-
tically instead of during contrived instructional
“skill and drill” activities (Price & Ruscher,
2006). Emergent literacy is associated with later
literacy achievement and the development of
other important skills. For example, children
who experience more high-quality reading
experiences early in childhood have larger
vocabularies than children with fewer experi-
ences (see Temple & Snow, 2003 for a review).
Emergent literacy activities provide a rich
context for learning and practicing joint attention
skills, which are particularly vulnerable in
children with autism spectrum disorders.
Historically, emergent literacy activities were
withheld from some children who did not
demonstrate signs of readiness, including oral
language abilities and behavioral precursors.
However, there is no evidence to suggest that
any child should be excluded from emergent
literacy activities. Because children with autism
spectrum disorders are at risk for reduced
opportunity for literacy achievement, providing
rich and diverse emergent literacy activities is
one way to support the literacy access for this
population.
1079 E
See Also
▶ Literacy
▶ Reading
▶ Shared Storybook Reading
References and Readings
Justice, L. M. (Ed.). (2006). Clinical approaches to
emergent literacy intervention. San Diego, CA: Plural E
Publishing.
Price, L. H., & Ruscher, K. Y. (2006). Fostering phonolog-
ical awareness using shared book reading and an
embedded explicit approach. In A. van Kleeck (Ed.),
Sharing books and stories to promote language and
literacy (pp. 15–76). San Diego, CA: Plural Publishing.
Temple, J. D., & Snow, C. E. (2003). Learning words from
books. In A. van Kleeck, S. Stahl & E. Bauer (Eds.),
On Reading books to children: Parents and teachers,
Mahwah, NJ: Lawrence Erlbaum.
van Kleeck, A. (Ed.). (2006). Sharing books and stories to
promote language and literacy. San Diego, CA: Plural
Publishing.
van Kleeck, A., Stahl, S. A., & Bauer, E. B. (Eds.). (2003).
On reading books to children: Parents and teachers.
Mahwah, NJ: Lawrence Erlbaum Associates.
Emotion
Sander Begeer
Developmental Psychology, VU University
Amsterdam, Amsterdam, The Netherlands
Autism Research Amsterdam, Amsterdam,
The Netherlands
School of Psychology, University of Sydney,
Australia
Definition
Emotions are a complex set of behaviors pro-
duced in response to some external or internal
event that serve to motivate and direct thoughts
and actions. The word “emotion” stems from the
Latin e- (out) and movere (move). Emotions are
generally thought to be processes, rather than
states. Emotions are not equal to feelings.
E 1080
Feelings are the subjective representation of the
emotional process. Emotions refer to the range of
chemical and neural responses that are produced
by the brain in response to a relevant stimulus.
Emotions are comprised of a broad array of com-
ponents including subjective experience, verbal
description, physiological response, motivational
influences, and behavioral expression. Emotions
are often understood as social processes (Salovey,
2003). Throughout the lifespan, most emotional
experiences and responses are contextually
anchored in social relationships, and emotions
become meaningful in the interaction with other
people (Ekman, 1992; Frijda, 1986). Vice versa,
emotions serve to regulate social interactions, and
the way emotions are exchanged defines our
social relationships. In short, emotions are
dynamic processes that create and are created
by the relationships with others. A general
differentiation is made between basic emotions
(happiness, sadness, fear, and anger, sometimes
completed with disgust and surprise) and
secondary emotions (also referred to as complex,
cognitive or self-conscious emotions), including
pride, shame, guilt, and jealousy. Secondary emo-
tions require the awareness of others’ perspective
on your situation. For instance, experiencing
shame is related to seeing oneself through the
eyes of an audience, which could be real or
imagined.
Historical Background
Historically, emotions are often contrasted with
cognition or rationality. Over 2,000 years ago,
Stoic and Epicurean philosophers even argued
that emotions are damaging to humans because
of their irrational nature. This perspective is still
apparent in contemporary sayings like “let’s be
rational” or “don’t get all emotional.” The con-
trast between emotion and rationality or cogni-
tion has been debated since the writings of
Aristotle and medieval rationalist philosophers
to Darwin and Freud. More recently, the discus-
sion revolved around the issue whether emotions
precede cognition or vice versa. For example,
during the encounter with a bear, do we become
Emotion
frightened because we know the animal is dan-
gerous, or do we feel our fear and then realize
the animal is dangerous? James (1884) argued
that the stimulus (the bear) elicits a physical
arousal that causes the feeling of fear. Later,
Arnold (1960) argued that one infers
(“appraises”) that the bear is dangerous, which
causes a tendency to run away resulting in the
feeling of fear. Cognition precedes emotion.
Subsequently, this cognitive approach to emo-
tions was invalidated by an experiment that
ingeniously showed that emotional preferences
can occur without the cognitive appraisal of a
stimulus (Zajonc, 1980).
Scientists are increasingly skeptical about the
possibility to untangle emotional and cognitive
processes. Damasio (1994) argued that the anat-
omy and functionality of emotions are strongly
related to physical and rational processes. This
perspective is widely embraced in the field of
affective neuroscience (Davidson, 2000). In this
conception, emotions become an important drive
rather than a damaging force to our rationality.
One of the first to argue for the functional nature
of emotions was Darwin (1872), reflecting on
the animal sources of human emotions. In line
with his conception, Frijda (1986) defined emo-
tions as states of action readiness or inborn behav-
ioral programs, which allow flexible adaptation
to a rapidly changing environment. For example,
aggression can motivate us to remove objects that
prevent us from achieving our goals. Sadness helps
us to abandon goals that are out of reach. Fear
enables the body for a fight or flight response, and
happiness increases cohesion and prolongs favor-
able situations.
Research on emotions in autism has
increased dramatically during the last two
decades. While the second half of the twentieth
century started with an emphasis on psychoan-
alytical aspects of autism, much research con-
sequently focused on autism as an information
processing disorder. While this cognitive
approach led to a fruitful line of studies, emo-
tional aspects of the disorder were neglected
until emotion became an important topic in
psychology in the 1980s and the rise of affec-
tive neuroscience in the 1990s.
Emotion
Current Knowledge
Below, a snapshot of current knowledge regard-
ing emotions and autism is described with respect
to the following broad domains: diagnostic
criteria, expression, experience, perception,
responding, understanding, psychophysiology,
and neuroscientific findings.
Diagnostic Criteria. It is generally agreed
upon that individuals with autism spectrum dis-
orders (ASD) are characterized by abnormalities
in their interaction and communication with other
people and their flexibility in thought and action,
all present from early childhood. Emotions play
a pivotal role in the definition, the diagnostic
criteria, the etiology, the development, and the
possibilities for treatment in autism. Leo Kanner
even defined autism as an inability to “form
affective contact with people” (Kanner, 1943,
p. 250). The diagnostic criteria for ASD as
described in the diagnostic manual for mental
disorders (DSM-IV-TR; APA, 2000), the
International Classification of Diseases-10
(Sponheim, 1996), and leading assessment tools,
such as the Autism Diagnostic Interview-Revised
(ADI-R) (Rutter, Lecouteur, & Lord, 2003) or the
Autism Diagnostic Observation Scale (ADOS)
(Lord et al., 2000), all include emotional prob-
lems as a possible aspect of the qualitative
impairments in autism. The proposed criteria for
the new DSM-5, to appear in 2013, will include
emotional problems as a necessary criteria for
autism: “Deficits in social-emotional reciprocity;
ranging from abnormal social approach and fail-
ure of normal back and forth conversation
through reduced sharing of interests, emotions,
and affect and response to total lack of initiation
of social interaction.”
Expression. The expression of emotions can
be conceived of as the first communicative action
of newly born infants. From the beginning of life,
expressing emotions has a strong impact on the
development of social interactions and social
relations. Emotional expressions evoke reactions
from the social environment (e.g., a crying baby
evokes caring behavior). This behavior informs
others on the subjective state of an individual but
also serves to maintain emotional reciprocity and
1081 E
attachment. Typically developing children rap-
idly adapt emotional expressions to their social
environment. Only a few weeks after birth, they
are able to modify their expression to the
responses of their environment. While the com-
ponents of expressing emotions seem to be pre-
sent at birth, at 4 years old, typically developing
children are able to express emotions at the same
level as adults. Research on the early develop-
ment of emotional expression in ASD is limited
E
because most children receive their diagnosis
later. However, various studies have analyzed
video material of infant period in children who
were later diagnosed with ASD (Baranek, 1999).
Surprisingly, the expressiveness of infants later
diagnosed with ASD does not seem to differ
much from typically developing comparison
groups. At school ages, in particular, cognitively
delayed children with ASD show more neutral
and idiosyncratic emotions. They may be
laughing during inappropriate situations and
seem less aware of their social context. Normally
intelligent individuals with ASD (high function-
ing ASD, HFASD) are generally found to show
adequate emotional expressions, though compar-
ison groups showed more positive affect (Capps
et al., 1993). In general, most research on emo-
tions highlights the perception of or responses to
emotional expressions by others. How individ-
uals with ASD express their own emotions has
been studied less often.
Experience. A persistent misconception on
individuals with ASD is that they experience
less emotions than typically developing indi-
viduals. Though it is not possible to directly
measure differences in experience (the qualia
problem), indirect measures of behavior, ret-
rospective, verbal, and observational outcomes
indicate that individuals with ASD are highly
emotional but likely express their emotions
in atypical manners. One line of research
has highlighted alexithymia in autism.
Alexithymia refers to the inability to differen-
tiate and describe one’s own subjective feel-
ing state. A lower awareness of one’s own
emotions has been reported in several studies,
but there is no consensus that autism overlaps
with alexithymia.
E 1082
Perception. Typically developing humans
show a strong preference for social stimuli from
birth. During infancy, they rapidly increase in
their ability to recognize human stimuli and dif-
ferentiate between the emotional states of others.
Evidence for impaired emotion perception skills
in ASD is conflicting. Abnormal perception of
emotions has particularly been shown with
respect to facial stimuli. In particular, reduced
attention to eye regions, poor memory, and
abnormal emotion processing were shown.
Impaired perception was also found in other sen-
sory modalities, like voices or bodily gestures.
However, cognitive ability and test conditions
play an important role (Begeer, Koot, Rieffe,
Terwogt, & Stegge, 2008). In general, given
structured situations and average or above cogni-
tive abilities, basic emotions are perceived in
ASD at equal levels as comparison groups. How-
ever, cognitive delay and unstructured dynamic
real-life settings result in less adequate, delayed
processing of perceptual information. It should
be noted that scientific research is often
conducted under strict, standardized, and
straightforward conditions, to ensure validity
and reliability of findings. A strong disadvantage
of this approach is that it creates an optimal
situation for individuals with autism. Their
capacities in the psychological laboratory may
overestimate their daily life skills.
Responding. Typically developing children
show reciprocal or empathic responses to others’
emotions during infancy. Around their first year
of life, children start to alter their behavior based
on emotional responses of others. For example,
they alter their approach of an object based on the
emotional response of their caregiver. This
shared or joint attention with another person
toward a third party, which may be another
object, event, or person, is associated with posi-
tive affect in typically developing children. When
the child monitors the affect of another person
toward a third party, this is called “social
referencing.” While impaired responsiveness to
emotions in others is an apparent criterion of an
ASD diagnosis, responding to others’ emotions
strongly depends on age and intelligence. Struc-
tured observations indicated that infants with
Emotion
ASD (with mixed IQs) were less oriented to
others than control infants (Baranek, 1999;
Palomo, Belinchon, & Ozonoff, 2006). While
responses to other’s emotions are certainly not
absent in the early life of individuals with ASD,
they generally respond less empathically ade-
quate. Their attention to negative emotions or
distress in another person is generally lower,
and they show less change in their own affect in
response to other people’s distress (Hutman et al.,
2010). Measuring physiological responses
seems a promising way to examine automatic
responding to emotions, but results so far have
not indicated cohesive impairments in ASD. Age,
IQ, motivation, and the explicitness of task
demands improve the performance of children
with ASD. It seems particularly important to
stress whether responses are based on isolated
explicit requests in structured situations, which
is generally the case in empirical research, or
informants’ observations of spontaneous behav-
ior in unstructured situations, as generally relied
on in diagnostic assessment procedures.
Emotion Regulation. Emotion regulation
will be discussed as a separate entry in this
encyclopedia.
Understanding. Diagnostic criteria focus on
behavior rather than cognition. However, many
related assessment tools such as the ADI-R (Rutter
et al., 2003) or the ADOS (Lord et al., 2000)
also rely on children’s abilities to describe and
explain emotions. This can be problematic because
children’s adequate understanding of emotions
decreases the likelihood of an ASD diagnosis.
Recent years have seen a vast increase in studies
on the understanding of emotions in ASD. Individ-
uals with ASD and average or above intelligence
were often shown to display adequate levels of
emotional understanding. The understanding of
emotions in others is strongly dependent on the
ability to attribute subjective states to others. This
ability relies on imagination and perspective tak-
ing or theory of mind skills that are known to be
impaired or atypical in ASD. Indeed, intellectually
disabled individuals with ASD fail to show an
understanding of emotions beyond the simple
acknowledgment of prototypical causes. Where
typically developing children may gain a better
Emotion
understanding of emotions through experience,
intellectually disabled children with ASD show
little progress during the preschool years. In con-
trast, individuals with ASD and average of above
average IQ do acquire skills to provide theoretical
responses to emotions, even though their explana-
tions can at times be idiosyncratic, superficial, or
scripted. Unsurprising, their emotional under-
standing is often correlated to their cognitive skills
(Capps et al., 1993). The understanding of mixed
emotions, i.e., feeling angry and sad simulta-
neously, is relatively poor (Rieffe, Meerum
Terwogt, & Kotronopoulou, 2007). Emotional dis-
play rules, the social guidelines for expressing
behavior are generally known in school-aged chil-
dren with HFASD (Begeer et al., 2011), though
they may be applied less. The understanding of
secondary emotions like shame, embarrassment,
or jealousy is poor, which is related to impaired
perspective taking and poor imagination. For
example, a child may feel hurt or sad when falling
down, but to feel embarrassed about the situation,
it needs to image how others perceive that situa-
tion. To improve diagnostic procedures of children
with HFASD in particular, a strong focus on the
analysis of the reasoning process that results in
children’s responses about emotions is necessary.
Neuroscience. With the rise of interest in
affective neuroscience, the focus on brain imag-
ing studies related to the processing of emotions
took a sharp rise in autism. A coherent overview
of neural underpinnings of autism is not available
yet. Findings are often not integrated into
a framework, and the heterogeneity of the autism
spectrum complicates the search for common
underlying neural mechanisms, which may in
turn be diverse. To further complicate the field,
inconsistent findings can also be explained by the
use of different methodology. Therefore, a short
overview of main topics is presented here. Brain
mechanisms that are related to emotional func-
tioning in autism are mainly studied by neuroim-
aging studies. Neuroimaging is a technique that
can measure volume, structures, and functioning
of brain areas. The neural underpinnings of emo-
tions include systems at different levels, ranging
from the regulation of core somatic circuits to
regulate the interaction with others (Herbert,
1083 E
2004). Anatomical abnormalities have been
found in a number of brain areas that are related
to emotional functioning, in particular the cere-
bella and limbic systems. Links between brain
activation and performance on emotional
processing tasks (e.g., judging other’s emotions)
have been reported in autism, but the findings are
not consistent. It has been suggested that individ-
uals with ASD use different neural networks and
strategies when processing emotions (Wang,
E
Dapretto, Hariri, Sigman, & Bookheimer, 2004).
Mirror neurons. A topic that raised consider-
able interest is the idea that autism may be related
to impairments in a “mirror neuron” system. Mir-
ror neurons fire both when an individual executes
an action and when the individual observes the
same action performed by somebody else
(Rizzolatti & Craighero, 2004). This may provide
a system that, among other things, may facilitate
the understanding of emotions in others. It has
been put forward as the neural subtract of empa-
thy (Bastiaansen, Thioux, & Keysers, 2009).
Abnormal functioning of the mirror neuron sys-
tem has been suggested for individuals with ASD
(Hadjikhani, Joseph, Snyder, & Tager-Flusberg,
2006). However, others challenge this assump-
tion (Fan, Decety, Yang, Liu, & Cheng, 2010),
and recent findings suggest a delay rather than an
impairment of mirror neurons in ASD
(Bastiaansen et al., 2011).
Future Directions
Increasing the coherence of findings on many
domains of research on autism and emotions is
an important task for future studies. The use of
large scale and longitudinal data collections, fol-
lowing young infants through their course of life,
can provide a clearer perspective on many
domains (Harms, Martin, & Wallace, 2010). In
addition to these general directions, various new
approaches may be worthwhile pursuing,
although it should be noted that new findings
often tend to be interpreted with too much enthu-
siasm. The focus on mirror neurons has been
discussed before, and research teams around the
world currently pursue this topic. More recently,
E 1084
the use of oxytocin, a hormone related to female
reproduction, has been suggested to improve
social functioning, including emotion recognition
(Guastella et al., 2010), in autism. This topic is
gaining considerable attention and will be on the
agenda of many research groups. The use of
virtual reality and other technological innova-
tions, like robotics, to study and intervene in the
emotional functioning of individuals with ASD
may provide further fields of research. However,
delineating which individuals with ASD are
impaired on what specific domains, specifying
age, IQ, and research context, in order to provide
treatments that fit specific needs in specific indi-
viduals remains the main challenge for future
research.
See Also
▶ Affective Development
▶ Emotion Regulation
▶ Emotional Intelligence
References and Readings
American Psychiatric Association (2000). Diagnostic and
statistical manual of mental disorders (4th ed., TR).
Washington, DC: American Psychiatric Association.
Arnold, M. B. (1960). Emotion and personality.
New York: Columbia University Press.
Baranek, G. T. (1999). Autism during infancy:
A retrospective video analysis of sensory-motor and
social behaviors at 9–12 months of age. Journal of
Autism and Developmental Disorders, 29, 213–224.
Bastiaansen, J. A. C. J., Thioux, M., & Keysers, C. (2009).
Evidence for mirror systems in emotions. Philosophi-
cal Transactions of the Royal Society B-Biological
Sciences, 364, 2391–2404.
Bastiaansen, J. A. C. J., Thioux, M., Nanetti, L., van der
Gaag, C., Ketelaars, C., Minderaa, R., et al. (2011).
Age-related increase in inferior frontal gyrus activity
and social functioning in autism spectrum disorder.
Biological Psychiatry, 69(9), 832–838.
Begeer, S., Banerjee, R., Rieffe, C., Meerum Terwogt, M.,
Potharst, E., Stegge, H., & Koot, H. (2011). The under-
standing and self-reported use of emotional display
rules in children with autism spectrum disorders. Cog-
nition and Emotion, 25, 947–956.
Begeer, S., Koot, H. M., Rieffe, C., Terwogt, M. M., &
Stegge, H. (2008). Emotional competence in children
with autism: Diagnostic criteria and empirical evi-
dence. Developmental Review, 28, 342–369.
Emotion
Capps, L., Kasari, C., Yirmiya, N., & Sigman, M. (1993).
Parental perception of emotional expressiveness in
children with autism. Journal of Consulting and
Clinical Psychology, 61, 475–484.
Damasio, A. (1994). Descartes’ error – emotion, reason
and the human brain. New York: G.P. Putnam’s Sons.
Darwin, C., (1872). The expression of emotions in man
and animals (3rd ed.). London: Oxford University
Press.
Davidson, R. J. (2000). Cognitive neuroscience needs
affective neuroscience (and vice verse). Brain and
Cognition, 42, 89–92.
Ekman, P. (1992). Are there basic emotions? Psycholog-
ical Review, 99, 550–553.
Fan, Y. T., Decety, J., Yang, C. Y., Liu, J. L., &
Cheng, Y. W. (2010). Unbroken mirror neurons in
autism spectrum disorders. Journal of Child Psychol-
ogy and Psychiatry, 51, 981–988.
Frijda, N. H. (1986). The emotions. Cambridge:
Cambridge University Press.
Guastella, A. J., Einfeld, S. L., Gray, K. M.,
Rinehart, N. J., Tonge, B. J., Lambert, T. J., et al.
(2010). Intranasal oxytocin improves emotion recog-
nition for youth with autism spectrum disorders.
Biological Psychiatry, 67, 692–694.
Hadjikhani, N., Joseph, R. M., Snyder, J., & Tager-
Flusberg, H. (2006). Anatomical differences in the
mirror neuron system and social cognition network in
autism. Cerebral Cortex, 16, 1276–1282.
Harms, M. B., Martin, A., & Wallace, G. L. (2010). Facial
emotion recognition in autism spectrum disorders:
A review of behavioral and neuroimaging studies.
Neuropsychology Review, 20, 290–322.
Herbert, M. R. (2004). Neurointaging in disorders of
social and emotional functioning: What is the ques-
tion? Journal of Child Neurology, 19, 772–784.
Hutman, T., Rozga, A., DeLaurentis, A. D., Barnwell, J. M.,
Sugar, C. A., & Sigman, M. (2010). Response to distress
in infants at risk for autism: A prospective longitudinal
study. Journal of Child Psychology and Psychiatry, 51,
1010–1020.
James, W. (1884). What is an emotion? Mind, 9, 188–205.
Kanner, L. (1943). Autistic disturbances of affective
contact. Nervous Child, 2, 217–307.
Lord, C., Risi, S., Lambrecht, L., Cook, E. H.,
Leventhal, B. L., DiLavore, P. C., et al. (2000). The
autism diagnostic observation schedule-generic:
A standard measure of social and communication
deficits associated with the spectrum of autism.
Journal of Autism and Developmental Disorders, 30,
205–223.
Palomo, R., Belinchon, M., & Ozonoff, S. (2006). Autism
and family home movies: A comprehensive review.
Journal of Developmental and Behavioral Pediatrics,
27, S59–S68.
Rieffe, C., Terwogt, M. M., & Kotronopoulou, C. (2007).
Awareness of single and multiple emotions in high-
functioning children with autism. Journal of Autism
and Developmental Disorders, 37, 455–465.
Emotional Intelligence
Rizzolatti, G., & Craighero, L. (2004). The mirror-neuron
system. Annual Review of Neuroscience, 27, 169–192.
Rutter, M., Lecouteur, A., & Lord, C. (2003). Autism
diagnostic interview-revised manual. Los Angeles:
Western Psychological Services.
Salovey, P. (2003). Introduction: Emotion and social
processes. In R. Davidson, H. H. Goldsmith, &
K. Scherer (Eds.), The handbook of affective science
(pp. 747–751). Oxford, UK: Oxford University Press.
Sponheim, E. (1996). Changing criteria of autistic disor-
ders: A comparison of the ICD-10 research criteria and
DSM-IV with DSM-III-R, CARS, and ABC. Journal
of Autism and Developmental Disorders, 26, 513–525.
Wang, A. T., Dapretto, M., Hariri, A. R., Sigman, M., &
Bookheimer, S. Y. (2004). Neural correlates of facial
affect processing in children and adolescents with
autism spectrum disorder. Journal of the American
Academy of Child and Adolescent Psychiatry, 43,
481–490.
Zajonc, R. B. (1980). Feeling and thinking – preferences
need no inferences. American Psychologist, 35, 151–175.
Emotion and Decision Making
▶ Frontal Lobe Findings in Autism
Emotion Regulation
▶ Mutual Regulation
Emotional Intelligence
Liz Pellicano
Centre for Research in Autism and Education
(CRAE), Department of Psychology and Human
Development, Institute of Education, University
of London, London, UK
Definition
Emotional intelligence is defined as “the capacity
to reason about emotions, and of emotions to
enhance thinking. It includes the ability to accu-
rately perceive emotions, to access and generate
emotions so as to assist thought, to understand
emotions and emotional knowledge, and to
1085 E
reflectively regulate emotions so as to promote
emotional and intellectual growth” (Mayer,
Salovey, & Caruso, 2004, p. 197).
Historical Background
Mayer and colleagues (Mayer et al., 2004;
Mayer & Salovey, 1993) view emotional intelli-
gence as belonging to what they term “hot
E
intelligences,” which essentially operate at the
intersection of emotion processing and higher-
level cognition, that is, between thinking and feel-
ing. This conceptualization is reflected in their
“four-branch ability model” in which they propose
the following components of emotional intelli-
gence: (1) perceiving emotion, (2) using emotion
to assist thought, (3) understanding emotions, and
(4) managing emotions in oneself and in others.
Current Knowledge
The concept of emotional intelligence
(or “EQ”) has captured the imagination of non-
psychologists, who have broadened the term to
include not only the ability to understand and use
emotional information but also to describe per-
sonality attributes and the capacity to relate to
others in social situations (e.g., Goleman, 1998).
The concept is not without controversy, however.
Academic scholars have been less willing to
adopt the term “emotional intelligence” in scien-
tific parlance, and the construct as described
above has not been the subject of sustained, sys-
tematic investigation. Indeed, it has been
described as an “elusive concept” (Davies,
Stankov, & Roberts, 1998, p. 989), one which
“appears more myth than science. . .” (Matthews,
Zeidner, & Roberts, 2002, p. 547).
Emotional Intelligence in Autism
Perhaps unsurprisingly, the term “emotional
intelligence” has not been embraced by
researchers in the field of autism. In fact,
a PubMed search for articles from January 1970
until August 2011 with the terms “emotional
E 1086
intelligence” AND “autistic disorder” OR
“autism” yielded 17 articles of which only one
directly investigated emotional intelligence in
autism (Petrides, Hudry, Michalaria, Swami, &
Sevdalis, 2011). These authors reported lower
scores on a trait emotional intelligence measure
by adults with Asperger syndrome relative to
typical adults.
This is not to say that the majority of the
“processes” in Mayer et al.’s “branches” have
not been systematically studied in autism, albeit
under different – and arguably better validated –
guises.
First, there is an extensive body of work inves-
tigating how people with autism perceive and
recognize emotion in faces, voices, and other
nonverbal cues (Branch 1). Second, the critical
role that emotion plays in decision making and
executive functions more broadly has been well
documented in the burgeoning social neurosci-
ence literature (e.g., Damasio, 1994; Pessoa,
2008). There have been several recent investiga-
tions of social decision making – problems that
involve the regulation of affect and motivation –
in autism (using the Iowa gambling task, for
example), although there have been compara-
tively fewer investigations of the development
of these processes either under the headings of
“self-regulation” (Posner & Rothbart, 2000) or
“hot executive function” (Carlson, Davis, &
Leach, 2005; Happaney, Zelazo, & Stuss, 2004)
(Branches 2 and 4). Finally, Baron-Cohen’s
(2002) “empathizing” construct covers many of
the abilities described in Branch 3 – those that are
important for both identifying the thoughts and
feelings of others and using that information to
respond in appropriate ways – which may overlap
with other heavily researched constructs like
“theory of mind.” Indeed, Blair (2002) considers
whether theory of mind might be a necessary
prerequisite for the development of emotional
intelligence.
Future Directions
Despite the limited empirical focus on the nature
of the construct of emotional intelligence in
Emotional Intelligence
autism, references to autistic individuals’ “lack
of emotional intelligence” abound in the popular
press and on the Internet. Caution is warranted,
however, on the use of these and other extreme
statements (e.g., “zero degrees of empathy”;
Baron-Cohen (2011), etc.) (see Pellicano &
Stears, 2011): They are often considered dispar-
aging to the individuals concerned and often
accurately reflect neither the empirical data
nor the inner emotional lives of many people
with autism (Cohen-Rottenberg, 2011). Future
research will need to take a more nuanced
approach.
See Also
▶ Affective Development
▶ Emotion
▶ Emotional Regulation
▶ Empathizing-Systemizing Theory
▶ Empathy
▶ Executive Function (EF)
▶ Motivation
▶ Self-Concept
▶ Social Cognition
▶ Theory of Mind
References and Readings
Baron-Cohen, S. (2002). The extreme male brain theory of
autism. Trends in Cognitive Sciences, 6, 248–254.
Baron-Cohen, S. (2011). Zero degrees of empathy: A new
theory of human cruelty. London: Penguin Books.
Blair, R. J. R. (2002). Theory of mind, autism and emo-
tional intelligence. In L. F. Barrett & P. Salovey (Eds.),
The wisdom in feeling: Psychological processes in
emotional intelligence (pp. 406–434). New York:
The Guildford Press.
Carlson, S. M., Davis, A. C., & Leach, J. G. (2005). Less is
more: Executive function and symbolic representation
in preschool children. Psychological Science, 16,
609–616.
Cohen-Rottenberg, R. (2011). The empathy issue is
a human rights issue. Accessed September 8, 2011,
from http://www.journeyswithautism.com/2011/09/
05/the-empathy-issue/
Damasio, A. R. (1994). Descartes’ error. New York:
Putnam.
Emotional Regulation
Davies, M., Stankov, L., & Roberts, R. D. (1998).
Emotional intelligence: In search of an elusive con-
struct. Journal of Personality and Social Psychology,
75, 989–1015.
Goleman, D. (1998). Working with emotional intelligence.
New York: Bantam Books.
Happaney, K. R., Zelazo, P. D., & Stuss, D. T. (2004).
Development of orbitofrontal function: Current
themes and future directions. Brain and Cognition,
55, 1–10.
Matthews, G., Zeidner, M., & Roberts, R. D. (2002).
Emotional intelligence: Science and myth. Cambridge,
MA: MIT Press.
Mayer, J. D., & Salovey, P. (1993). The intelligence of
emotional intelligence. Intelligence, 17, 433–442.
Mayer, J. D., Salovey, P., & Caruso, D. R. (2004). Emo-
tional intelligence: Theory, findings, and implications.
Psychological Inquiry, 15, 197–215.
Pellicano, E., & Stears, M. (2011). Bridging autism,
science and society: Moving towards an ethically-
informed approach to autism research. Autism
Research, 4, 271–282.
Pessoa, L. (2008). On the relationship between emotion
and cognition. Nature Reviews Neuroscience, 9,
148–158.
Petrides, K. V., Hudry, K., Michalaria, G., Swami, V., &
Sevdalis, N. (2011). A comparison of the trait emo-
tional intelligence profiles of individuals with and
without Asperger syndrome. Autism 15, 671–682.
Posner, M. I., & Rothbart, M. K. (2000). Developing
mechanisms of self-regulation. Development and
Psychopathology, 12, 427–441.
Emotional Regulation
Walter Gilliam
Child Study Center, Yale University School of
Medicine, New Haven, CT, USA
Synonyms
Affective regulation; ER
Definition
Emotional regulation (ER, also known as affec-
tive regulation) is an area of research that has
experienced significant growth in interest during
the last two decades. In brief, ER is a person’s
attempt to regulate or influence the type and
1087 E
degree of emotional response he or she has to
a stimulus, the timing of that emotional response,
how that emotional response is experienced, or
how that emotional response is expressed to
others (Gross, 2007). ER capacity is a person’s
ability to regulate their emotions toward adaptive
ends.
ER is an aspect of self-regulation. All living
organisms engage in processes of self-regulation
in order to adapt to environmental demands. In
E
humans, self-regulation is a developmental pro-
cess, by which individuals gain greater control
over their own physiological, emotional, cogni-
tive/attentional, and behavioral responses to their
environments. These response domains and their
regulation are interrelated. When the environ-
ment poses manageable challenges to which
a person can draw upon his or her personal
resources to meet these challenges, self-
regulatory capacities are strengthened and adap-
tive development occurs. When the environment
poses challenges beyond the capacities of the
individual to adapt, maladaptive or disordered
patterns of behavior may become evident
(National Research Council & Institute of
Medicine, 2000).
Emotions play an important role in social
relationships, both as a way to respond to others
and as a way to elicit social connections from
others. During typical development, emotional
expression develops from generalized arousal
states (e.g., a “fussy” baby) to more differenti-
ated emotional responses (e.g., anger, sadness,
frustration, fear), while the development of cog-
nitive capacities helps the person to better
understand the environmental antecedents of
their emotional responses, identify emotional
states in others, and develop self-coping strate-
gies. These self-coping strategies are often
mediated by language (self-talk), and evidence
has long suggested that delayed or impaired lan-
guage development may have a negative impact
on the development of ER.
Aspects of ER capacity include the ability to
identify one’s own feelings, to identify feelings in
others and empathize, and to manage one’s own
feelings toward constructive or adaptive ends. As
in other areas of self-regulation, the development
E 1088 Emotional Synchrony

of ER capacities evolves from mostly external emotional states in themselves and others, to
regulation (e.g., reliance on caregivers to soothe choose between a variety of potential emotional
and modulate emotional response) to increas- and behavioral responses, to delay gratification,
ingly internal regulation (e.g., self-soothing and and to use self-relaxation techniques.
self-modulation of emotional expression). In
most young children, external regulation of emo-
tion can be easily seen during frequent social See Also
referencing – the tendency to look at a trusted
caregiver for cues as to the appropriate emotional ▶ Emotional Intelligence
response. Temperament (an individual’s typical ▶ Empathy
responses to environmental demands and novel ▶ Executive Function (EF)
stimuli and ability to regulate emotional and ▶ Temperament
arousal responses to these stimuli) is a related
construct.
Self-inhibitory skill (also described as effort- References and Readings
ful control) is central to the development of ER.
This is the ability to behaviorally inhibit a natural Gross, J. J. (2007). Emotion regulation. In M. Lewis, J. M.
Haviland-Jones, & L. F. Barrett (Eds.), Handbook of
emotional response in order to obtain a more
emotions (3rd ed., pp. 497–512). New York: Guilford
socially desirable outcome (e.g., not hitting Press.
someone when angry). Individuals who are poor National Research Council, & Institute of Medicine.
at effortful control often experience difficulty (2000). From neurons to neighborhoods: The science
of early childhood development. Committee on Inte-
with social relationships with peers, caregivers,
grating the Science of Early Childhood Development.
and authority figures. ER, however, is not about In J. P. Shonkoff & D. A. Phillips (Eds.), Board
the suppression of emotion, but rather about on Children, Youth, and Families, Commission on
understanding emotions within social contexts Behavioral and Social Sciences and Education.
Washington, DC: National Academy Press.
and how to modulate emotional expression in
adaptive ways. A greater capacity for ER helps
one to be able to better regulate strong emotions,
deal with fearful and frustrating events, and form
and maintain meaningful and beneficial social
relationships. Emotional Synchrony
ER capacity is influenced by a person’s tem-
perament, diagnosable disorders that may impact ▶ Mutual Regulation
a person’s ability to attend to socially salient
information, the degree of demands placed upon
the individual by his or her environment,
and executive functioning skills (e.g., attending
to important environmental details, forming Emotionally Withdrawn/Inhibited
a symbolic understanding of the environment Attachment Disorder
and how aspects of the environment interrelate,
planning behavioral responses, sustaining and ▶ Attachment Disorder
shifting attention, inhibiting, and self-reflecting).
Cultural values also exert a strong influence by
influencing caregiver responses to emotions and
preferred methods for dealing with strong
emotion. Empathizing-Systemizing Theory
Efforts to facilitate ER capacities have
included teaching children to identify and label ▶ Systems Intervention
Empathy
Empathy
Nurit Yirmiya and Ifat Seidman
Department of Psychology, The Hebrew
University of Jerusalem, Jerusalem, Israel
Definition
Empathy, the capacity to share the feelings of
others, is considered a significant core ability in
the development of social and emotional func-
tioning. In general, individuals with autism expe-
rience difficulties in their capacity to empathize,
thus failing to successfully engage in social inter-
actions (Charman et al., 1997; Jones, Happe,
Gilbert, Burnett, & Viding, 2010; Yirmiya,
Sigman, Kasari, & Mundy, 1992).
In everyday language, as well as in the
research literature, the term empathy is used syn-
onymously for both mental and emotional states.
However, cognitive empathy pertains to the
capacity to represent others people’s thoughts,
beliefs, and intentions, whereas emotional empa-
thy is defined as experiencing what it feels like
for another person to experience a certain emo-
tion, including a bodily sensation. Both indices
tap overlapping processes and are considered
interrelated aspects of the same complex con-
struct of empathy (Singer, 2006). Yet, there are
quantitative differences. For example, sharing
a close friend’s feelings of grief is felt much
differently than the recognition or comprehen-
sion of this person’s thoughts and feelings in
this painful situation. Understanding of these dif-
ferences has led to the establishment of a more
multidimensional approach to the definition of
empathy, acknowledging that all these aspects
are separate but related constructs of the integral
concept of empathy (Eisenberg, Fabes, &
Spinrad, 2006).
Sharing feelings with others may be
manifested in facial and/or vocal expressions or
in body movements and gestures. People can feel
empathy for others in a range of emotional con-
texts, from basic sensations such as sadness or joy
1089 E
to more complex emotions such as love and
remorse. Empathy has a variety of definitions
such as the ability to place oneself in another’s
place (“put oneself in another’s shoes”), the
experiencing of another’s affective or psycholog-
ical states, or one’s emotional responses to the
emotional displays of others (Eisenberg & Fabes,
1990; Moore, 1990; Zahn-Waxler, Radkeyarrow,
Wagner, & Chapman, 1992). Additional defini-
tions describe empathy as an affective response
E
more appropriate to someone else’s situation than
to one’s own situation, or when another person’s
emotion evokes an analogous affective experi-
ence in oneself (Eisenberg et al., 2006). It is
important to note that although in empathizing
one may “feel the same” as another, the affective
states of the self and other are nevertheless
distinguishable. That is, the emotion that was
induced in the self by the perception of the other’s
emotional state can be distinguished from the
same feeling originating in oneself. A related
concept to empathy is sympathy, which is simi-
larly described as an emotional response of sor-
row or concern toward someone in distress.
Sympathy usually stems from empathy, yet
both empathy and sympathy differ from personal
distress, which is a self-focused and somewhat
aversive reaction of anxiety in response to a sim-
ilar emotional state of distress in another
(Eisenberg et al.).
The concept of empathy plays a significant
role in developmental social cognition theories
such as theory of mind (ToM) and the empathiz-
ing-systemizing theory and is associated with
concepts such as mind reading, mentalizing, and
perspective taking (Baron-Cohen, 1995, 2002;
Frith, 1994). These theories suggest that the
characteristic deficits in mentalizing skills
that are associated with poor interpersonal
relationships hinder the ability of individuals
with autism to understand and engage in
interpersonal relationships. In order to
engage in reciprocal social interactions and
to successfully navigate social exchanges,
one should possess the capacity to recognize
and accurately interpret and predict what the
other is thinking and feeling and how he or
she might respond.
E 1090
Historical Background
In their initial writings, Leo Kanner as well as
Hans Asperger described autism as affective
impairment pertaining to difficulties in social
and communicative functions as well as to diffi-
culties in empathy. Kanner described “children’s
inability to relate themselves in the ordinary way
to people and situations from the beginning of
life.” He noted that “It is not a ‘withdrawal’ from
formerly existing participation. There is from the
start an extreme autistic aloneness that whenever
possible, disregards, ignores, shuts out anything
that comes to the child from the outside”
(Asperger, 1944; Kanner, 1943; Wing, 1981). In
his description, Asperger specifically addressed
“autistic psychopathy” of children who
manifested “severely disturbed and considerably
limited interaction. . ..and characteristic difficul-
ties of social integration” including patterns of
lack of empathy and difficulties in “reading
between the lines.”
Empathy is long considered an important pro-
cess known to facilitate interpersonal relation-
ships, particularly prosocial behavior. Religious,
philosophical, and psychological theories have
long debated whether humans are basically
good, empathic, and altruistic in nature or
whether all prosocial actions essentially derive
from underlying egoism and self-interest. Twen-
tieth century psychological theories such as
Freud’s psychoanalytic theory viewed human
development mainly as an interplay between
two innate trends, “egoistic” and “altruistic,”
although later psychoanalytic theories acknowl-
edged prosocial actions as defense mechanisms
used to deal with irrational demands such as
feelings of guilt, self-destructive tendencies, and
sexual strivings – all believed to underlie altruism
and empathy. These theories also put forward the
importance of the early mother-child relationship
for the development of empathy, through mental
mechanisms of identification and internalization.
Furthermore, contemporary psychoanalytic theo-
ries consider empathy as crucial to the develop-
ment of insight, for people may come to
see themselves through eyes of others via empa-
thy. Empathy is also considered an important
Empathy
condition for effective therapeutic intervention
in psychotherapy. Piaget’s theory on cognitive
development emphasized the transition from
infants’ egocentric orientation to the more social
orientations characteristic of later periods,
through the acquisition of perspective-taking
abilities during the preschool years; thus,
prosocial behaviors were assumed to emerge at
the beginning of the school years (Eisenberg
et al., 2006).
Current Knowledge
Empathy in Individuals with Autism
A considerable body of research investigated dif-
ficulties in empathy among individuals with
autism, who are characterized by qualitative
impairments in social interaction and communi-
cation (Baron-Cohen & Wheelwright, 2004;
Charman et al., 1997; Jones et al., 2010; Kasari,
Chamberlain, & Bauminger, 2001; Rogers,
Dziobek, Hassenstab, Wolf, & Convit, 2007;
Shamay-Tsoory, Tomer, Yaniv, & Aharon-
Peretz, 2002; Yirmiya et al., 1992). It was
suggested that individuals with autism exhibit
deficits in their capacity to mentalize and empa-
thize and that these core deficits hinder them in
developing adequate reciprocal interactions.
Individuals with autism reveal difficulties in
interpreting social cues and in “mind reading”
of others’ emotions; hence, it is more difficult
for them to achieve a clear and accurate under-
standing of what other individuals think, feel, and
experience.
Clinical observations suggested that children
with autism do not respond to other people’s
affect in the same way as children with typical
development or children with mental retardation
(Sigman & Capps, 1997). The empathic response
to negative affect (distress of other) was investi-
gated in children with autism in comparison to
children with typical development and children
with mental retardation, matched on mental age
(Kasari, Sigman, & Yirmiya, 1993). It was found
that more children with autism ignore, or did not
notice, the negative affect of the adults and
appeared less concerned than the other children
Empathy
in response to distressed adult. It was suggested
that children with autism lack the cognitive and
affective prerequisites that are necessary for
being attentive and empathic to the emotion of
others. Other studies investigated difficulties in
the capacity to empathize in high-functioning
children with autism and adolescents compared
to typically developing children at the same age
(Yirmiya et al., 1992). Children’s ability to dis-
criminate between different emotional states,
perspective-taking abilities of emotional states,
and emotional responsiveness were compared.
The strong associations between cognitive abili-
ties and empathy that was found in the autism
group compared to the typical development
group may have suggested that children with
autism use their cognitive abilities and cognitive
strategies to successfully understand and engage
in social situations more than is necessary for
children with typical development (Sigman &
Capps, 1997).
Individuals with autism present difficulties in
understanding the feelings and perspectives of
others, labeling the emotions felt by others, and
responding with empathy. They also react unex-
pectedly to interpersonal situations. It is impor-
tant to note that although individuals with autism
manifest difficulties in empathy, this does not
mean that their behavior in real-life situations is
cold or uncaring or that their lack of empathy is
related to antisocial behavior (Jones et al., 2010;
Rogers et al., 2007). Many individuals with
autism appear to show as much warmth, compas-
sion, caring, and concern for others as typically
developing individuals, especially when the
information is presented in a way that allows
them to better understand the feelings and per-
spectives of others. An alternative explanation
for the lower empathy levels reported in autism
than in typical development may be that these
research findings could reflect difficulties in artic-
ulating emotions rather than in feeling them. Evi-
dence for this possibility may be that individuals
with autism who exhibit greater self-awareness as
well as higher cognitive and verbal abilities are
able to report their feelings more accurately and
thus to appear more empathic than individuals
with autism with lower cognitive and verbal
1091 E
abilities who exhibit lower levels of self-
awareness and who show difficulties articulating
their emotions (Travis, Sigman, & Ruskin, 2001;
Yirmiya et al., 1992). Furthermore, comparing
boys with autism and boys with psychopathic
tendencies revealed that the latter had significant
impairments in emotional empathy with intact
perspective-taking abilities, whereas the boys
with autism had a reverse pattern – significant
impairments in cognitive perspective-taking abil-
E
ities and intact emotional empathy (Jones et al.,
2010).
Recently, Simon Baron-Cohen introduced the
extreme male brain (EMB) theory of autism
(Baron-Cohen, 2002), suggesting that individuals
with autism may manifest an exaggerated male
brain psychometric profile, demonstrating
extreme properties in two psychological dimen-
sions: extremely low empathizing (defined as the
drive to identify another’s mental state and to
respond with an appropriate emotion) and
extremely high systemizing (defined as mecha-
nistic thinking; the drive to analyze, explore, and
construct a system in terms of its underlying
regularities).
The Development of Empathy
It is well known that infants and toddlers are
sensitive and responsive to emotional cues or
signals of others, thus yielding behaviors that
resemble empathic expressiveness. An infant’s
reflexive crying or arousal-containing sucking
behavior in response to the crying of another
infant are considered early precursors of
empathic reactivity (Ungerer et al., 1990; Zahn-
Waxler et al., 1992). This emotional contagion,
or emotional resonance, refers to the infant’s
ability to imitate another’s emotional distress,
without awareness of the other, and therefore is
not considered “true” empathy. This kind of emo-
tional involvement, which is strongly linked to
infants’ early developmental and cognitive abili-
ties, diminishes after the first year as differentia-
tion between self and other increases and toddlers
come to perceive themselves as separate beings.
Thus, empathy emerges throughout the second
year of life, as well as sympathetic concern and
E 1092
comforting behaviors in response to others’ dis-
tress (Eisenberg & Fabes, 1990; Zahn-Waxler &
Radkeyarrow, 1990; Zahn-Waxler et al., 1992).
Longitudinal studies revealed that empathic
behaviors increase and become more sophisti-
cated and explicit during the first years, and this
increase is associated with the developmental
changes that are prerequisites for empathy.
These cognitive and emotional prerequisites are
self-other differentiation, perspective-taking
ability, and emotion regulation, as well linguistic
ability and social engagement skills. All these
skills are necessary for the child to empathize,
comfort others, inquire about others’ feelings,
and provide others with adequate support
(Knafo, Zahn-Waxler, Van Hulle, Robinson, &
Rhee, 2008; Zahn-Waxler et al., 1992). Further-
more, secure attachment relationships and early
parent-infant interactions contribute to later
development of empathy, through the synchro-
nized exchange of shared emotions (“the dance”)
between the parents and infant in the first year. In
the second year, emotion regulation pertains to
the capacity for role-taking and the emergence of
higher-order self-conscious emotions such as
guilt or shame as well as empathy. Socialization
and environmental influences also play an impor-
tant role in the second year, when parents already
expect their children’s behavior to be socially and
interpersonally appropriate (Eisenberg et al.,
2006).
Although the observation of early empathic
manifestations in infants and toddlers is not
straightforward due to children’s limited
verbal skills, some researchers demonstrated the
presence of different early manifestations of
emphatic behaviors (Zahn-Waxler & 20-month-old toddlers with developmental
Radkeyarrow, 1990; Zahn-Waxler et al., 1992).
For example, toddlers older than 1 year who
observed a peer or adult in distress revealed vary-
ing behaviors: Some toddlers became quiet and
observed the situation with a concerned facial
expression; others expressed their discomfort by
disquiet and agitated behaviors; and others
ignored the distressed person and continued
with their own activities. The earliest emphatic
reactions are mostly physical in nature, such as
hugs and pats. After age 2 years, toddlers reveal
Empathy
more explicit empathic and prosocial behaviors
such as verbally comforting, reaching for some-
one to get help, giving a victim toys, or trying to
find ways to cheer someone up. Some of these
behaviors may be still egocentric in nature;
young children may try to comfort the other
with things that make them feel better. With
age, as ToM abilities become more developed
(regarding the differentiation between one’s
own and others’ states of mind) and as affective
arousal becomes more modulated, children’s
emphatic and prosocial behaviors become more
attuned to the other person’s needs (Eisenberg
et al., 2006). There is some evidence regarding
sex differences in empathy in the preschool
years as well as in adulthood. Girls usually
reveal more empathic reactions than boys, such
as concern and joining into the emotional expe-
riences of others, and these sex differences
are present as early as 14 months. It may be
assumed that these differences reflect both bio-
logically based predispositions as well as social-
ization influences for females to be responsive
to the physical and emotional needs of others
(Eisenberg et al.).
Not many studies have investigated children
with autism in terms of the emergence of empa-
thy in the first years and the early manifestations
of sympathetic concern and comforting behaviors
in response to others’ distress (Yirmiya et al.,
1992), as well as developmental trajectories for
the ability to empathize in children with autism.
Twenty-month-old toddlers with autism had
difficulties looking to other person’s face and
showing expressed facial concern in response to
feigned distress compared to control groups of
delays and typical development (Charman et al.,
1997). In a recent prospective study of young
siblings of children with autism – a group con-
sidered at higher risk for autism – infants later
diagnosed with autism paid less attention and
showed less affective response to the examiner’s
display of a distress reaction as early as 12 months
of age compared to infants who were not later
diagnosed with autism (Hutman et al., 2010).
Furthermore, it was found that atypical response
to another person’s distress differentiated infants
Empathy
subsequently diagnosed with autism from those
infants who were not later diagnosed with autism
spectrum disorder at 36 months. Thus, it was
suggested that low levels of responsiveness to
another person’s distress at 12 and 18 months
are indicative of elevated risk for autism spec-
trum disorder at 36 months. These findings need
to be replicated in other low-risk and high-risk
infant populations.
Measuring Empathy
Several research instruments have been used to
measure empathy in children and adults in gen-
eral and in individuals with autism. The Feshbach
and Powell Audiovisual Test for Empathy
(Feshbach, 1982) was designed to measure chil-
dren’s empathy and emotional responsiveness. It
consists of 10 videotaped segments presenting
short stories about children experiencing differ-
ent events and emotions such as happiness, anger,
or sadness (e.g., a boy is sad because he lost his
dog). After watching each story, the child is asked
to report how he or she feels. In some adaptations
of this procedure (Yirmiya et al., 1992), usually
when examining children with autism, partici-
pants are first asked about the nature of the pro-
tagonists’ feelings (labeling the emotion) in
addition to the nature of their own emotional
response to the video vignette (empathic reac-
tion). This adaptation prevents the examiner
from identifying children as failing to empathize
in cases when the child recognizes and reports
a different emotion from the target emotion yet
reveals the capacity to refer to the protagonist’s
emotional state.
Marian Sigman and her colleagues designed
specific research procedures for measuring
empathy among young children with autism
(Sigman, Kasari, Kwon, & Yirmiya, 1992). The
researchers recorded and then coded the child’s
reactions to a distress situation that was enacted
by the mother. In this enactment, after a short
period of play with a wooden pounding toy and
hammer, the mother pretended to hurt herself by
hitting her finger with the hammer, and she
displayed facial and vocal expressions of distress
without using words. Children with autism
1093 E
tended to ignore or not notice adults showing
these negative affects more often than children
with mental retardation or children with typical
development.
Carolyn Zahn-Waxler and her colleagues
(Zahn-Waxler et al., 1992), who investigated the
early development of empathy in children and
twins, used similar procedures where both an
experimenter and the mother presented simulated
situations of distress such as bumping into a
E
chair. In addition, they used mothers as system-
atic observers, training them to collect data
regarding their child’s responses to the emotions
of others, emotions both caused and witnessed by
their children. This methodology may be of inter-
est to investigators to employ in future studies of
empathy in children with autism.
Children’s limited verbal ability precludes the
use of self-report measures, which are more com-
mon in the examination of empathy in adoles-
cents and adults. The Interpersonal Reactivity
Index (IRI; Davis, 1983) is a self-report measure
of empathy comprising four subscales: perspec-
tive-taking, empathic concern, personal distress,
and fantasy. Although some of these subscales
may not directly assess emotional empathy, indi-
ces such as imagination or emotional self-control
correlate with empathy. A more recent self-report
instrument for measuring empathy is the 60-item
Empathy Quotient questionnaire (EQ; Baron-
Cohen & Wheelwright, 2004). This scale
includes items like: “It is hard for me to see
why some things upset people so much” or
“I find it easy to put myself in somebody else’s
shoes” and thus may be measuring prosocial
behaviors and social skills in addition to empa-
thy. Adults with Asperger’s syndrome or high-
functioning autism scored significantly lower
on the EQ than individuals with typical devel-
opment matched for age and sex; in addition, in
the typical development group, women score
significantly higher than men. Assessing indi-
viduals’ beliefs about their own empathy might
differ from their actual empathic reactions to
emotional situations. Indeed, it is an important
methodology strength of developmental
research over the report measures used with
older individuals.
E 1094
Current Knowledge
Recent longitudinal and twin studies have identi-
fied continuity in empathic development over
time and the relationship between empathy and
prosocial behavior (Knafo et al., 2008). It was
suggested that empathy is a relatively stable dis-
position across both time and different contexts,
with heritability that tends to increase with age.
Yet, environmental factors such as parenting
practices, peer and sibling relationships, and edu-
cational programs contribute to empathic abili-
ties (Knafo & Uzefovsky, 2012). Several
biological and genetic mechanisms were pro-
posed as relevant to the development of empathy.
Empathy was found to be associated with
temperamental characteristics: For example,
inhibited and unreactive temperament features
in the first year were negatively associated with
empathy at the age of 2 years (Young, Fox, &
Zahn-Waxler, 1999). Other studies have focused
on the neuronal correlates and neural mecha-
nisms underlying the ability to understand the
mental and emotional states of others (Blair,
1999; Singer, 2006). Different neural circuitries
were associated with the cognitive and emotional
aspects of empathy: Perspective-taking abilities
were found to involve structures of the superior
temporal sulcus and the medial prefrontal
cortex, whereas emotional empathy involved
sensory-motor cortices as well as limbic and
paralimbic structures (the “social” or “emo-
tional” brain). Moreover, it was found that the
limbic structures develop earlier than the tempo-
ral lobe and prefrontal structures – in line with
developmental studies that demonstrated the
early precursors of emotional empathy during
the first year as well as the later emergence of
cognitive perspective-taking abilities (Decety,
2010; Singer, 2006).
Some speculations were raised about the asso-
ciations between empathy and autism and the
network of visuomotor cells known as mirror
neurons (MNs). The MNs are activated and
discharged when the individual performs
a particular motor action as well as when observ-
ing somebody else perform a similar action.
Thus, it was suggested that the MNs as an execu-
tion/observation matching system may be
Empathy
connected to social and emotional functioning
such as imitation and empathy, which are consid-
ered as impaired in autism (Perkins, Stokes,
McGillivray, & Bittar, 2010). Finally, molecular
genetics studies have demonstrated the associa-
tions between social behavior and two
nonapeptides of arginine: vasopressin and oxyto-
cin (Israel et al., 2008; Yirmiya et al., 2006). It
was suggested that the arginine vasopressin
receptor 1a (AVPR1a) gene and the oxytocin
receptor (OXTR) gene are possible contributors
to altruistic behavior. Furthermore, family stud-
ies of individuals with autism and their relatives
revealed the role of the AVPR1a gene in mediat-
ing the association of socialization skills in
autism. Other genetic studies examined candidate
genes in a group of individuals with Asperger’s
syndrome and a population sample. Nineteen
genes showed nominally significant associations
with self-report measures of empathy (Empathy
Quotient questionnaire) and autistic traits (the
Autism Quotient questionnaire) (Chakrabarti
et al., 2009).
Future Directions
Although difficulties in empathy are detectible
among individuals with autism, not much is yet
known about the developmental trajectories of
empathy in infants or toddlers who are later diag-
nosed with autism (Hutman et al., 2010). The
search for empathy precursors in autism is closely
linked to the investigation of early manifestations
of autism in the first year/s of life. Future research
would do well to track infants who are
underresponsive to emotional cues such as
others’ distress and to explore these infants’
developmental trajectories and later diagnoses.
It will be of great importance to know whether
early underresponsiveness during the first year
predicts future diagnoses of autism or other
developmental difficulties. Furthermore, within
the field of autism, treatment studies should be
initiated to explore strategies to improve the
capacity to empathize and thus to facilitate the
various aspects of social interactions and
relationships.
Empathy
See Also
▶ Affective Development
▶ Empathizing-Systemizing Theory
▶ Extreme Male Brain (EMB) Theory
▶ Face Perception
▶ Face Recognition
▶ Friendships
▶ Interpersonal Skills
▶ Mindblindness
▶ Social Cognition
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empathy. Motivation and Emotion, 14(2), 75–80.
Perkins, T., Stokes, M., McGillivray, J., & Bittar, R.
(2010). Mirror neuron dysfunction in autism spectrum
disorders. Journal of Clinical Neuroscience, 17(10),
1239–1243.
Rogers, K., Dziobek, I., Hassenstab, J., Wolf, O. T., &
Convit, A. (2007). Who cares? Revisiting empathy in
Asperger syndrome. Journal of Autism and Develop-
mental Disorders, 37(4), 709–715.
Shamay-Tsoory, S. G., Tomer, R., Yaniv, S., & Aharon-
Peretz, J. (2002). Empathy deficits in Asperger
syndrome: A cognitive profile. Neurocase, 8(3),
245–252.
E 1096
Sigman, M., & Capps, L. (1997). Children with autism:
A developmental perspective (Development of social
and emotional understanding, pp. 34–60). Cambridge,
MA: Harvard University Press.
Sigman, M. D., Kasari, C., Kwon, J. H., & Yirmiya, N.
(1992). Responses to the negative emotions of others
by autistic, mentally-retarded, and normal-children.
Child Development, 63(4), 796–807.
Singer, T. (2006). The neuronal basis and ontogeny of
empathy and mind reading: Review of literature and
implications for future research. Neuroscience and
Biobehavioral Reviews, 30(6), 855–863.
Travis, L., Sigman, M., & Ruskin, E. (2001). Links
between social understanding and social behavior in
verbally able children with autism. Journal of Autism
and Developmental Disorders, 31(2), 119–130.
Ungerer, J. A., Dolby, R., Waters, B., Barnett, B., Kelk, N.,
& Lewin, V. (1990). The early development of empa-
thy: Self-regulation and individual differences in the
first year. Motivation and Emotion, 14(2), 93–106.
Wing, L. (1981). Asperger syndrome: A clinical account.
Psychological Medicine, 11, 115–130.
Yirmiya, N., Rosenberg, C., Levi, S., Salomon, S.,
Shulman, C., Nemanov, L., et al. (2006). Association
between the arginine vasopressin 1a receptor
(AVPR1a) gene and autism in a family-based study:
Mediation by socialization skills. Molecular Psychia-
try, 11(5), 488–494.
Yirmiya, N., Sigman, M. D., Kasari, C., & Mundy, P.
(1992). Empathy and cognition in high-functioning
children with autism. Child Development, 63(1),
150–160.
Young, S. K., Fox, N. A., & Zahn-Waxler, C. (1999). The
relations between temperament and empathy in 2-year-
olds. Developmental Psychology, 35(5), 1189–1197.
Zahn-Waxler, C., & Radkeyarrow, M. (1990). The origins
of empathic concern. Motivation and Emotion, 14(2),
107–130.
Zahn-Waxler, C., Radkeyarrow, M., Wagner, E., &
Chapman, M. (1992). Development of concern for
others. Developmental Psychology, 28(1), 126–136.
Empirically Supported Treatments
Brian Reichow
Child Study Center, Associate Research
Scientist, Yale University School of Medicine,
New Haven, CT, USA
Definition
Evidence-based practice (EBP) refers to
a multistep process used to make decisions that
Empirically Supported Treatments
involves the appraisal of current evidence, refer-
ence to clinical expertise, and consideration of
patient values and choice (Sackett et al., 1996).
Historical Background
The conceptualization, ideals, and guidelines that
have become evidence-based practice (EBP)
emerged first in the medical field as evidence-
based medicine. EBP is a multistep process that
involves the appraisal of current evidence,
reference to clinical expertise, and consideration
of patient values and choice (Sackett et al., 1996).
Since moving to the social sciences, EBP, albeit
under various names (e.g., empirically supported
treatment, scientifically based research), has been
further refined and expanded to match the ideol-
ogies and traditions of the various disciplines
within the social sciences. Most organizations
representing individuals practicing in the social
sciences now have a definition of EBP, although
the amount and type of evidence needed for
a practice to be recognized as evidence-based
often differ across organizations. Given the
multitude of disciplines working in the field of
autism, this likely hindered early efforts at
identifying EBP.
Current Knowledge
Recently, a number of practices and treatments
for individuals with ASDs have been identified
EBP. Two recent books (e.g., Evidence-Based
Practices and Treatments for Children with
Autism (Reichow, Doehring, Cicchetti, &
Volkmar, 2011) and Effective Practices for
Children with Autism (Luiselli, Russo, Christian,
& Wilczynski, 2008)) have shown that many
autism treatments can now be considered
evidence-based (see also Educating Children
with Autism; National Research Council, 2001).
Evidence of EBP in autism in peer-reviewed
publications has also emerged. In 2000, Filipek
and colleagues applied the American Academy of
Neurology standards to screening and diagnostic
procedures, and Rogers and Vismara (2008)
Empirically Supported Treatments
outlined the evidence for autism treatments for
the 10-year follow-up of APA Division 53 assess-
ment of EBP. The new report suggested early
intensive behavioral intervention based on
applied behavior analysis, pivotal response treat-
ment, and parent education could now be consid-
ered evidence-based. Shortly thereafter, two
independent comprehensive reviews by the
National Professional Development Center on
ASD (2008) and the National Autism Center
(2009) identified dozens of focal treatments that
are evidence-based, including, but not limited to,
visual schedules, social narratives, prompting,
and reinforcement (complete lists available
at websites listed below). Updates to both
of these guides is currently underway which
should further our knowledge about the most
effective treatments for children with ASD.
Government-led health agencies (e.g., Agency
for Healthcare Research and Quality, 2011;
National Institute for Health and Clinical Excel-
lence, 2011; Scottish Intercollegiate Guidelines
Network, 2007) have also issued guidelines,
often with accompanying parent-friendly guides,
thus helping ensure consumers are able to access
this critical information necessary to be an active
participant in the EBP process.
Future Directions
The amount of research on ASD continues to
expand. Thereby, continued identification of
EBP for individuals with ASDs will be needed.
Currently, little is known a priori concerning
which EBP will be the most successful treatment
for specific individuals. Future EBP guides
should strive to help identify the individual char-
acteristics of the client, therapist, and/or setting
that will help maximize outcomes. Given the
research to practice gap, further dissemination
of EBPs are also needed, especially in formats
that are accessible to practitioners and parents. As
society continues to expand its use and emphasis
of technology, it will also be important to begin to
understand how the World Wide Web and social
media (e.g., Facebook, Twitter) might be utilized
to disseminate EBP to parents and practitioners.
1097 E
Research has shown that parents utilize the World
Wide Web more than any other source to gain
information on ASD, but recent analyses of the
quality of the information on autism websites
suggest caution and vigilance are needed as
consumers are likely to access sites with mixed
or poor quality (Reichow et al., 2012).
See Also E
▶ Practice Guidelines in Autism
▶ Treatment Effectiveness
References and Readings
Agency for Healthcare Research and Quality. (2011).
Therapies for children with autism spectrum disorders
(Comparative effectiveness review number 26).
Rockville, MD: Author.
Filipek, P. A., Accardo, P. J., Ashwal, S., Baranek, G. T.,
Cook, E. H., Jr., Dawson, G., et al. (2000). Practice
parameter: Screening and diagnosis of autism.
Neurology, 55, 468–479.
Luiselli, J. K., Russo, D. C., Christian, W. P., &
Wilczynski, S. M. (2008). Effective practices for
children with autism: Educational and behavior
support interventions that work. New York: Oxford
University Press.
National Autism Center. (2009). National standards
report. Retrieved January 6, 2010, from: http://www.
nationalautismcenter.org/pdf/NAC%20Standards%
20Report.pdf
National Institute for Health and Clinical Excellence.
(2011). Autism: Recognition, referral and diagnosis
of children and young people on the autism spectrum
(CG128). London: Author.
National Research Council. (2001). Educating young
children with autism. Washington, DC: National
Academy Press.
Reichow, B., Doehring, P., Cicchetti, D. V., & Volkmar,
F. R. (Eds.). (2011). Evidence-based practices and
treatments for children with autism. New York:
Springer.
Reichow, B., Halpern, J., Steinhoff, T., Letsinger, N.,
Naples, A., & Volkmar, F. R. (2012). Characteristics
and quality of autism websites. Journal of Autism and
Developmental Disorders, 42(6), 1263–1274.
Rogers, S. J. (1998). Empirically supported comprehen-
sive treatments for young children with autism.
Journal of Clinical Child Psychology, 27, 168–179.
Rogers, S. J., & Vismara, L. A. (2008). Evidence-based
comprehensive treatments for early autism. Journal of
Clinical Child and Adolescent Psychology, 37, 8–38.
E 1098
Sackett, D. L., Rosenberg, W. M. C., Gray, J. A. M.,
Haynes, R. B., & Richardson, W. S. (1996). Evidence
based medicine: What it is and what it isn’t. British
Medical Journal, 312, 71–72.
Scottish Intercollegiate Guidelines Network. (2007).
Assessment, diagnosis and clinical interventions for
children and young people with autism spectrum
disorders: A national clinical guideline. Retrieved
January 5, 2010, from http://www.sign.ac.uk/pdf/
sign98.pdf
Employ
▶ Employment
Employee Development
▶ Feedback on Provider Work Performance
Employee Performance
▶ Feedback on Provider Work Performance
Employment
Paul Wehman
Department of Physical Medicine and
Rehabilitation, Virginia Commonwealth
University, Richmond, VA, USA
Synonyms
Employ; Pay; Service; Working for pay
Definition
An agreement between a person and
a representative of a business who has hiring
authority (i.e., owner, manager, personnel direc-
tor, etc.) to exchange labor for a wage that is in
Employ
alignment with others who are performing com-
parable work in the workplace and at least meets
the federal minimum wage standard.
An arrangement where a person engages in
providing a service and/or producing a product
for another entity (person, the public, business,
etc.) in exchange for monetary payment to earn
a livable income.
See Also
▶ Supported Employment
▶ Transition Planning
▶ Vocational Rehabilitation Act of 1973
References and Readings
Inge, K., & Moon, S. (2011). Preparing students with low
incidence disabilities to work in the community. In
J. M. Kauffman & D. P. Hallahan (Eds.), Handbook
of special education. New York/London: Routledge.
Wehman, P. (2012). Life beyond the classroom: Transi-
tion strategies for young people with disabilities.
Baltimore: Paul H. Brookes.
Wehman, P., Smith, M., & Schall, C. (2009). Transition
from school to adulthood for youth and young adults
with autism: Growing up in the real world. Baltimore:
Paul Brookes.
Employment Consultant
▶ Employment Specialist
Employment in Adult Life
Paul Wehman
Department of Physical Medicine and
Rehabilitation, Virginia Commonwealth
University, Richmond, VA, USA
Definition
There is limited research outlining the specific
services and supports required by individuals
Employment in Adult Life
with ASD. However, some examples of
a supported employment approach have been
described (e.g., Hillier et al., 2007a, b; Howlin,
Alcock, & Burkin, 2005; Keel, Mesibov, &
Woods, 1997; Lawer, Brusilovskiy, Salzer, &
Mandell, 2009; Nesbitt, 2000; Smith, 1994;
Schaller & Yang, 2005; Wehman, Datlow
Smith, & Schall, 2009). Using this advocacy
level service, a vocational rehabilitation profes-
sional known as an employment specialist or job
coach provides and/or facilitates a unique mix of
supports that vary in type, level, and intensity
uniquely designed to assist the person with
gaining and maintaining employment (Wehman
et al., 2009).
Additionally, case studies conducted with
adults with ASD provide tremendous insight
regarding vocational needs (Hurlbutt &
Chalmers, 2002, 2004; M€ uller, Schuler, Burton,
& Yates, 2003, Wehman et al., 2009). From this
research, recommendations for vocational sup-
ports can be ascertained and grouped into four
major themes: (1) job placement (Schaller &
Yang, 2005) and match (Howlin et al., 2005;
Keel et al., 1997; Mawhood & Howlin, 1999;
M€ uller et al., 2003), (2) supervisors and
coworkers (Bolman, 2008; Burt, Fuller, &
Lewis, 1991; Hagner & Cooney, 2005; Hillier
et al., 2007a, b; Howlin et al., 2005; Keel et al.,
1997; Mawhood & Howlin, 1999; M€ uller et al.,
2003; Nesbitt, 2000), (3) on-the-job provisions
(Burt et al., 1991; Fast, 2004; Hagner & Cooney,
2005; Hillier et al., 2007a, b; Lawer et al., 2009,
Nuehring & Sitlington, 2003; Smith, Belcher, &
Juhrs, 1995), (4) work place modifications (Fast,
2004; Hagner & Cooney, 2005; M€ uller et al.,
2003; Nuehring & Sitlington, 2003) and predict-
ability (Burt et al., 1991; Foley & Staples, 2003;
Hagner & Cooney, 2005; Hume & Odom, 2007),
and (5) long-term support (Hillier et al., 2007a, b;
Howlin et al., 2005; Keel et al., 1997; M€ uller
et al., 2003; Smith & Philippen, 1999; Smith
et al., 1995).
While the small body of existing research
gives shape to this topic, there are limitations.
The number of peer-reviewed articles on this
topic is scarce and hampered by limited sample
sizes and restricted population ranges. Existing
1099 E
research covers an array of topics, yielding few
solid conclusions in any given area. However, to
some degree, the evidence does seem to endorse
supported employment as a promising practice to
assist individuals with ASD with employment
and career advancement. If this supported
employment is going to become a viable option
for individuals with ASD, then key stakeholders
including individuals with ASD, family mem-
bers, educators, vocational rehabilitation service
E
providers, and others will need to learn how to
individualize an array of specific supports at work
designed to meet each person’s unique needs.
It will also require education of employers to
understand how employing an individual with
ASD can bring value to business. In summary,
to date, few solid conclusions have been reached,
and more research is needed.
Historical Background
There is limited research outlining the specific
services and supports required by individuals
with ASD. However, some examples of
a supported employment approach have been
described (e.g., Hillier et al., 2007a, b; Howlin
et al., 2005; Keel et al., 1997; Lawer et al., 2009;
Nesbitt, 2000; Smith, 1994; Schaller & Yang,
2005; Wehman et al., 2009). Using this advocacy
level service, a vocational rehabilitation profes-
sional known as an employment specialist or job
coach provides and/or facilitates a unique mix of
supports that vary in type, level, and intensity
uniquely designed to assist the person with
gaining and maintaining employment (Wehman
et al., 2009).
Additionally, case studies conducted with
adults with ASD provide tremendous insight
regarding vocational needs (Hurlbutt &
Chalmers, 2002, 2004; M€uller et al., 2003,
Wehman et al., 2009). From this research, recom-
mendations for vocational supports can be
ascertained and grouped into major themes:
(1) job placement (Schaller & Yang, 2005) and
match (Howlin et al., 2005; Keel et al., 1997;
Mawhood & Howlin, 1999; M€uller et al., 2003),
(2) supervisors and coworkers (Bolman, 2008;
E 1100
Burt et al., 1991; Hagner & Cooney, 2005; Hillier
et al., 2007a, b; Howlin et al., 2005; Keel et al.,
1997; Mawhood & Howlin, 1999; M€ uller et al.,
2003; Nesbitt, 2000), (3) on-the-job provisions
(Burt et al., 1991; Fast, 2004; Hagner & Cooney,
2005; Hillier et al., 2007a, b; Lawer et al., 2009;
Nuehring & Sitlington, 2003; Smith et al., 1995),
(4) work place modifications (Fast, 2004; Hagner
& Cooney, 2005; M€ uller et al., 2003; Nuehring &
Sitlington, 2003) and predictability (Burt et al.,
1991; Foley & Staples, 2003; Hagner & Cooney,
2005; Hume & Odom, 2007), and (5) long-term
support (Hillier et al., 2007a, b; Howlin et al.,
2005; Keel et al., 1997; M€ uller et al., 2003; Smith
& Philippen, 1999; Smith et al., 1995).
While the small body of existing research
gives shape to this topic, there are limitations.
The number of peer-reviewed articles on this
topic is scarce and hampered by limited sample
sizes and restricted population ranges. Existing
research covers an array of topics, yielding few
solid conclusions in any given area. However, to
some degree, the evidence does seem to endorse
supported employment as a promising practice to
assist individuals with ASD with employment
and career advancement. If this supported
employment is going to become a viable option
for individuals with ASD, then key stakeholders
including individuals with ASD, family
members, educators, vocational rehabilitation
service providers, and others will need to learn
how to individualize an array of specific supports
at work designed to meet each person’s unique
needs.
It will also require education of employers to
understand how employing an individual with
ASD can bring value to business. In summary,
to date, few solid conclusions have been reached,
and more research is needed.
Current Knowledge
Predicting outcome and planning for adult ser-
vice needs for children with autism spectrum
disorders (ASD) is limited by gaps in current
knowledge. The best quality information about
autism in adulthood comes from a few
Employment in Adult Life
population-based longitudinal studies that esti-
mate the full picture of outcomes. However,
changes in diagnostic criteria in the 1990s from
a comparatively narrow definition to the broader
current criteria for ASD means that studies of
adults originally diagnosed as children with his-
torical criteria have limited application to later
generations. In addition, longitudinal research
that depends on information from aging
caregivers has inherent challenges. For example,
recall of symptoms from earlier life may be
compromised by memory problems and health
problems of the aging informant. An alternative
research design using cross-sectional samples of
adults diagnosed with current, broader criteria
can provide data relevant to the future of children
being diagnosed today. Such cross-sectional
studies are useful adjuncts to population-based,
longitudinal research as they give a more com-
prehensive understanding of ASD in adulthood
and can bring focus to specific issues. For exam-
ple, the prevalence and variety of behaviors that
lead to encounters with law enforcement have
been described by Allen et al. (2009).
Two useful prognostic factors for adult out-
come in ASD are childhood intellectual ability
and onset of communicative speech. Like other
people with intellectual disabilities (ID), people
with ASD and ID generally achieve a limited
range of independence and “success” in adult
life as defined in developed Western societies
inclusive of gainful employment, a household
independent of their parents, and a circle of recip-
rocal friendships and romantic relationships.
Those with average-range intellectual abilities
(i.e., 70) have widely varying adult outcomes.
Several longitudinal studies have demonstrated
that communicative phrase speech before age 6
and an average-range childhood intelligence quo-
tient (IQ) are necessary for a chance at adult
independence but in no way guarantee it
(Billstedt, Gillberg, & Gillberg, 2005; Farley
et al., 2009; Howlin, Goode, Hutton, & Rutter,
2004; Kobayashi, Murata, & Yoshinaga, 1992).
When assessed in adulthood, barriers to indepen-
dence in people with ASD and average-range
intellectual abilities appear to include
co-occurring psychiatric conditions, difficulty
Employment in Adult Life
with initiation of goal-oriented activities, and
poor social skills. There may also be specific
genetic variations, developmental processes,
educational opportunities, ecological factors,
and specialized adult supports that influence
levels of independence in adulthood.
Natural Course
While ASD is a lifetime diagnosis, several longi-
tudinal studies have shown improvements in
autistic symptoms over the lifespan (Billstedt
et al., 2005; Cederlund, Hagberg, Billstedt,
Gillberg, & Gillberg, 2008; Piven, Harper,
Palmer, & Arndt, 1996; Rumsey, Rapaport, &
Sceery, 1985; Seltzer et al., 2004). The trend is
toward improvement in symptom severity in par-
ticipants as a group, with the greatest amount of
behavioral improvement in individuals who had
the highest IQs and the least severe symptom
presentation at the initial evaluation. These stud-
ies also show that a small proportion of affected
individuals no longer meet full diagnostic criteria
in adulthood. Importantly, most of these individ-
uals retain subtle impairments that continue to
present daily challenges to fully independent
functioning.
There also appears to be a small subgroup that
experiences significant deterioration in cognitive
or behavioral functioning in adolescence
(Ballaban-Gil, Rapin, Tuchman, & Shinnar,
1996; Kobayashi et al., 1992; Venter, Lord, &
Schopler, 1992). Causes for this deterioration are
unknown as yet, but appear unrelated to adoles-
cent seizure onset that occurs in some individuals
with ASD.
Mortality
Studies of mortality in autism have identified
a higher rate of mortality for populations with
ASD than in the general population, owing
largely to complications related to epilepsy and
other medical conditions and to accidental deaths
that may be associated with ID. Standardized
1101 E
mortality ratios (i.e., the ratio of observed deaths
in a specific sample to expected mortality in the
general population matched on variables such as
age, gender, and length of follow-up period)
range from 1.9 to 2.4, approximately twice the
expected rate for the general population (Isager,
Mouridsen, & Rich,1999; Pickett, Paculdo,
Shavelle, & Strauss, 2006; Shavelle, Strauss, &
Pickett, 2001). Females have had higher mortal-
ity rates than males in studied populations, prob-
E
ably associated with a higher rate of ID.
Selected Longitudinal Outcome Studies
A number of authors have categorized outcomes
of adults with AD using broad social and educa-
tional or occupational criteria (Howlin et al.,
2004). Outcome classifications usually include
five nodes and range from Very Poor (i.e., the
person cannot function independently in any
way) to Very Good (i.e., achieving great indepen-
dence, having friends and a job). Findings from
outcome studies are quite disparate, in spite of
considerable similarities between outcome
criteria and samples. A consistent finding from
published outcome studies is that outcome for
a majority (approximately 60%) of individuals
with ASD was Fair, Poor, or Very Poor (Billstedt
et al., 2005; Eaves & Ho, 2008; Howlin et al.,
2004).
Gillberg and Steffenburg (1987) studied out-
come for a population-based sample of 23 people
with ASD. As children, one-third obtained IQ
scores in the mildly mentally retarded range,
and 26% achieved scores in the normal or near
normal ranges. Eight (35%) had communicative
speech at age 6. These 23 participants were aged
16–23 years at the time of the follow-up. One
person (4% of the sample) obtained a “Good”
outcome. Thirty-five percent experienced the
“Fair, but restricted outcome” (i.e., characteris-
tics of “poor” outcome status, but accepted by
and included in some social community).
Thirteen percent had a “Fair” outcome, and 44%
had “Poor” or “Very Poor” outcomes. Childhood
IQ and use of communicative speech at age 6
E 1102
were useful predictors of outcome status. Epilep-
tic seizures were present in one-third of the pop-
ulation, often associated with severe mental
retardation and pubertal symptom aggravation.
Kobayashi et al. (1992) conducted a follow-up
investigation of 201 adults identified with ASD in
childhood through clinical services in Japan.
Four of the people had died. The mean age for
the remaining 197 young adults was 21 years and
8 months (SD ¼ 3.6). About one-fourth of the
sample had an IQ score of 70 or better at age 6,
and about 20% were able to speak without echo-
lalia at that age. An additional 31% used commu-
nicative language at age 6 but also used echolalic
speech. Forty percent of the sample began school
in a general education class, but only 27%
remained in general education at the age of 12.
At follow-up, 43 (21%) were employed and
11 (6%) were enrolled in higher education or
vocational training programs. Outcome adjust-
ment was “Good” or “Very Good” for 47%, was
“Fair” for 32%, and was “Poor” or “Very Poor”
for 46%. Childhood IQ was the only strong pre-
dictor of outcome in this investigation. Although
there were similarities between the sample in this
study and others reported, the outcome for these
participants was strikingly better, overall.
The authors provided some possible explanations
including sociodemographic factors in Japan,
advances in public education standards for people
with disabilities, intensive intervention histories,
and a high proportion of people with ASD and
average-range IQ scores at baseline.
Howlin et al. (2004) studied adult outcome for
68 people with ASD who also had a childhood
nonverbal IQ score of 50 or better. The mean age
at the initial evaluation was 7.24 (SD ¼ 3.10) and
at follow-up was 29.33 (SD ¼ 7.97). Nonverbal
IQ scores averaged 80.21 (SD ¼ 19.28).
At follow-up, the average nonverbal IQ was 75
(SD ¼ 21.52). Almost all of the subjects were
known to have attended compulsory schooling;
however, only 22% left school having achieved
formal qualifications. At the time of the follow-
up investigation, 23 people were employed. Eight
worked in regular, independent jobs, one was
self-employed as an artist but was unable to
earn a living wage, and 14 worked in sheltered
Employment in Adult Life
or supported employment. Twenty-seven people
were occupied in general work/leisure programs
at day centers for adults with disabilities. Out-
come adjustment ratings for the sample were that
22% had “Good” or “Very Good” outcomes, 19%
had “Fair” outcomes, and 58% had “Poor” or
“Very Poor” outcomes. Analyses of the assess-
ment results revealed that childhood IQ was
a useful predictor of adult adjustment in
that those with childhood nonverbal IQ scores
of 70 or more were more likely to do well than
those with scores below 70. Furthermore, a score
of 100 or better did not increase the likelihood
that a person would do well in adulthood.
For those who were capable of completing
a childhood verbal IQ measure, the combination
of verbal and nonverbal IQ scores in childhood
provided a more precise indication of outcome
classification, with scores above 70 in both
domains yielding the greatest likelihood of
a “Fair” outcome or better. Specifically, among
those with childhood nonverbal IQ scores of 70 or
more, 7 had a “Very Good” outcome, 7 had
a “Good” outcome, 10 obtained a “Fair” out-
come, and 20 had “Poor” or “Very Poor”
outcomes. Language level at age 5 was useful in
predicting overall outcome and residential status,
but none of the other outcome variables studied
demonstrated predictive utility.
Eaves and Ho (2008) followed 48 individuals
with autism spectrum disorders from childhood
(mean age ¼ 6.8) to adulthood (mean age ¼ 24)
in Canada. Fifty-seven percent of this sample had
autistic disorder, while the remainder had less
severe variants of ASD. Eight of the participants
had a childhood IQ score above 70. All partici-
pants received special education support during
their compulsory schooling years, and 30%
engaged in some kind of post-secondary educa-
tional program. Overall outcome adjustment rat-
ings were that 21% had “Good” or “Very Good”
outcomes, 32% had “Fair” outcomes, and 46%
had “Poor” outcomes. No participants fell within
the “Very Poor” outcome categorization. Sixty
percent of the sample resided at home with their
parents, 19% lived in group homes, and 13%
lived in foster care. Almost 80% received
a government disability pension and used the
Employment in Adult Life
services of social workers. In this sample, child-
hood verbal IQ was most predictive of outcome
status. However, the proportion of individuals
who were capable of completing an assessment
of verbal IQ was not reported.
Also in 2008, Cederlund et al. released their
study of outcome for 70 adults with autism and
70 adults with Asperger syndrome, after 5 or
more years time elapsed from original diagnosis.
This research team used the same outcome
categorization scheme as Gillberg and Steffenberg
(1987), with categories of “Good,” “Fair,”
“Restricted,” “Poor,” and “Very Poor.” Twenty-
seven percent (n ¼ 19) of this sample obtained an
outcome categorization of “Good,” and 47%
(n ¼ 33) were categorized as having a “Fair”
outcome. Sixteen people, or 23%, obtained
“Restricted” outcome status, and 2 people, or
3%, fell within the “Poor” category. There were
no participants with “Very Poor” outcome ratings.
Farley et al. (2009) studied 41 adults who had
been identified through a population-based study
of ASD in Utah in the 1980s. All of these indi-
viduals had previous IQ scores of 70 or greater.
Mean age at the first assessment was 7.2 years
(SD ¼ 4.1) and in adulthood was 32.5 years
(SD ¼ 5.7). Outcome adjustment was somewhat
better for this sample than previous samples, with
48% in the “Very Good” and “Good” categories,
34% in the “Fair” category, and 17% in the
“Poor” category. No participants fit within the
“Very Poor” category of outcome categorization.
Six participants did not meet diagnostic criteria
for current ASD using gold-standard diagnostic
procedures, but five of these still retained signif-
icant social difficulties reported by themselves or
significant others. Half were employed on a full-
or part-time basis, and 39% had attended some
kind of formal post-secondary education. Over
half of the sample (56%) continued to live with
their parents, and almost 25% lived in supported
living arrangements including a state residential
center for people with significant disabilities.
Almost 60% of the sample reported co-occurring
psychiatric diagnoses. Reported chronic medical
conditions were those commonly seen in the
general population (e.g., seasonal allergies,
gout, high blood pressure).
1103 E
Cognitive Function
Evidence to date reflects uneven development of
cognitive abilities across people with ASD. Ini-
tial evaluations during childhood often indicate
better nonverbal than verbal abilities. However,
many studies show evidence increases in verbal
ability and decreases in nonverbal ability during
adolescence and adulthood. Group results for
individuals with ASD and average-range IQ
E
scores demonstrate consistency in the distribu-
tion of subtest scores on Wechsler scales. How-
ever, some individuals who have relatively high
IQs in childhood demonstrate significant
increases in overall ability at follow-up. Dispar-
ities among findings may have several causes.
Selection of tests at initial evaluation and fol-
low-up for their appropriateness to the research
question and participants’ behavior may influ-
ence results. Furthermore, tests may not be suffi-
ciently parallel for comparison so that some of
the variance is attributable to inequality across
measures. Variation of tests from the initial eval-
uation to follow-up further obscures results since
within-group variation on measures may be con-
siderable (Howlin et al., 2004). Age at initial IQ
also appears to be an important factor, with non-
verbal abilities varying more among children ini-
tially tested before age 5 (Howlin et al., 2004).
Associated Co-occurring Conditions
Many of the outcome studies concerning adults
with AD provide information concerning co-
occurring medical and psychiatric conditions.
Few have analyzed the specific contributions
these disorders make to restrictions in overall
outcome (Danielsson, Gillberg, Billstedt,
Gillberg, & Olsson, 2005). One of the clearest
indicators of the presence of significant
co-occurring psychiatric and medical diagnoses
is the proportion of individuals who are pre-
scribed anticonvulsant and psychotropic medica-
tions. Eaves and Ho (2008) reported that 40% of
their sample was prescribed medication for
behavioral difficulties. Similarly, 40% of the par-
ticipants in the population-based study by
E 1104
Billstedt et al. (2005) were prescribed medication
for psychiatric disorders, and 40% of the adoles-
cents and adults in another study were prescribed
psychotropic medications to control behavior
(Ballaban-Gil et al., 1996). Thirty-seven percent
of those studied by Farley et al. (2009) were
described as taking prescription medications
aimed at managing behavioral difficulties.
Epilepsy is a chronic condition involving
recurring seizures and is more common in indi-
viduals with ASD than in the general population,
with an average prevalence rate of 16.8% across
epidemiological studies of ASD (Fombonne,
2005). This disorder occurs more frequently
in individuals with ASD and ID. The onset
of seizures typically occurs early in childhood
(i.e., before age 2) or in adolescence (Danielsson
et al., 2005; Kobayashi et al., 1992). Seizures
remit in a fraction of those afflicted (Danielsson
et al., 2005). Kobayashi et al. (1992) reported that
19% of their sample, representing the full range
of functioning within ASD, had epilepsy, and all
took antiepileptic medication. Nine percent of
a sample of adults with ASD and average-range
IQ scores who were taking antiepileptics (Howlin
et al., 2004).
Affective disorders challenge a person’s
capacity to regulate mood and include depres-
sion, mania, and bipolar disorder. It is estimated
that over 60% of people with AD suffer from
a co-occurring affective disorder. In a study of
35 individuals with Asperger syndrome,
Ghaziuddin, Weidmer-Mikhail, and Ghaziuddin
(1998) found that affective disorders were the
most common type of psychiatric condition
co-occurring in adults, affecting over half of
their sample. Figures from outcome studies with
adult samples range from 1% to 30% (Billstedt
et al., 2005; Farley, 2009).
Results of several outcome studies demon-
strate that anxiety disorders are present in
a large proportion of adults with AD. Rumsey
et al. (1985) determined that 50% of their sample
was suffering from chronic, generalized anxiety
which they suggested could account for the atten-
tion difficulties observed in one fifth of the sam-
ple. Another study of adults with ASD and
average-range IQ scores concluded that 40% of
Employment in Adult Life
their sample had OCD or chronic anxiety.
Figures from other outcome studies are much
smaller; however, these results may be con-
founded by the presence of ritualistic character-
istics and hyperactivity commonly associated
with ASD (Ghaziuddin et al., 1998).
Hyperactivity and short attention span are
common in people with ASD. These have been
most commonly noted in children, yet some
adults present with behavioral characteristics of
attention deficit-hyperactivity disorder (ADHD)
as well (Ghaziuddin et al., 1998). Forty (33%) of
the adults in the study by Billstedt and colleagues
(2005) presented with hyperactivity.
Psychiatric conditions evident in a small num-
ber of people with ASD include tic disorders,
psychotic features, and catatonia. Almost 20%
of the sample examined by Billstedt et al.
(2005) demonstrated tics, and 10% of the adults
studied by Eaves and Ho (2008) had Tourette’s
disorder. One of the 15 adults in another investi-
gation presented with Tourette’s disorder
(Ghaziuddin et al., 1998). A small number of
individuals with ASD genuinely have
co-occurring psychotic conditions. Eight percent
of the sample in the study of adults with
ASD conducted by Billstedt and colleagues
(2005) and 38% of those examined by Szatmari
et al. had characteristics of psychosis. Catatonia
is another type of psychiatric disturbance that
is rarely observed, but notable, in ASD. One of
the 15 adults studied by Howlin et al. (2000)
had a sudden-onset catatonic episode during
puberty. Billstedt et al. (2005) reported a much
higher percentage (12%) in their sample of
120 adults.
While not psychiatric disorders in their own
right, maladaptive behaviors are significant devi-
ations from expected behavior for a person’s
developmental level. They are often disruptive
and sometimes dangerous. Maladaptive behav-
iors are frequently observed in people with ASD
of all levels of ability and developmental age. In
general terms, maladaptive behaviors have been
reported in up to 69% of adults with ASD with no
overall difference in frequency between males
and females (Ballaban-Gil et al., 1996; Eaves &
Ho, 2008). Maladaptive behaviors may be
Employment in Adult Life
relatively infrequent in adults with ASD and
average-range IQ scores, but odd or severe
enough to preclude acceptance into general social
settings over time (Rumsey et al., 1985). Self-
injurious behaviors were reported to have
occurred in 50% of the sample studied by
Billstedt et al. (2005) and have been reported to
be more common in females than in males
(Ballaban-Gil et al., 1996). Difficulties with
toileting and feeding appear to persist in lower-
functioning individuals, but difficulties with
compulsive rituals may develop around these
tasks in higher-functioning adults as well.
Aggression among adults is rarely designed to
harm others, but property damage or harm to
self may occur intermittently, sometimes in
response to unimportant changes or problems in
the environment (Rumsey et al., 1985).
Social Relationships
Few adults with ASD develop significant rela-
tionships outside of the family of origin in spite
of common increases in interest in developing
social relationships as individuals with AD age
(Rumsey et al., 1985). Almost 75% of family
members interviewed in the study by Eaves and
Ho (2008) reported that they enjoyed good
to excellent relationships with their affected
relative; however, only one-third of the sample
of affected adults had one or more friendships
outside of the family. Similar results have been
found in other studies of adults with ASD
(Howlin et al., 2004). Females have reportedly
experienced greater success with peer relation-
ships than males (Piven et al., 1996). Ten percent
of adults in the study by Eaves and Ho (2008) had
a romantic relationship at some time in the past,
but none of the participants were romantically
involved at the time of the investigation. Nine-
teen percent of the men with Asperger syndrome
disorder in the Cederlund et al. (2008) study and
3% of the men with autistic disorder were or had
been in long-term romantic relationships. Thirty-
two percent of those studied by Farley et al.
(2009) had dated, and 20% were involved in
a serious relationship at the time of the study. In
1105 E
general, very few adults with ASD have been
reported to have successful, long-term romantic
relationships (Howlin et al., 2004).
Education and Employment
Approximately 15% of adults with ASD studied
in outcome research attend post-secondary
education programs (Ballaban-Gil et al., 1996;
E
Farley et al., 2009; Kobayashi et al., 1992;
Rumsey et al., 1985; Venter et al., 1992). In
general, gainful employment for adults with
ASD is rare, as is sheltered employment, occupy-
ing less than 40% of adults with AD (Howlin
et al., 2004). While outcome studies of autism
into adulthood conducted since 1992 reflect some
steady improvements in employment rates, with
22% to 54% of participants reporting gainful
employment on a full- or part-time basis
(Ballaban-Gil et al., 1996; Farley et al., 2009;
Howlin et al., 1994; Kobayashi et al., 1992; Ven-
ter et al., 1992), many of these individuals are
underemployed based on their cognitive abilities
and academic credentials.
Forensic Problems
Involvement with police officers and other law
enforcement agents has been recognized as
a major concern for parents of adolescents and
adults with ASD. A study of offending behavior
in 33 individuals with Asperger syndrome (Allen
et al., 2009) revealed that most engaged in violent
or threatening behavior that was related to inter-
personal problems including social or sexual
rejection, bullying, or family conflict. Investiga-
tors have suggested such offending behavior was
likely to result from coercion by others, misinter-
pretation of social situations, or obsessional inter-
ests, while many with ASD may be protected
from these by their tendency to adhere strictly to
rules. Allen et al. (2009) found evidence of this
insight in that the least common offenses identi-
fied among their population of offenders with
Asperger syndrome were drug offenses, theft,
fraud, sexual offending, and motor offenses.
E 1106
Cederlund et al. (2008) found that 10% (n ¼ 7) of
their sample with Asperger syndrome had been
involved with law enforcement officers, but the
remainder was described as very law abiding.
None of the individuals in their lower-
functioning sample with autistic disorder had
committed legal offenses. In the study by Farley
et al. (2009), 29% of the sample was involved
with law enforcement offices for infractions after
childhood, but these were related exclusively to
“suspicious” behaviors deriving from special
interests, participants being coerced to engage
in antisocial behavior by peers, and social
misunderstandings.
Future Directions
The prognosis for a majority of adults with ASD
based on studies conducted to date is guarded.
Future studies are needed to further define the
subtypes of ASD and the factors that influence
adult outcome. Studies of genetics, brain imag-
ing, and responses to interventions are likely to
yield important information.
See Also
▶ Adulthood, Transition to
▶ Advocacy
▶ Asperger Syndrome Follow-Up Studies
▶ Community Services
▶ Community-Integrated Residential Services
for Adults with Autism
▶ Competitive Employment
▶ Comprehensive Transition Program
▶ Course of Development
▶ Employment
▶ Employment Specialist
▶ Functional Life Skills
▶ Group Homes
▶ Guardianship
▶ Independent Living
▶ Individualized Plan for Employment (IPE)
▶ Job Carving
▶ Job Coach
Employment in Adult Life
▶ Law Enforcement Agencies and Autism
▶ Legal Competency
▶ Living Arrangements in Adulthood
▶ Residential Services
▶ Secure Employment
▶ Self-Advocacy
▶ Sexuality in Autism
▶ Sheltered Employment
▶ Sheltered Workshops
▶ Support Trust
▶ Supported Employment
▶ Transition Planning
▶ Transitional Living
▶ Travel Training
▶ Trust
▶ Violent/Criminal Behavior in Autism
▶ Vocational Evaluator
▶ Vocational Rehabilitation Act of 1973
▶ Vocational Training
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Employment Services
▶ Department of Vocational Rehabilitation
Employment Specialist
Pamela Targett
Virginia Commonwealth University, Richmond,
VA, USA
Synonyms
Employment consultant; Job coach; Vocational
rehabilitation specialist
Definition
An employment specialist is a vocational reha-
bilitation professional, who assists individuals
with the most severe disabilities with gaining
and maintaining employment in the community
by providing supported employment services.
The employment specialist who may also be
known as a job coach or employment consultant
provides individualized services to an individual
with a severe disability with all phases of the
employment process which include (a)
preemployment, (b) employment, and (c)
postemployment. Although the type of support
service provided is individualized typically the
employment specialist is engaged in the follow-
ing activities.
During phase one, the employment specialist
conducts preemployment activities. This requires
spending time setting up and implementing
a variety of functional assessment activities.
These practical experiences offer both the job
1109 E
seeker and employment specialist with opportu-
nities to learn more about his or her (the job
seeker’s) abilities, interests, work preferences,
and potential on the job support needs. Then
with a vision of the jobseeker in mind, the
employment specialist spends time meeting with
potential employers to learn more about their
business needs and positions him or herself as
someone who has services to meet a range of
business needs including the referral of potential
E
employees with disabilities. During this time, the
employment specialist explores ways a particular
job seeker may be able to make a contribution to
the workplace. An informational interview and
workplace analysis take place to provide the
employment specialist with insight into whether
or not the job seeker may be able to fill an existing
position or possible ways to restructure or create a
job for the job seeker. At this time, there is also a
review of what type, level, and intensity of both
on and off the job supports the job seeker may
require if hired. If an employer seems willing to
move forward with a proposition on hiring the
person, then the possibilities for employment
are discussed further with the job seeker and or
his or her family. In particular, the pros and cons
associated with the potential job offer are
reviewed. If the job seeker is interested in explor-
ing it, then an introductory meeting is arranged
which depending on the circumstances may be an
introductory meeting and/or a job interview.
Once hired, or during the employment phase,
the employment specialist provides and facili-
tates a variety of on or off the job supports spe-
cifically designed to assist the new hire with
learning how to do the job to meet the employer’s
expectations, including nonwork-related tasks
such as following procedures (i.e., upon arrival
and departure, taking breaks, requesting time off,
etc.) and working with others (i.e., getting to
know coworkers, asking for help if needed, etc.)
This support often involves providing the new
hire with intensive on the job site skills training
(including positive behavior support) that com-
mences after both the new hire and employment
specialist participate in the employer’s new
employee orientation and training program. At
this time, the employment specialist may also
E 1110 Encephalography

help the new hire complete his or her job respon-

sibilities. This work completion guarantee Encephalography
is designed to keep an employer satisfied while
the new hire is learning how to do the job. The ▶ Pneumoencephalography
employment specialist collects data to evaluate
what the new hire has learned and the effective-
ness of the training as well as design a schedule to
Enclave
fade his or her presence away from the job site.
Overtime, as the new hire learns the job and job-
▶ Mobile Work Crew Model
related tasks the employment specialist is there
less and less time. Eventually, the job seeker is
working all or most of the time on his or her own.
The employment specialist remains in touch with Encopresis
the new hire and employer and if indicated offers
additional on the job skills training or support Irma Isasa
to the worker. In a holistic approach to Polyclinic Gipuzkoa Paseo Miramón, 174,
implementing supported employment, the Donostia, Spain
employment specialist is involved in all three
phases of employment. In a partitioned approach,
different employment specialists may only pro- Synonyms
vide a support during a specific phase or phases of
employment. Among other traits, an employment Fecal incontinence; Soiling
specialist should possess a 4-year degree in busi-
ness, education, or related area and a valid
driver’s license and have excellent communica- Short Description or Definition
tion skills and the ability to independently solve
problems. Encopresis, as defined by the DSM-IV-TR
(American Psychiatric Association [APA],
2000), consists in the repeated passage of feces
See Also
in inappropriate places. Although soiling is
▶ Job Coach usually involuntary, it may be intentional in
some cases. Soiling must occur once a month
▶ Supported Employment
▶ School to Work Transition Process for at least 3 months and the chronological age
of the child must be at least 4 years. In the case of
children with developmental delays, a mental age
References and Readings of at least 4 years is required in order to charac-
terize for a diagnosis of encopresis. Any physical
Targett, P. S., & Wehman, P. (2009). Integrated employ-
disorder, explaining incontinence must be ruled
ment. In P. Wehman, M. D. Smith, & C. Schall (Eds.),
Autism and the transition to adulthood: Success out and the soiling should not be due to the direct
beyond the classroom (pp. 163–188). Baltimore: Paul effects of a substance (e.g., laxatives).
H. Brookes Publishing.
Wehman, P. (2012). Life beyond the classroom.
Baltimore: Paul H. Brookes Publishing.
Wehman, P., Inge, K. J., Revell, W. G., & Brooke, V. Categorization
(2007). Real work for real pay: Inclusive employment
for people with disabilities. Baltimore: Paul H. Encopresis can be categorized as primary or
Brookes Publishing.
secondary. In the case of primary encopresis the
Wehman, P., Targett, P., & Young, C. (2007). Off to work
for individuals with Autism: A supported employment fecal continence has never been obtained; and in
approach. Autism Advocate, 46(1), 54058. secondary encopresis, there has been a period of
Encopresis
fecal continence (defined as having reached con-
tinence for at least a period of 12 months) pre-
ceding the recurrence of soiling.
The DSM-IV-TR describes two subtypes of
encopresis:
– Encopresis with constipation and overflow
incontinence, which has been referred in the
literature as “retentive encopresis.” On physi-
cal examination there is evidence of large
stool mass on abdominal or rectal examina-
tion, and a history of stool frequency of less
than three per week. Usually, there are periods
of retention which last several days, followed
by a painful expulsion and then the period of
retention starts again.
– Encopresis without constipation and overflow
incontinence, which has been referred in the
literature as “non-retentive encopresis.” Here,
there is no evidence of constipation on physi-
cal examination or by history, and the feces
are likely to be of normal consistency. Here
the main characteristic is the lack of psycho-
logical, physiologic, or combined control of
the expulsion.
Epidemiology
It is estimated that 1% of 5-year-old children
have encopresis, and the disorder is more
frequent in males (APA, 2000).
There are different studies involving children of
different ages, with a prevalence varying between
1.5% and 4.1% and a male–female ratio of 3:1.
The prevalence of encopresis is higher among
younger children (Bellman 1996; Mikkelsen
2007; Van Der Wall, Benninga, Hirasing, 2005).
Special Characteristics of Encopresis in
Children with Autism
The figures reported before pertain to the general
population. In children with autism, there are just
a few studies to review. Data collected from these
studies suggest that constipation in this popula-
tion has a behavioral etiology, rather than a
primary organic gastrointestinal etiology. The
overall incidence of gastrointestinal symptoms
among children with autism did not differ from
1111 E
childrens without the disorder (Ibrahim, Voigt,
Katusic, Barbaresi, & Weaver, 2009). Children
with autism have an increased incidence of
difficulties regarding, not only constipation,
but also feeding behavior and food selectivity,
that are understood as related to behavioral prob-
lems, rather than to organic gastrointestinal
pathology (Ibrahim, Voigt, Katusic, Barbaresi,
& Weaver, 2009).
E
Natural History, Prognostic Factors,
and Outcomes
There have been several studies (Mikkelsen
2007; Loening-Baucke 1987a, 1987b) to find
out the basis for the encopresis. It seems clear
that retentive encopresis has a direct relationship
with abnormal contractions and an inability to
relax the external sphincter. Even more, this prob-
lem very often generates a constipation problem,
with painful defecation, which leads again to
retention, making the problem bigger and bigger.
The consistency of the stool becomes harder, mak-
ing the process more painful and difficult. And the
child avoids defecation, until leakage occurs.
In the non-retentive encopresis, psychological
issues such as oppositional defiant or conduct
disorder can be identified. Also, in the case of
developmental disabilities one can suspect that
proper toileting behavior has never been mastered.
Clinical Expression and
Pathophysiology
Constipation and Functional fecal retention
(FFR) has been included as causes leading
to the development of retentive encopresis.
It should include a period of a minimum of
12 weeks of constipation history, large stools,
abdominal pain, soiling, and the need to use
laxatives or enemas to treat the problem.
It seems clear that constipation and painful
defecation are associated with stool toileting
refusal (STR) and in most cases, hard and/or
painful bowel movements occur before the
onset of STR. Therefore, an effective treatment
E 1112
for constipation may be an option to decrease the
duration and/or the incidence of STR (Blum,
Taubman, & Nemeth, 2004). Constipation is
a frequent and significant problem that happens
in children suffering from autism. It is difficult to
recognize its impact and how it functionally
affects the rectosigmoid colon. It is often associ-
ated with mega-rectum. Since there is no signif-
icant correlation between the degree of fecal
impaction and the clinical history, the importance
of an abdominal radiography during the assess-
ment, to evaluate the degree of constipation is
essential (Afzal et al. 2003).
Behavioral problems may be the primary or
sole symptom of the underlying medical condi-
tion (Buie et al. 2010).
Evaluation and Differential Diagnosis
Soiling can be an original problem or a symptom
of a different cause. Therefore, it is important to
rule out possible physical or psychological
causes. In typically developed children, there
may be times when soiling and/or wetting acci-
dents can occur, and if these are repetitive, the
clinician must identify possible coincidental
stresses. Usually the problem remits when the
stressor is removed. Other times, there may be
physical or medical causes such as Hirschsprung
Disease, stenosis of the rectum, endocrine abnor-
malities, and other medical conditions that must
be ruled out. Also, for a variety of different rea-
sons, other problems such as Attention Deficit
Hyperactive Disorder (ADHD), Oppositional
Defiant Disorder (ODD) and, again, Develop-
mental Disorders like Mental Retardation or
Autistic Spectrum Disorders (ASD) can be asso-
ciated with encopresis.
Soiling in children suffering from an Autistic
Spectrum Disorder (ASD) can include all the
physical and psychological causes that must be
considered in typically developing children. Pecu-
liar aspects playing a role in ASD may include:
– Rigidity that leads where and when they
defecate, leading to constipation
– Refusal to seat on the toilet
– Absence of appropriate learning of the toilet
use
Encopresis
– Diet problems, leading to constipation
– Soiling challenging behavior, such as
smearing feces and playing with them
– Social cognition limitations hampering their
understanding about using toilets, and when
and how the toilet should be used
– Sensory anomalies involving olfactory, tactile
sensations, or even the noise produced by the
toilet that can generate refusal among ASD
children
It is important to find out what are the possible
one or more involved factors and include them
into a coherent treatment plan.
Treatment
Once medical problems have been ruled out, we
should check for psychological/behavioral expla-
nation of the problem and treat accordingly.
Treating Anxiety Symptoms
We should keep a very close attention to anxiety
symptoms that could lead to suffering and avoid-
ance of toilet use. We should encourage the use of
the toilet in a positive and progressive way, cou-
pling the toilet situation with rewarding and
pleasant stimuli. Since changing routines is diffi-
cult for these children, they will need more time
and effort to adapt to this challenging task.
Minimizing Understanding Difficulties
When giving tips or messages regarding the use
of the toilet, it is important to ensure proper
understanding. Therefore, the use of augmenta-
tive communication systems, using for example,
gestures, objects, pictograms, or pictures may be
quite helpful.
Treating Physical Causes
If poor diet is the problem leading to constipation,
the bowel may be blocked with hard stools, pain-
ful to pass and that may even cause fissures in the
perianal area. The child, therefore, will try to
avoid passing them because it is painful and the
stools will become harder and may even further
challenge passage through the bowel. There is
usually leaking through the passage that stains
Encopresis
the underpants. In children suffering from ASD,
the fact that their clothes get stained may not be
an issue for them, due to social unawareness, but
there will be negative feedback obtained from
peers or non-informed adults.
Measures to resolve this problem may be
increasing high-fiber foods such as bran, whole
wheat products, vegetables, and fruits or even
increasing the liquids in the diet adding water or
juices. Also the reduction in constipating foods
like bananas, dairy, and peanuts can help. Most
people react with a gastrocolic reflex, by feeling
the need to defecate just after having a meal; and
this can be used as a simple mechanism to favor
appropriate defecation.
These general dieting advices may be impor-
tant when diapers are removed for the first time
and training is attempted.
Treating Sensory Problems
The physical structure of the toilet is very
important and involves “isolating” the place
(avoiding distracters) and the behavior (sits on
the toilet to defecate or urinate only). It is not
easy to assign a half-bath in every house but if
possible it can be very helpful, to avoid distrac-
tions and confusing issues. Creating a secure
and not over-stimulating environment is impor-
tant, to make the child more relaxed and com-
fortable. Therefore, think of the plumbing
noises, echoes, and lights. Even playing soft
music can help.
Treating Rigidity Problems
Establishing a visually supported routine can be
crucial. We must create a visual sequence of steps
that help the child to complete the goal. Since
children presenting ASD have preferences for
routines or rituals, we can create new ones to
make a bridge between the old and the new
ones. We could start with a transition object (a
photograph, a picture, or an object of the toilet)
that serves to initiate the bathroom routine. Once
the transition to the toilet has been made it
is important to continue with the visual aids
to visually support each step of the toileting
routine. Those aids can be placed in a ziplock
bag or glued shut.
1113 E
Treating Refusal to Sit on the Toilet
When resisting to sit on the toilet is an issue, we
must break the target into as many steps as
needed. Sometimes these children have motor
planning difficulties and although they may
know the next step, they seem unable to physi-
cally move themselves. Therefore, we should
physically help them to initiate the movement.
Other times we may use desensitization,
a behavioral technique useful to help the child
E
decrease the fears over different situations such
as sitting on a toilet and the noise of flushing it,
step by step. For example, tips like sitting on the
toilet without removing the clothes; using timers;
using the length of one song on the CD player;
entertaining the child; taking turns sitting on
the toilet; and using dolls for modeling can be
helpful. The adult must recognize that it may take
time for the child to extinguish his or her fears.
We also should be aware that they have difficul-
ties imitating and generalizing behaviors.
If flushing the toilet is an issue because the
child is afraid of it, one can try starting the flush
while the child is away from the toilet and grad-
ually help him or her to get closer. Give warming
in advance. Show him how to do it and make a
“game” of it. If the problem is the opposite, and
flushing is an intense interest, use visual sequence
to show the child when to flush, and what follows
afterward (washing hands, lights off, leave toilet),
to help him to get distracted from this interest.
Treating Social Difficulties
The use of social stories about the use of the toilet
can also help. By them, children with ASD can
understand when and how to use a toilet; who can
support them if they need help; how to ask if they
need using the toilet; and where to locate one
when they are not at home.
Treating Other Difficulties
There may be other difficulties such as playing
with the toilet paper or even resisting being
cleaned that need to be tackled. In those cases
one can try using Kleenex, wet wipes, or
a sponge. At the same time we should reinforce
all the desired behaviors such as spending more
time sitting on the toilet, flushing it without fear,
or doing so for the appropriate length of time.
E 1114
When planning a structured program for potty
training in children with ASD, three basic com-
ponents should be covered: Order, predictability,
and routine. Each program has to be individual-
ized, and we should not forget that potty training
is a process, not an event. It should include visual
supports, social stories, and very important indi-
vidualized personal potty stories.
For parents it is also important, before begin-
ning with the plan, to write the reasons that have
caused them anxiety over potty training and under-
stand why training has not been successful in the
past. It is useful for them to anticipate any obsta-
cles that will be found and consider ways to over-
come them. Also it should help to write the
strategies to be followed and think about the ben-
efits generated when potty training is achieved.
It is mandatory to keep track of the progress
(and difficulties) and to share them with the cli-
nician or educator. First, a base-line observation
time recording the time or times in the daywhere
the “accident” takes place, then, most people find
that it is useful to consider this “likely times” and
proceed before they happened, using the previ-
ously mentioned tips.
The investment in this training sooner or later
pays back and this achievement helps the dignity,
autonomy, health, and social status of the child
with previous encopresis.
See Also
▶ Constipation
▶ Toilet Training
References and Readings
Afzal, N., Murch, S., Thirrupathy, K., Berger, L.,
Fagbemi, A., & Heuschkel, R. (2003). Constipation
with acquired megarectum in children with autism.
Pediatrics, 112, 939–942.
American Psychiatric Association. (2000). Elimination
disorders. In American Psychiatric Association (Ed.),
DSM-IV-TR diagnostic and statistical manual of men-
tal disorders. Text revision (4th ed., pp. 116–118).
Washington, DC: Author.
Batts, B. (2010). Ready, set potty! Training for children
with autism and other developmental disorders.
London/Philadelphia, PA: Jessica Kingsley.
Endophenotypes
Bellman, M. (1996). Studies on encopresis. Acta
Paediatrica Scandinavica, 56(Suppl 170), 1–151.
Blum, N. J., Taubman, B., & Nemeth, N. (2004). During
toilet training, constipation occurs before stool
toileting refusal. Pediatrics, 113, e520–e522.
Buie, T., Campbell, D. B., Fuchs, G. J., Furuta, G. T.,
Levy, J., VandeWater, J., et al. (2010). Evaluation,
diagnosis, and treatment of gastrointestinal disorders
in individuals with ASDs: A consensus report. Pediat-
rics, 125(Suppl), S1–S18. doi:10.1542/peds.2009-
1878C.
Gray, C., & White, A. L. (2002). My social stories book.
London/New York, NY: Jessica Kingsley.
Ibrahim, S. H., Voigt, R. G., Katusic, S. K., Barbaresi,
W. J., & Weaver, A. L. (2009). Incidence of gastroin-
testinal symptoms in children with autism:
A population based study. Pediatrics, 124, 680–686.
doi:10.1542/peds.2008-2933.
Loening-Baucke, V. A. (1987a). Factors responsible for
persistence of childhood constipation. Journal of Pedi-
atric Gastroenterology and Nutrition, 6, 915–922.
Loening-Baucke, V., Cruikshank, B., & Savage, C.
(1987b). Defecation dynamics and behavior profiles
en encopretic children. Pediatrics, 80, 672–679.
Mikkelsen, E. J. (2007). Elimination disorders: Enuresis
and encopresis. In A. Martin & F. R. Volkmar (Eds.),
Lewis child and adolescent psychiatry. A comprehen-
sive textbook (4th ed., pp. 662–665). Philadelphia, PA:
Wolters Kluwer Health/Lippincott Williams & Wilkins.
Parenting and Child Health. http://www.cyh.com/
HealthTopics/HealthTopicdetails.aspx. Last revision
March 14, 2011.
Strategies for dealing with soiling (encopresis). http://
www.autism-help.org/behavior-soiling-encopresis.htm.
Last revision March 14, 2011.
Van Der Wall, M. F., Benninga, M. A., & Hirasing, R. A.
(2005). The prevalence of encopresis in a multicultural
population. Journal of Pediatric Gastroenterology and
Nutrition, 40(Suppl 3), 345–348.
Wheeler, M., & Kranowitz, C. S. (2007). Toilet training
for individuals with autism or other developmental
disorders. Arlington, TX: Future Horizons.
Endophenotypes
Paul El-Fishawy
State Laboratory, Child Study Center,
Yale University, New Haven, CT, USA
Definition
A phenotype is a characteristic of an organism or
individual that can be observed. In psychiatry, the
Endophenotypes
term is often used to refer to a set of behaviors
that constitute a categorical diagnosis. An
endophenotype is a measureable characteristic
that exists somewhere along the biological path-
way from gene risk to the overall phenotype or
categorical diagnosis. It is a characteristic that
may reflect an underlying or component feature
of a disorder, such as autism. The characteristic
can be of many types, including biochemical,
neurophysiological, neuroanatomical, and cogni-
tive (Viding & Blakemore, 2007). It can be
a subset of the clinical symptoms but not the
full syndrome itself. For example, “age at first
word” has been proposed as an autism
endophenotype (Alarcón, Cantor, et al., 2002).
While it clearly relates to language disability, it
is not the entire autism phenotype. Some terms
have similar meanings but do not focus on the
genetic connection. These include “intermediate
phenotype,” “biological marker,” “subclinical
trait,” and “vulnerability marker” (Gottesman &
Gould, 2003).
Historical Background
The term endophenotype was introduced into the
psychiatric lexicon in a 1972 book on the genetics
of schizophrenia by Irving Gottesman and James
Shields (Gottesman & Shields, 1972). They
borrowed the term from a paper by John and
Lewis who had used it to describe concepts in
evolution and insect biology (Lewis, 1966).
Gottesman and Shields proposed the
endophenotype concept in an effort to speed
discovery of genes that contributed to neuropsy-
chiatric disorders, especially Schizophrenia
(Gottesman & Gould, 2003).
The idea was that the complexity of neuropsy-
chiatric behavioral phenotypes would likely
result from the dysfunction of a greater number
of genes than would less complex
endophenotypes of these disorders (Gottesman
& Gould, 2003). The discovery of genes that
contributed to endophenotypes, therefore, would
help speed gene discovery in neuropsychiatric
disorders both because the genes that contributed
1115 E
to endophenotypes would presumably also
contribute to the disorder and because the genetic
research and analysis involved in the discovery of
genes resulting in an endophenotype (with fewer
genes contributing) would be easier than the
discovery of genes resulting in a full-blown
neuropsychiatric phenotype (with multiple
genes contributing).
In 2003, Gottesman and Gould published a
paper updating and further elucidating the
E
endophenotype concept in psychiatry (Gottesman
& Gould, 2003). They proposed the following five
principles, some of which were adapted from those
suggested by others, that they state make an
endophenotype useful for genetic research:
1. The endophenotype is associated with illness
in the population.
2. The endophenotype is heritable.
3. The endophenotype is primarily state-
independent (manifests in an individual
whether or not illness is active).
4. Within families, endophenotype and illness
co-segregate, (meaning that those with the
endophenotype have the illness and those
without it do not have the illness).
5. The endophenotype found in affected family
members is found in nonaffected family mem-
bers at a higher rate than in the general
population (Gottesman & Gould, 2003).
As pointed out by Gottesman and Gould, the
endophenotype concept lay dormant and largely
unutilized from the time of their introduction of
the concept to the psychiatric literature in the
1970s until the start of the twenty-first century
(Gottesman & Gould, 2003). However, in the
new century, researchers began to utilize the con-
cept significantly more frequently. Gottesman
and Gould attribute this change to the lack of
success of numerous genetic studies utilizing
phenotypes as opposed to endophenotypes in dis-
covering genes that contributed to neuropsychi-
atric disorders despite significant investments
and large-scale projects (Gottesman & Gould).
The slowness of the progress was certainly
evident in research into the genetics of autism
(El-Fishawy & State, 2010). Regardless of the
reason, the use of endophenotypes proliferated
substantially after the year 2000 in
E 1116
neuropsychiatric research in general and in
genetic research in autism in particular, as
described below (Gottesman & Gould, 2003).
Current Knowledge
The endophenotype concept has been used in
multiple studies seeking to identify genes
contributing to autism spectrum disorders. For
example, a study by Alarcon et al. linked
a region on chromosome 7 to an autism
endophenotype, “age at first word” (Alarcón
et al., 2002). Subsequently, this group found
evidence for association of this endophenotype
to a specific gene in this interval called contactin-
associated protein-like 2 (CNTNAP2). A series
of subsequent studies have pointed to the involve-
ment of CNTNAP2 in language development and
autism (Abrahams & Geschwind, 2010).
Multiple other endophenotypes have been
explored with regard to autism genetics. For
example, there has been a long-standing interest
in the observation of increased platelet serotonin
levels in individuals with ASD (Anderson,
Freedman, et al., 1987) and whether this might
serve as a useful endophenotype for gene discov-
ery (Freitag, 2006). Similarly, enlarged head size,
or macrocephaly, has been demonstrated in
a subset of autistic children (Sacco, Militerni,
et al., 2007). In this regard, rare cases of muta-
tions in the gene PTEN (phosphatase and tensin
homolog) have been found in individuals with
macrocephaly and autism. These findings have
been robust enough to warrant the recommenda-
tion that individuals with these features should
have a genetic evaluation including sequencing
of this gene.
Quantitative scales have also been devel-
oped focusing on identifying potential
endophenotypes in autism. For instance, scores
on the Social Responsiveness Scale (Constantino
& Todd, 2005), aimed at measuring the severity
of social impairment, have been shown to be
heritable and continuously distributed in the pop-
ulation, with parents of autistic children showing
significant shifts toward pathological scores
(Constantino & Todd).
Endophenotypes
Future Directions
Several avenues of autism research have charac-
terized traits that could potentially serve as novel
endophenotypes. For example, eye-tracking
experiments and functional neuroimaging have
identified potential signatures of autism risk.
Simultaneous advances in genomic technologies
will increasingly allow these to be explored.
Importantly, as specific risk genes and regions
have been identified based on the categorical
diagnosis of ASD, it has become clear that these
genetic factors also increase the liability for
a wide range of disorders that were previously
conceptualized as being distinct. For example,
duplications of a section on the short arm of
chromosome 16, 16p11.2, have been shown to
increase the risk for both autism and schizophre-
nia. Studies are just now being undertaken exam-
ining whether these and similar findings may, in
part, reflect shared endophenotypes among dis-
parate clinical syndromes (State & Levitt, 2011).
See Also
▶ Biological Motion
▶ Candidate Genes in Autism
▶ DNA
▶ Event-Related Functional Magnetic
Resonance Imaging (MRI)
▶ Genetics
▶ Social Responsiveness Scale
References and Readings
Abrahams, B. S., & Geschwind, D. H. (2010). Connecting
genes to brain in autism spectrum disorders. Archives
of Neurology, 67(4), 395–399.
Alarcón, M., Abrahams, B. S., et al. (2008). Linkage,
association, and gene-expression analyses identify
CNTNAP2 as an autism-susceptibility gene. American
Journal of Human Genetics, 82(1), 150.
Alarcón, M., Cantor, R. M., et al. (2002). Evidence for
a language quantitative trait locus on chromosome 7q
in multiplex autism families. American Journal of
Human Genetics, 70(1), 60.
Alarcon, M., Yonan, A. L., et al. (2005). Quantitative
genome scan and ordered-subsets analysis of autism
Enhanced Perceptual Functioning
endophenotypes support language QTLs. Molecular
Psychiatry, 10(8), 747.
Anderson, G. M., Freedman, D. X., et al. (1987). Whole
blood serotonin in autistic and normal subjects. Journal
of Child Psychology and Psychiatry, 28(6), 885–900.
Arolt, V., Lencer, R., et al. (1996). Eye tracking dysfunc-
tion is a putative phenotypic susceptibility marker of
schizophrenia and maps to a locus on chromosome 6p in
families with multiple occurrence of the disease. Amer-
ican Journal of Medical Genetics, 67(6), 564–579.
Butler, M. G., Dasouki, M. J., et al. (2005). Subset of
individuals with autism spectrum disorders and
extreme macrocephaly associated with germline
PTEN tumour suppressor gene mutations. Journal of
Medical Genetics, 42(4), 318.
Conciatori, M., Stodgell, C. J., et al. (2004). Association
between the HOXA1 A218G polymorphism and
increased head circumference in patients with autism.
Biological Psychiatry, 55(4), 413–419.
Constantino, J. N., & Todd, R. D. (2005).
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Enhanced Perceptual Functioning
Cora Mukerji1, Laurent Mottron2,3 and
James C. McPartland4
1
Yale Child Study Center, New Haven, CT, USA
2
Center of Excellence in Pervasive
Developmental Disorders of University of
Montreal, QC, Canada
3
Department of Psychiatry, Riviere-des-Prairies
Hospital, University of Montreal, Montreal, QC,
Cananda
4
Yale Child Study Center, Yale University,
New Haven, CT, USA
Synonyms
EPF model
Definition
The enhanced perceptual functioning (EPF)
model of autism proposes that superior function
and increased independence of auditory and visual
perceptual processes are responsible for the dis-
tinct pattern of cognitive, behavioral, and neural
performance observed in autism. The EPF model
emphasizes the primacy of perceptual processes,
rather than social or higher order cognitive pro-
cesses, in giving rise to the autistic phenotype.
Initially proposed by L. Mottron and
colleagues as an alternative to the weak
central coherence (WCC) model of perceptual
E 1118
functioning, the EPF outlines eight principles of
perception in autism:
1. More locally oriented perception is the default
for individuals in autistic populations relative
to typical populations.
2. Neural complexity is inversely related to
performance in low-level perceptual tasks.
3. Early atypical behaviors regulate perceptual
input.
4. In autism, primary and associative brain
regions involved in perception are atypically
activated during social and nonsocial tasks.
5. Higher order processing is variable in autism
and mandatory in typical development.
6. Perceptual expertise underlies savant syndrome.
7. Savant syndrome is an autistic model for
subtyping within pervasive developmental
disorder (PDD).
8. Enhanced functioning of perceptual brain
regions may contribute to abnormalities in
perception in autism.
Evidence in support of this model stems from
the demonstration of enhanced visual functioning
across multiple tasks (Caron, Mottron,
Berthiaume, & Dawson, 2006) and enhanced
brain activity in brain regions implicated in pat-
tern processing in autism (Samson, Mottron,
Soulières, & Zeffiro, 2011).
See Also
▶ Auditory Processing
▶ Autistic Savants
▶ Perception
▶ Perceptual Development
▶ Social Cognition
▶ Visual Processing
▶ Weak Central Coherence
References and Readings
Caron, M. J., Mottron, L., Berthiaume, C., & Dawson, M.
(2006). Cognitive mechanisms, specificity and neural
underpinnings of the block design peak in autism.
Brain, 129, 1789–1802.
Mottron, L., & Burack, J. A. (2001). Enhanced perceptual
functioning in the development of autism. In J. A.
Entrepreneurial Model
Burack, T. Charman, N. Yirmiya, & P. R. Zelazo
(Eds.), The development of autism: Perspectives from
theory and research (pp. 131–148). Mahwah, NJ:
Erlbaum.
Mottron, L., Dawson, M., Soulières, I., Hubert, B., &
Burack, J. A. (2006). Enhanced perceptual functioning
in autism: An updated model and eight principles
of autistic perception. Journal of Autism and
Developmental Disorders, 36(1), 27–43.
Samson, F., Mottron, L., Soulières, I., & Zeffiro, T. A.
(2011). Enhanced visual functioning in autism: an
ALE meta-analysis. Human Brain Mapping.
doi:10.1002/hbm.21307.
Entrepreneurial Model
Paul Cavanagh
New York Institute of Technology, Central Islip,
NY, USA
Synonyms
Entrepreneurial supports; Supported employ-
ment; Supported work
Definition
The term Entrepreneurial Model refers to creation
of a new business entity as a means of providing
work for an individual, or a group of individuals,
with a diagnosis of a developmental disability. In
this model, the skills and interests of the individ-
ual, or a group of individuals, with an autism
spectrum disorder are used as a basis for the crea-
tion of a new business. The goal of the endeavor is
to create enough revenue from the business to both
pay the workers with a disability and support staff
who assist them. An advantage of the Entrepre-
neurial Model is that the work involved is specif-
ically chosen to match with the skills and interests
of the individual (or individuals) with an autism
spectrum disorder. The biggest challenge for an
Entrepreneurial Model is that it faces the same
start-up costs and difficulties in reaching profit-
ability of any new business endeavor.
An Entrepreneurial Model is one work option
along a continuum of ▶ supported employment
Entrepreneurial Supports
for individuals with a disability. In addition to the
Entrepreneurial Model, the most common types
of supported employment models are an individ-
ual placement model, an enclave placement
model, and a mobile work crew.
See Also
▶ Entrepreneurial Supports
▶ Mobile Work Crew Model
▶ Supported Employment
References and Readings
Advancing Futures for Adults with Autism, an advocacy
organization. http://www.afaa-us.org/site/c.llIYIkNZ
JuE/b.5063863/k.BE3C/Home.htm
Autism Transition Handbook, an on-line resources
supported by Devereux, Inc. http://www.autism
handbook.org/index.php/Main_Page
Gehardt, P. F. (2009). The current state of services for
adults with autism. Organization for Autism Research.
Retreived May 29, 2011, from http://www.mo-feat.
org/files/oar_survey_11309.pdf
James, E., & Young, D. (2007). Fee income and commer-
cial ventures. In D. Young (Ed.), Financing nonprofits.
Lanham, MD: AltaMira Press.
McDonnell, J., & Hardman, M. L. (2010). Successful
transition programs: Pathways for students with intel-
lectual and developmental disabilities. Thousand
Oaks, CA: Sage.
Skloot, E. (1988). The nonprofit entrepreneur: Creating
ventures to earn income. New York: The Foundation
Center.
Wehman, P., Brooke, V., & West, D. (2010). Vocational
placements and careers: Toward inclusive employ-
ment. In P. Wehman (Ed.), Life beyond the classroom:
Transition strategies for young people with disabil-
ities. Baltimore: Brookes.
Entrepreneurial Supports
Ernst VanBergeijk
Vocational Independence Program, New York
Institute of Technology, Central Islip, NY, USA
Synonyms
Self-directed support corporation supports;
Self-employment supports
1119 E
Definition
Entrepreneurial supports are supports that
would enable individuals working under an
entrepreneurial model to become successful.
Success would be measured by the self-directed
business ability to generate enough revenue not
only for salaries of the individuals on the autism
spectrum in the corporation but also for salaries
of the staff hired to help them with this
E
endeavor.
Like any other business, support takes many
forms. It can include help developing a business
plan, securing loans or funding for start-up costs,
accounting support in terms of paying taxes and
other payroll issues, as well as taking advantage of
employer initiatives and tax incentives such as
Work Opportunity Tax Credits, Small Business
Tax Credits, and Architectural/Transportation
Tax Deduction: IRS Code Section 190, Barrier
Removal (Gerhardt, 2009). Support can also be
in terms of renting office space, buying furniture
and equipment, and advertising the product or
service. Job coaching may also be a necessary
support for individuals on the spectrum under
this model.
Prevocational supports may also be necessary
for individuals who are working under an entre-
preneurial model. Prevocational supports may
include travel training on mass transit in order
to reach work or business meetings. It may also
include how appropriate dress and hygiene for the
type of business the individual is engaged in.
Independent living skills might include money
management and budgeting skills for the individ-
ual (e.g., grocery shopping, bill paying, paying
for lunch) on top of money management skills or
supports for the business.
“Many people with disabilities, particularly
those in rural areas where jobs are often scarce,
have already created opportunities for themselves
through entrepreneurship. In fact, according to
the U.S. Census Bureau, people with disabilities
are nearly twice as likely to be self-employed as
the general population, 14.7 percent compared to
8 percent” (U.S. Department of Labor and Office
of Disability Employment Policy, 2011). Small
businesses account for 60–80% of the new jobs
E 1120
annually (U.S. Department of Labor and Office of
Disability Employment Policy).
Government supports for individuals with dis-
abilities who are engaged in the entrepreneurial
model often begin with Vocational Rehabilitative
(VR) services and programs:
• The Social Security Administration’s (SSA)
Plan for Achieving Self-Support (PASS) pro-
gram allows people with disabilities receiving
SSI benefits to set aside money and resources
to help achieve a particular work goal, includ-
ing self-employment.
• The Ticket-to-Work program connects SSI
and SSDI beneficiaries with Employment Net-
works (EN) for training and other support
services needed to achieve their employment
goals, including self-employment.
• More than 1,100 Small Business Development
Centers (SBDC) offer free or low-cost
counseling, training, and technical assistance
to individuals seeking to start their own busi-
ness in communities across the nation.
• The Service Corps of Retired Executives
(SCORE), comprising more than 10,000 coun-
selors at 389 offices nationwide, provides free
small business start-up advice through one-on-
one counseling, group workshops, and online
resources.
• Local One-Stop Career Centers funded through
the U.S. Department of Labor’s (DOL)
Employment and Training Administration
(ETA) assist people in training for and
obtaining employment, including self-
employment (U.S. Department of Labor and
Office of Disability Employment Policy, 2011).
See Also
▶ Entrepreneurial Model
References and Readings
Brown, R. I. (1997). Quality of life for people with devel-
opmental disabilities: Models, research, and practice
(2nd ed.). Cheltenham, UK: Stanley Thorne.
Center for Self-Determination. (2011). http://www.
centerforself-determination.com/
Enuresis
Edmonds, G., & Beardon, L. (Eds.). (2008). Asperger
syndrome and employment: Adults speak out about
asperger syndrome. London: Jessica Kingsley.
Gerhardt, P. (2009). The current state of affairs for adults
with autism (draft). Advancing futures for adults with
autism: Think Tank. New York, January 21, 2009.
Grandin, T., & Duffy, K. (2008). Developing talents:
Careers for individuals with Asperger syndrome and
high functioning autism. Overland Park, KS: Autism
Asperger Publishing.
Rizzo, D. C. (2002). With a little help from my friends:
Supported self-employment for people with severe
disabilities. Journal of Vocational Rehabilitation,
17(2), 97–105.
U.S. Department of Labor, Office of Disability Employ-
ment Policy. (2011). Entrepreneurship: A flexible
route to economic independence for people with dis-
abilities. Retrieved July 28, 2011, from http://www.
dol.gov/odep/pubs/misc/entrepre.htm
Enuresis
Fred R. Volkmar
Director – Child Study Center, Irving B. Harris
Professor of Child Psychiatry, Pediatrics and
Psychology, School of Medicine,
Yale University, New Haven, CT, USA
Synonyms
Bed-wetting
Short Description or Definition
It is typical in developed countries that toilet
training begins in the toddler period and usually
is completed by age 3; there is some variation in
this age (and in toilet training) across cultures.
Various factors can interfere with the process
including motor difficulties, cognitive and social
problems, and lack of motivation (any combina-
tion of which may be present in younger children
with ASDs). When toilet training is not achieved
or was once achieved and then lost, a diagnosis of
enuresis is made.
Categorization
A distinction is made between primary enuresis
(the child has never been fully trained) and
Enuresis
secondary enuresis (the child had been trained for
a prolonged period – usually at least a year).
Nighttime or nocturnal enuresis is much more
common than the daytime form. Isolated and
very occasional episodes of bed-wetting, partic-
ularly in younger boys, may not merit either
a diagnosis or treatment since there is an expec-
tation that the problem be sufficiently severe as to
merit attention (either because of frequency or
because it serves as a source of distress). The
diagnosis is not made in very young children
and cannot be made if the voiding is due to
medical problems.
Epidemiology
Longitudinal studies have shown that boys are
more likely than girls to exhibit the problem. By
age 6 years, the vast majority of children (90 %)
are dry at night, and this number continues to rise
so that in adolescence (age 15) only about 1 % of
boys and 0.5 % of girls have episodes of enuresis
on at least a weekly basis. There is some sugges-
tion of familial risk and association with both
stress and psychosocial adversity.
Natural History, Prognostic Factors,
and Outcomes
Spontaneous remission of bed-wetting is com-
mon and often occurs by age 7. It is typical in
longitudinal studies that during a given year,
about 15 % of children will have their symptoms
remit. Behavioral treatments are typically
regarded as a first line of intervention. The pres-
ence of multiple risk factors in the child, stress,
and psychosocial adversity can complicate inter-
vention. Behavioral psychologists can be
involved in situations where developmental
delays are present to help both in an assessment
of the child’s potential for understanding and
participating in a treatment program and in
a broader analysis of any associated behavioral
difficulties.
1121 E
Clinical Expression and
Pathophysiology
A range of theories have been proposed – from
those that focus on anatomic abnormality, psy-
chological or neurological immaturity, to psy-
chodynamic explanations. Developmental delay
is a risk factor, and some data suggest complex
interactions of factors in pathogenesis. A genetic
component can be present.
E
Evaluation and Differential Diagnosis
Laboratory analysis of urine (to rule out infec-
tion) is a first step. There is not a high yield from
more medically invasive studies in the absence of
an indication for the same. Those children who
have both day- and nighttime difficulties are
more likely to have anatomical or other physical
problems. Sometimes enuresis can be associated
with other medical conditions or medications.
Urinalysis is an obvious first step in evaluation
of enuresis, e.g., to rule out urinary tract infection
as a cause. In general invasive laboratory studies
do not have a particularly high yield and would
not be indicated unless other indications were
present. Children who have problems in both
night- and daytime may be more likely to exhibit
structural or other problems of the urinary tract.
Ultrasound evaluation is less invasive than past
procedures.
At times enuresis may arise following other
medical problems, e.g., hyperthyroidism,
although this is infrequent. A physical examina-
tion should look for potentially treatable under-
lying conditions. Associations to other factors,
e.g., nocturnal enuresis that follows administra-
tion of a new medication, should be explored as
relevant.
Treatment
Two approaches have been used for treatment:
behavioral and pharmacological. Behavioral
E 1122
treatments have long been used and combine
aspects of classical and operant condition in
the “bell and pad” approach. The child sleeps
on a pad that, if it becomes wet, closes an
electrical circuit and rings a bell, thus awak-
ening the child. A majority of children do
respond, and the response is frequently
maintained after the treatment is discontinued.
Other behavioral approaches include use of
a timer to awaken the child periodically to
void.
Drug treatments have included several agents.
The tricyclic antidepressant imipramine has been
used for many decades. An ECG is obtained at
baseline and the dose of the medicine gradually
increased. Many children respond positively. In
such cases periodic attempts to discontinue it
should be made. The mechanism of action
remains unclear.
A more recent pharmacological treatment
has used desmopressin acetate (DDAVP) (an
analogue of a pituitary hormone involved in
kidney function). The agent frequently is asso-
ciated with a positive response, but symptoms
do tend to turn once the intervention is
discontinued and various side effects can be
noted.
In the absence of other indications, psycho-
therapy is not usually indicated.
See Also
▶ Toilet Training
References and Readings
Robson, W. L. M. (2009). Clinical practice. Evaluation
and management of enuresis. New England Journal
of Medicine, 360(14), 1429–1436.
Volkmar, F. R., & Martin, A. (2011). Essentials of child
and adolescent psychiatry. Philadelphia: Lippincott,
Williams, and Wilkins.
Ward-Smith, P., & Barry, D. (2006). The challenge
of treating enuresis. Urologic Nursing, 26(3),
222–224.
Weaver, A., & Dobson, P. (2007). Nocturnal enuresis
in children. Journal of Family Health Care, 17(5),
159–161.
Environmental Engineering/Modifications
Environmental Engineering/
Modifications
Christine Barthold
Center for Disabilities Studies, University of
Delaware, Newark, DE, USA
Definition
Environmental engineering/modification strate-
gies, also known as antecedent interventions,
are defined as changes to the immediate environ-
ment that allow the individual with ASD to
process stimuli, predict future events, and
respond appropriately. The purpose of environ-
mental engineering strategies is to provide
additional information about the appropriate and
expected response in any given situation (Neitzel,
2009; Quill, 1995). They are considered
proactive strategies to prevent problem behavior
and increase appropriate behavior before
correcting strategies are needed (Bregman,
Zager, & Gerdtz, 2005).
There are a myriad of interventions that fall
under the heading of environmental engineering.
Such interventions include, but are not limited to,
social stories and video modeling, functional
communication training, consistent scheduling,
choice, and organization, and visual supports.
These interventions are often used to prevent
problem behavior, but can also be used to
increase adaptive behavior and as academic
supports for learners of all ages. It has also been
suggested that environmental engineering may
increase independence and generalization of
learned skills (Quill, 1995). The majority of
studies on antecedent interventions, though,
focus upon their use to decrease problem behav-
ior, such as stereotypy or self-injurious behav-
iors (Neitzel, 2009). Although used widely by
educators and considered to be effective and
easy to implement, there is comparatively
little research on the effects of antecedent
manipulations on the behavior of children
with ASD.
Environmental Engineering/Modifications
Historical Background
Antecedent interventions have, in some way,
been an important part of interventions for indi-
viduals with ASD throughout the short history of
intervention for the disorder. Division TEACCH,
considered by some to be the first program to
provide structured interventions for individuals
with ASD, has been incorporating environmental
engineering strategies since the 1960s (Mesibov,
Shea, & Schopler, 2005). In applied behavior
analysis, the antecedents which evoke both
problem behavior and appropriate responding
are considered to be critical to intervention.
Tools such as antecedent-behavior-consequence
(ABC) data collection and scatterplot data
determine what types of environmental events
evoke problem behavior and what environmental
changes could prevent reoccurrence of these
types of behavior (Bijou, Petersen, & Ault,
1968; Touchette, McDonald, & Langer, 1985).
Current Knowledge
Whatever form of environmental engineering is
used, it should be universally accepted by the
members of the individual’s community and
implemented consistently. Those strategies that
are most socially valid are more likely to be
implemented consistently. Therefore, any
strategy should take into account the child’s
environment, preferences, and community at
large (Quill, 1995).
It is also very important that any strategy
selected is age-appropriate, especially for
older learners with more severe impairments.
For example, a 16-year-old with a visual system
that includes pictures of preschool cartoon
characters may serve to stigmatize the individual
and decrease opportunities for social interaction.
A more socially appropriate alternative might be
using pictures of the adolescent themselves or
other individuals in the class (Wehman, 2006).
Before making environmental modifications,
a thorough functional behavioral assessment
(FBA) should be conducted to determine
what environmental variables reliably evoke
1123 E
problematic behavior for the individual in ques-
tion (Bregman et al., 2005; Umbreit, Ferro,
Liaupsin, & Lane, 2007). In FBA, detailed data
are taken to determine both the environmental
events and the consequences that might be
maintaining problem behavior. In more difficult
cases, a functional analysis might be conducted.
Functional analysis consists of a series of short,
tightly controlled sessions where situations
which are hypothesized to evoke the problem
E
behavior are recreated. Data are taken on the
antecedents, problem behavior, and conse-
quences. If specific situations, when compared
to control conditions, do, in fact, evoke problem
behavior, they are considered to be the function
(Iwata, Dorsey, Slifer, Bauman, & Richman,
1994). FBA, including functional analysis,
allows the practitioner to tailor the intervention
to the function of the behavior being assessed.
Structural analysis (SA; Stichter, Randolph, &
Kay, 2009) may also be of help, and implementa-
tion is very similar to a functional analysis. In SA,
the consequences for problem behavior are held
constant and the antecedents are systematically
manipulated. For example, an interventionist
might be interested in whether pictures or verbal
prompts are more effective in increasing on-task
behavior. In one condition, verbal prompts are
presented to the individual and on-task behavior
is reinforced by verbal praise. In the second condi-
tion, the same task is presented, but this time visual
cues are used to prompt responding. Reinforce-
ment stays constant for on-task behavior. The strat-
egy that produces more on-task behavior across
several presentations is considered to be the most
effective of the two interventions being evaluated.
There are several types of environmental
engineering strategies available to those who
work with individuals with autism. For the sake
of brevity, these will be broken into the following
categories: (1) priming strategies, (2) physical
environmental modifications, and (3) activity-
based strategies. What follows should not be con-
sidered to be an exhaustive list of strategies that
utilize environmental engineering; instead, it
should be considered to be a survey of the myriad
of environmental engineering interventions that
are available to the interested reader.
E 1124
Priming Strategies
Priming strategies consist of instruction on how
to behave appropriately in or preexposure to new
or stressful situations. They are designed to
provide advanced knowledge to the individual
with ASD that allows him or her to predict what
will happen in the future. Some examples of
priming strategies include video modeling,
Social Stories™, and functional communication
training.
In a traditional priming session, an individual
visits an unfamiliar situation (e.g., school) prior
to entering the situation. For example, a student
with ASD might visit the first-grade classroom he
or she will attend before the first day of school.
This allows the individual to become comfortable
with the environment so that navigating that
environment is less overwhelming. An example
is provided by Koegel, Koegel, Frea and
Green-Hopkins (2003). Students experiencing
difficulty in preacademic and academic situations
were exposed to the day’s lesson the night or day
before the lesson was presented in class. This
reduced problem behaviors such as stereotypic
behavior, repeated requests for the bathroom,
inappropriate verbalizations, and disruptive
behavior.
Video modeling uses a simple video of a social
situation or task to teach the student how to com-
plete the task or behave appropriately in
a particular situation. The student watches this
video several times and can pause, rewind, or
otherwise manipulate the video model.
The video model provides a concrete set of
parameters for responding that can be viewed
repeatedly to rehearse a social situation
(Cihak, 2011).
Recent research suggests that video models
are effective in a variety of environments and
with a variety of individuals. Most research
involves the teaching of adaptive skills such as
communication and social skills. It is considered
to be an evidence-based practice according to the
National Professional Development Center
on Autism Spectrum Disorders (Franzone &
Collet-Klingenberg, 2008).
Social Stories™ are simple stories that are
read by the individual prior to entering a social
Environmental Engineering/Modifications
situation. The story highlights at a minimum what
the individual should try to say or do and how
their behavior affects others. According to Carol
Gray, the developer of Social Stories™, the
following minimum elements must be present:
(1) descriptive statements, which present factual
information about the situation, (2) perspective
statements, which provide information about the
emotions and behavior of others, and (3) directive
statements, which guide the student regarding
strategies to try in the situation (Gray, 2000;
Kokina & Kern, 2010). These stories are always
written as suggestions for the student in order to
encourage flexibility and generalized responding.
Social Stories™ are reviewed by the individual
before the challenging situation presents itself in
a calm and nonthreatening environment (e.g., the
social story is best read to the child right before
lunch if the cafeteria is a problematic
environment).
Teachers and other practitioners report that
Social Stories™ are an easy, cost-effective way
to increase appropriate behavior and teach social
skills, especially skills which require taking the
perspective of others. Research on Social
Stories™ is limited; however, that which does
exist suggests that Social Stories™ are best as
brief interventions. According to Kokina and
Kern (2010), those developed using functional
behavioral assessment (FBA) data and
addressing problem behavior versus complex
social skills seemed to be most effective. How-
ever, Karkhaneh et al. (2010) found in their
review of the literature that Social Stories™
increased behaviors such as game playing,
reading comprehension, and reading and
comprehending social situations. Individuals
with moderate social skill problems and moderate
reading ability seemed to benefit more from
Social Stories™ than those with low social skills
and lower reading ability (Kokina & Kern, 2010).
No evidence is available at present regarding the
generalization and long-term maintenance of the
effects of Social Stories™. The evidence base for
Social Stories™ is at present rather small;
however, its use as a brief intervention for
individuals with higher communication and
social skills is promising.
Environmental Engineering/Modifications
Functional communication training (or FCT)
is a strategy in which the individual with ASD is
taught to request preferred items or activities.
These items are often identified as those
requested through problem behavior in the past.
Based upon the hypothesis that the majority of
problem behavior is communicative in nature,
FCT provides for a more socially appropriate
way to communicate wants and needs for
individuals who may have limited expressive
skills. In most cases, some sort of alternative or
augmentative communication system, such as
paper-based picture symbols or voice output
device, is selected for functional communication
training. The individual is then taught to manip-
ulate the communication system to request pre-
ferred items that in the past triggered problem
behavior. Research supports that replacing
problem behavior with appropriate requesting
skills can decrease the amount of problem
behavior in individuals with ASD (Mancil,
2006). For example, teaching a child to request
a break rather than engage in self-injury can
result in a decrease in the problem behavior
and an increase in the likelihood that the child
will request a break appropriately (Carr &
Durand, 1985).
Even when problem behavior is not a concern,
augmentative and alternative communication
devices (AAC) may be used for individuals
without spoken speech. These devices range
from low-technology (such as the picture
exchange communication system or PECS;
Frost & Bondy, 2002) to sophisticated high-tech
devices. As with all accommodations and modi-
fications, the system is based upon a thorough
evaluation of the child’s needs. A qualified
speech-language pathologist often evaluates the
child and determines the best intervention
method for that individual.
The Picture Exchange Communication
System (PECS) is a common and well-known
system for communication by individuals with
ASD, although its use is not limited to just indi-
viduals with ASD. In PECS, individuals are sys-
tematically instructed to (1) hand their
communicative partner a picture to request
items, (2) to recruit attention if the
1125 E
communicative partner is otherwise engaged,
(3) discriminate between cards, (4) increase com-
plexity and combinations of cards, and (5) use
picture cards to comment on the environment
(Frost & Bondy, 2002). A recent review identi-
fied over 30 articles showing the effectiveness of
PECS. Although all presented positive results,
many abandoned the protocol in the early phases,
leaving the later and more sophisticated aspects
of PECS untested. The authors suggested
E
a number of research questions, including
research into generalization of the effects of
PECS, using PECS with high-tech communica-
tion devices, and investigations into what ele-
ments of PECS affect the development of
spoken speech for those who acquire it (Sulzer-
Azaroff, Hoffman, Horton, Bondy, & Frost,
2009).
At present, there is a debate as to whether
visually based communication systems (such as
PECS and picture symbol-based devices, also
sometimes called aided devices; Mirenda, 2003)
are better for individuals with ASD than more
transient devices and systems such as signed
exact english (SEE; also called unaided devices).
The rationale is that picture-based symbols use
the visual channel (considered to be a strength
of individuals with ASD) and are more static (i.e.,
they do not disappear).
Recent research suggests that neither system is
best for teaching functional communication;
rather, choosing a system is an individually
based clinical decision. Limited evidence sug-
gests that for children who have more advanced
fine motor imitation skills, sign may have the
advantage of being easier to learn and general-
ized. However, these conclusions are based upon
small studies with identified methodological
difficulties (Tincani, 2004).
Voice output communication devices (VOCA;
Mirenda, 2003) are an often chosen modality for
individuals on the autism spectrum. A VOCA
produces either a synthesized or recorded vocal-
ization when an individual presses a button.
These buttons usually have some sort of graphic
display. For example, pushing the button with
a picture of a drink may produce a sound file
where a voice says, “I want a drink.” According
E 1126
to Mirenda (2003), VOCAs have the potential to
encourage more social interactions. Individuals
may respond more readily to an auditory bid for
interaction than a sign or pictorial one. There is
some evidence that VOCA devices may assist the
functional communication of individuals with
ASD in school or clinic settings. However,
the research on VOCA for children with ASD
is somewhat sparse, especially in the area of
generalization to home and community
(Mirenda, 2003). Further research is critical in
this age of iPads, iPods, and apps that increase
communication for children with ASD. It is
important to understand the variables that predict
success with more high-tech communication
devices as well as what variables affect the selec-
tion of a functional communication system.
Whatever functional communication system is
used, the representational competence of
a learner must be taken into consideration.
Representational competence refers to the ability
of a learner to infer meaning from some sort of
symbol (Mineo Mollica, 2003). Although line
drawings are a popular way to create schedules,
they are in fact very advanced and abstract
representations. Most individuals learn concrete
objects first, then photos, then color line draw-
ings, then miniatures, then black and white line
drawings. For individuals who do not respond to
typically used picture symbols, it might be better
to use a more concrete representation such as
legible photographs or, in some cases, the actual
object (Mirenda & Locke, 1989).
Setting Modifications
Setting modifications, such as work systems,
visual schedules, and organization and structure,
refer to arrangements of the physical settings
encountered by learners with ASD so that salient
features of the environment are visually clear and
so that the individual with ASD clearly knows
what to do in each environment. The majority of
setting modifications are visual; however, some
are auditory in nature or a combination of both
(e.g., timers, transition music). Division
TEACCH uses many setting modifications, such
as color coding, stations, and visual cues, to
reduce the amount of verbal interaction (Mesibov
Environmental Engineering/Modifications
et al., 2005). The rationale for using visual setting
modifications is that most individuals with ASD
tend to more easily process stimuli visually rather
than verbally.
Visual schedules function in much the same
way as a “to-do list.” In a visual schedule, the
events of a person’s day (or in most cases,
a subset of the person’s day) are arranged on
a schedule either horizontally or vertically
(Hume, 2008). Visual schedules may also be
created for specific tasks. For example, the task
of hand washing may be broken into its compo-
nent parts and a visual of each part may be placed
in the bathroom to prompt the appropriate hand-
washing sequence. It allows the individual with
ASD to process and organize his or her time. In
most cases, pictures are used to represent each of
the activities; however, words can be used for
higher-functioning individuals and actual items
are sometimes used for individuals with less
processing and representational skill. As each
item is completed, the picture is removed and
put away, signaling its completion.
When creating a visual schedule, it is impor-
tant to consider the needs of the child. For exam-
ple, a younger or less experienced learner may
need to have a simple schedule that consists
solely of what is happening now and what will
happen next. A more advanced learner may be
able to process a full day’s schedule. In the case
of a task-based visual schedule, a less experi-
enced learner might need a more detailed analy-
sis, whereas the more advanced learner might be
able to anticipate and chunk information into
a single visual cue. Examples of how to create
and use appropriate visuals are available (see
Hodgdon, 1998). Representational competence,
described earlier in this article, should be consid-
ered as well.
Although visual cues are often associated with
schedules and/or task sequences, photographs
and other types of picture symbols can be used
to prompt appropriate behavior in a number of
ways. Many individuals with ASD respond well
when there are visual cues in the environment
that can help them understand how to respond
and when. Labels with picture symbols may
also be used to describe expectations in the
Environmental Engineering/Modifications
environment. For example, a child’s place at the
dinner table might be signaled with their picture
on a placemat. The child is then instructed to find
their picture and sit at that chair. West
(2003) found that pictorial cues were more effec-
tive than verbal prompts in teaching a variety of
skills to individuals with ASD. These skills both
generalized to novel skills and maintained over
time (West, 2008).
Visual cues seem to be effective for
individuals with autism across the lifespan
(Hume, 2008). For example, Ganz, Kaylor, Bour-
geois, and Hadden (2008) used visual social
scripts and cues to “be quiet” to increase
appropriate social statements and reduce
perseverative statements in three elementary
children with ASD. Modest generalization of
appropriate untrained social statements was
observed as well.
Organization of elements in the environment is
also considered to be an important part of
environmental engineering for individuals with
autism. Some advocate for more ambient light-
ing, reduced distractions, and less stimulating
environments. These changes are introduced to
reduce the amount of stimulating sensory
input and allow the child with autism to focus
upon those important parts of the environment
(Kluth, 2003).
Organizing the environment by activity and
reducing clutter is another element of environ-
mental engineering. For example, a teacher might
use bookcases to cordon off the reading area and
surround the area with red tape. The activity area
may include active toys and may be surrounded
by blue tape on the floor. These supports are
designed to give the individual with autism
more information about what is expected in cer-
tain areas of the classroom or home. These types
of visual supports are considered to be critical to
the structured teaching strategies developed by
division TEACCH (Mesibov et al., 2005). Some
interventionists have called eliminating clutter
and extraneous stimuli sterilizing the environ-
ment (Carbone, 2003).
As with all interventions, these supports
should be individualized; some individuals will
respond better to quiet environments while
1127 E
others work better with background noise
(Scheuermann & Hall, 2008).
Clear and consistent scheduling is also consid-
ered to be a critical environmental support.
Many individuals with autism have difficulty
processing open-ended instructions or activities;
therefore, supporting the understanding of the
beginning or end of an activity can help to
increase appropriate behavior. Visual schedules
can assist with this task, as well as timers and cues
E
such as music during transitions (Scheuermann &
Hall, 2008).
Any organizational strategy must be
flexible; that is, the individual with ASD
should be prepared in advance for changes or
out-of-the-ordinary events. For example,
a birthday party might be put on the calendar, or
a surprise icon might be placed on the visual
schedule to signal an unexpected event.
While providing clear visual cues and elimi-
nating extraneous stimli from the environment
are considered to be best for individuals with
ASD, there is little research to support effective-
ness at this time. Several literature searches with
terms such as “classroom organization and
autism,” “environment and autism,” and
“environmental organization and autism”
returned no empirical articles. Studies that inves-
tigate the effects of a carefully organized physical
environment need to be conducted.
Activity-Based Strategies
Activity-based strategies are those that are
embedded into everyday activities and provide
modifications or accommodations for individuals
with ASD. Some examples include academic
supports, task modifications, incorporating pref-
erence and choice, and prompting techniques.
A well-known intervention from TEACCH is
the work system. In the work system, a task is
broken down into its component parts and visuals
are created that communicate to the learner with
ASD (1) what is to be done, (2) how much work
needs to be done, (3) when he or she is finished,
and (4) what the person should do once the work
is complete. The goal of the work system is to
increase independence in children with ASD and
decrease prompts. It has been shown to be
E 1128
effective with elementary and middle school stu-
dents and can be used to teach a myriad of tasks
including vocational, self-help, and transitions
(Hume & Carnahan, 2008).
Academic supports and task modifications are
those supports that allow an individual to be
successful at a task. These supports might include
visual cues, such as reducing the amount of visual
stimuli to isolate visual tasks (such as folding
a piece of paper to cover up additional questions
on a test). Other visual supports include
highlighting pertinent information, color coding
salient information, etc. Other modifications may
include frequent proactive breaks (i.e., breaks set
at preset intervals as opposed to in response to
agitation) or using a task analysis, where a task is
broken into its component parts and taught in
a systematic fashion. Considerations for creating
academic and task modifications are available in
Vaughn and Bos (2012). Visual supports such as
the visual schedules described above can also be
used to modify tasks.
Incorporating preference and choice can
increase the success of a child with ASD. Those
items that a child is more likely to choose are
typically the most reinforcing (Mason & Egel,
1995). Using preferred items for teaching may
also increase the likelihood of attention. Giving
individuals simple choices, such as the order in
which to complete a task, can decrease problem
behavior and increase more socially appropriate
behavior (Smeltzer, Graff, Ahearn, & Libby,
2009; Ulke-Kurkcuoglu & Kircaali-Iftar, 2010).
There are many different types of assessments
of preference. Often, teachers and caregivers will
give families a checklist or open-ended question-
naire to complete. Professionals, however, should
be aware of respondent bias when questionnaires
are used. Free-operant preference assessments
consist of giving a child free access to a limited
number of items. Those manipulated or con-
sumed most frequently are considered to be the
most preferred. In a forced-choice preference
assessment, items are presented in pairs and the
child is asked to choose which one they would
like to manipulate or consume. It is important to
note that different types of preference assess-
ments may yield different results; therefore,
Environmental Engineering/Modifications
multiple modalities of preference assessment
may be in order when finding preferred items
proves difficult (Kodak, Fisher, Kelley, &
Kisamore, 2009).
Related to choice is the notion of environmen-
tal enrichment. In environmental enrichment,
additional items are provided that allow the
child to be appropriately engaged in activities as
opposed to engaging in repetitive, stereotypic
behavior (Neitzel, 2009). Visual cues, items to
hold, and timers may also be effective interven-
tions for difficulties with transitions and wait
time. Ringdahl, Vollmer, Marcus, and Roane
(1997) found that systematically providing envi-
ronmental enrichment in the form of preferred
items to manipulate reduced self-injurious behav-
ior in three participants with developmental dis-
abilities. A recent review of the literature found
environmental enrichment to be an effective
strategy for reducing stereotypic behavior in indi-
viduals with developmental delays (Lancioni,
Singh, O’Reilly, & Sigafoos, 2009).
Prompts are additional instructions provided
to a child with autism that allow them to be
successful in activities. The prompts and
prompting sequence is tailored to the learner
with ASD. Common strategies include the least-
to-most prompting sequence, where prompts are
introduced in order of intrusiveness (typically
from verbal to hand-over-hand guidance) until
the child is successful. Most-to-least prompting
reverses the sequence and systematically fades
prompts as the learner needs less and less assis-
tance to be successful. In time delay, the teacher
gradually increases the time between the instruc-
tion and the prompt until the learner anticipates
the prompt (Alberto & Troutman, 2009). The
evidence base supports the use of prompting for
most behaviors and individuals of all ages
(Neitzel & Wolery, 2009).
Future Directions
Anecdotal and empirical evidence support the use
of environmental engineering for individuals
with ASD; however, additional empirical evi-
dence is needed for specific environmental
Environmental Engineering/Modifications
engineering strategies. Antecedent-based inter-
ventions are popular among practitioners because
they are easy to implement, considered to be
cost-effective, and are perceived to be effective.
Although there is much evidence that antecedent-
based interventions are being utilized with
individuals on the autism spectrum, much more
research should be devoted to investigating why
and how these interventions are effective.
The best-researched environmental engineer-
ing interventions seem to be those surrounding
functional communication training, especially
PECS, and priming. Many interventions have
a modest evidence base, such as Social Stories
and video modeling. Others, such as environmen-
tal arrangements and academic supports, have
little evidence to support them. It seems as if, in
many ways, “the devil is in the details.” At pre-
sent, which interventions work best for specific
students and the details of implementation seem
to remain the domain of clinical judgment.
Evidence-based guidance for clinicians may
assist them in making more efficient, individual-
ized decisions for intervention. Considering
environmental engineering is deemed important
in many respected books and training manuals,
and more evidence is needed to support its use.
See Also
▶ Augmentative and Alternative
Communication
▶ Developmental Continuum (Principles of
TEACCH)
▶ Functional Analysis
▶ Functional Assessment and Curriculum for
Teaching Everyday Routines
▶ Functional Communication Training
▶ Video Modeling/Video Self-Modeling
▶ Visual Supports
References and Readings
Alberto, P. A., & Troutman, A. C. (2009). Applied behav-
ior analysis for teachers (8th ed.). Upper Saddle River,
NJ: Merrill-Prentice-Hall.
1129 E
Barthold, C. H., & Egel, A. L. (2001). Stimulus
overselectivity and generative language instruction
for students with autism: An issue that needs to be
revisited. The Behavior Analyst Today, 2, 33–39.
Bijou, S. W., Petersen, R. F., & Ault, M. H. (1968).
A method to integrate descriptive and experimental
field studies at the level of data and empirical concepts.
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Bregman, J. D., Zager, D., & Gerdtz, J. (2005). Behavioral
interventions. In F. R. Volkmar, R. Paul, A. Klin, &
A. Cohen (Eds.), Handbook of autism and pervasive
developmental disorders (3rd ed.). Hoboken, NJ:
Wiley. E
Carbone, V. J. (2003). Teaching verbal behavior to chil-
dren with autism and related disabilities. Unpublished
Workshop Manual.
Carr, E. G., & Durand, V. M. (1985). Reducing behavior
problems through functional communication training.
Journal of Applied Behavior Analysis, 18, 111–126.
Cihak, D. F. (2011). Comparing pictorial and video
modeling activity schedules during transitions for
students with autism spectrum disorders. Research in
Autism Spectrum Disorders, 5(1), 433–441.
Franzone, E., & Collet-Klingenberg, L. (2008). Overview
of video modeling. Chapel Hill, NC: The National Pro-
fessional Development Center on Autism Spectrum
Disorders, Frank Porter Graham Child Development
Institute, The University of North Carolina.
Frost, L. A., & Bondy, A. S. (2002). The picture exchange
communication system training manual (2nd ed.).
Newark, DE: Pyramid Educational Consultants.
Ganz, J. B., Kaylor, M., Bourgeois, B., & Hadden, K.
(2008). The impact of social scripts and visual cues
on verbal communication in three children with autism
spectrum disorders. Focus on Autism and Other
Developmental Disabilities, 23(2), 79–94.
Gray, C. (2000). The new social stories book. Arlington,
TX: Future Horizons.
Hodgdon, L. A. (1998). Visual strategies for improving
communication volume 1: Practical supports for
school and home. Troy, MI: QuirkRoberts.
Hume, K. (2008). Overview of visual supports. Chapel
Hill, NC: The National Professional Development
Center on Autism Spectrum Disorders, Frank Porter
Graham Child Development Institute, The University
of North Carolina.
Hume, K., & Carnahan, C. R. (2008). Overview of
structured work systems. Chapel Hill, NC: The
National Professional Development Center on Autism
Spectrum Disorders, Frank Porter Graham Child
Development Institute, The University of North
Carolina.
Iwata, B. A., Dorsey, M. F., Slifer, K. J., Bauman, K. E., &
Richman, G. S. (1994). Toward a functional analysis
of self-injury. Journal of Applied Behavior Analysis,
27, 197–209.
Karkhaneh, M., Clark, B., Ospina, M. B., Seida, J. C.,
Smith, V., & Hartling, L. (2010). Social stories[TM]
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spectrum disorder: A systematic review. Autism: The
International Journal of Research and Practice, 14(6),
641–662.
Kluth, P. (2003). You’re going to love this kid! Teaching
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Baltimore: Paul H. Brookes.
Kodak, T., Fisher, W. W., Kelley, M. E., & Kisamore, A.
(2009). Comparing preference assessments: Selection-
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Koegel, L. K., Koegel, R. L., Frea, W., & Green-Hopkins, I.
(2003). Priming as a method of coordinating educational
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EPF Model
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Tincani, M. (2004). Comparing the picture exchange
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Touchette, P. E., McDonald, R. F., & Langer, S. N. (1985).
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EPF Model
▶ Enhanced Perceptual Functioning
Epidemiology 1131 E
Kaneshiro, N. K. (2011). Epicanthal folds. MedlinePlus.
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ency/article/003030.htm
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Abha R. Gupta
Developmental-Behavioral Pediatrics, Child E
Study Center, Yale University, New Haven, CT, Epicanthus
USA
▶ Epicanthic Fold
Synonyms

Epicanthal fold; Epicanthus; Palpebronasal fold; Epidemiology

Plica palpebronasalis
Definition
A skin fold of the upper eyelid that covers the
inner corner (canthus) of the eye. It is seen nor-
mally in infants before the bridge of the nose
develops and in East Asian people. It can also
be a characteristic feature of some medical con-
ditions, such as Down syndrome, fetal alcohol
syndrome, Turner syndrome, Williams syn-
drome, and Noonan syndrome.
See Also
▶ Down Syndrome
▶ Fetal Alcohol Syndrome
▶ Noonan and Ras/Mapk Pathway Syndromes
▶ Turner Syndrome
▶ Williams Syndrome
References and Readings
Burn, J. (1986). Williams syndrome. Journal of Medical
Genetics, 23, 389–395.
Delabar, J. M., Theophile, D., Rahmani, Z., Chettouh, Z.,
Blouin, J. L., Prieur, M., et al. (1993). Molecular
mapping of twenty-four features of Down syndrome
on chromosome 21. European Journal of Human
Genetics, 1, 114–124.
Lisa Croen
Autism Research Program, Kaiser Permanente
Division of Research, Oakland, CA, USA
Definition
Epidemiology is a multidisciplinary field of study
that focuses on describing, investigating, and
preventing disease in populations. Studying dis-
eases on the population level creates a level of
complexity not seen on the individual level. In
order to understand the movement and patterns of
disease in a population, epidemiologists often
need to be well versed in biology (disease trans-
mission, symptoms, treatment), social sciences
(population dynamics, behavior), statistics (anal-
ysis of population level data, visualizing trends
and patterns), and rigorous scientific methods
(study design, causal pathways). Epidemiology
employs a scientific, evidence-based approach
to investigations of health and disease and thus
is sometimes referred to as the scientific arm of
public health.
Historical Background
The term “epidemiology” is of Greek origin and
means “the study of what is upon the people.”
E 1132
One of the first epidemiologists was thought to be
the Greek physician Hippocrates. Besides
coining the terms “epidemic” and “endemic” in
approximately 400 B.C., he also noted the asso-
ciation between yellow fever and malaria and
swamps and advocated their drainage.
Several other notable epidemiologists
included John Graunt (1620–1674), who was
the first to use life tables to support and refute
theories on certain diseases; James Lind
(1716–1794), who used an experimental study
design to determine that citrus could cure scurvy
in sailors; and Ignaz Semmelweis (1818–1865),
who cut maternal mortality rates by more than
ninefold over a 6-year time period by requiring
that physicians in his ward wash their hands with
chlorinated lime between patient examinations
Merril & Timmreck (2006).
Perhaps the most notable epidemiologist,
though, is John Snow (1813–1858), whose break-
through work on cholera in London helped
develop modern epidemiology as it is known
today. Snow gathered data on the incubation
period of cholera and time from infection to
death and even plotted mortality events on
maps. Not only did he study the disease exten-
sively, he also identified a potential cause of
illness – contaminated water. He found that
a brewery with its own water source was
protected from cholera, while approximately
500 people died over a 10-day span within close
proximity to the Broad Street water pump. This
led to the famous removal of the Broad Street
pump handle. Years later, John Snow conducted
one of the first major epidemiologic studies in
a randomized setting. Two companies were com-
peting to supply water to individuals in London.
The first company, Lambeth Water Company,
took water from the Thames River from
a relatively unpolluted upstream source. The sec-
ond company, Southwark and Vauxhall Water
Company, drew water contaminated with the
city’s effluent. Both companies ran water pipes
to the same areas, and thus citizens randomly
chose one company or the other to obtain water
(some citizens did not even recall which com-
pany they had chosen). Snow was able to obtain
Epidemiology
the addresses of those who died of cholera and
then determine what water company supplied
water to those households. In this way, he
was able to demonstrate that water from the
Lambeth Water Company was far safer than
the fecally contaminated water provided by the
Southwark and Vauxhall Water Company. This
seminal work, conducted in the mid-1800s, was
produced at a time when most physicians still
believed in the same miasma, or bad air, that
Hippocrates had believed in over 2,000 years
prior (Snow, 1855).
Since Snow’s time, modern epidemiology has
blossomed. In 1905, a school of tropical medicine
was created at the University of London, and in
1916, Johns Hopkins University created the first
school of public health. The Centers for Disease
Control was created in 1946, and the National
Institutes of Health was created soon after in
1948 Breslow & Cengage (2006). Several large
epidemiologic studies were subsequently
conducted that helped solidify the reputation of
epidemiology as a rigorous science. One of the
most definitive set of studies conducted in the
later half of the twentieth century were those
conducted by Doll and Hill (1950) and Hammond
and Horn (1954) which established smoking as
a strong risk factor for lung cancer.
The epidemiologic study of autism spectrum
disorders (ASDs) began in 1943 with Kanner’s
first description of autism in 11 children. Since
then, many hypotheses have been developed
regarding the potential causes of autism. Early
hypotheses suggested that cold detached par-
ents were a cause of autism. In 1964, an
epidemic of rubella infected both mothers and
their unborn or newly born infants, causing
20,000–30,000 congenital malformations. In
a study conducted by Stella Chess in 1971, out
of 243 preschool children who had experienced
congenital infection with rubella, ten were
found to have autism (as described by Kanner)
and eight demonstrated some autistic behavior.
This finding, along with others, began to sug-
gest that autism could be a disease rooted in
biology and not in parenting (Amaral et al.,
2011).
Epidemiology
Current Knowledge
The current practice of epidemiology employs
a variety of study designs to accurately determine
the relationship between exposures and health
outcomes. The tools of epidemiology have been
used to address a wide variety of research ques-
tions, ranging from genetic epidemiology to out-
break epidemiology, the epidemiology of aging,
and the epidemiology of childhood developmen-
tal disorders such as autism.
Study designs can be categorized into one of
two headings: experimental or observational.
Experimental study designs include randomized
controlled trials, or clinical trials, where partici-
pants follow well-defined protocols. These types
of studies are quite powerful because perfect
randomization allows investigators to examine
only the causal effect of exposure on the outcome
of interest and prevents other factors from
influencing the relationship between the exposure
and disease. These factors which influence both
exposure and disease are often referred to as
confounders, and presence of confounders may
bias the relationship between exposure and dis-
ease. However, there are several limitations to
the randomized controlled design. Studies like
these seek to mimic laboratory type conditions,
and more control requires more time and more
resources. Thus, randomized designs are often
quite expensive and difficult to conduct. In addi-
tion, many ethical issues can arise. For example,
individuals with illnesses that might benefit
from treatment cannot be expected to take
placebos.
Observational studies include many designs;
the most common being cohort studies, case-
control studies, and cross-sectional studies. The
goal of such observational studies is to determine
the causal relationships between exposures and
disease, though accomplishing this task with
observational study designs is much more diffi-
cult than with a randomized controlled trial due to
potential confounding.
Case-control studies involve finding individ-
uals who are diseased, cases, and then identifying
a group of nondiseased individuals, controls, who
1133 E
come from the same population that generated
the cases. The past exposure status for all study
participants is then determined, and a relationship
between exposure and disease can then be calcu-
lated. Case-control studies have the advantage of
being much faster and cheaper to conduct than
randomized trials or cohort studies. Case-control
studies are especially effective when the disease
of interest is rare. However, identifying an appro-
priate control population may be difficult.
E
Another limitation is that unless all confounders
are identified and accounted for, the relationship
between exposure and disease cannot be
described as causal. Thus, many case-control
studies and observational studies in general
report associations between exposure and dis-
ease, not causal relationships.
Cohort studies differ from case-control studies
in that the opposite approach is taken. Rather than
identify diseased and nondiseased individuals to
begin with, cohort studies begin by identifying at-
risk exposed and unexposed individuals. These
nondiseased groups are then followed until the
end of the study. Illness in the exposed and
nonexposed groups is then compared. Cohort
studies are often more expensive than case-
control studies, but are much less expensive
than randomized trials. Like case-control studies,
they suffer from the limitation of potential
unmeasured confounders. However, one critical
advantage of cohort studies is that exposure is
known to precede disease, a critical criteria for
a causal relationship. In addition, investigators do
not have to rely on study participants to remem-
ber prior exposure status, as in a case-control
study.
Cross-sectional studies are similar to taking
a picture of the population at one point in time.
Information on exposure and disease is often
collected at the same time, and temporal ordering
may or may not be recorded. They differ from
case-control studies in that cross-sectional stud-
ies often attempt to collect data on the entire
population of interest. They are often even less
expensive to conduct than case-control studies.
An example of a cross-sectional design is mailing
a questionnaire to all employees of a company,
E 1134
inquiring about current exposure and health
status. Another example involves use of census
data to determine the relationship between an
exposure and disease. However, one major limi-
tation to cross-sectional studies that use “high-
level” data such as census data is the ecological
fallacy. The ecological fallacy exists when
a relationship is seen at a population level that
does not exist at the level of individual persons.
An example of this is measuring the average
IQ score for a population. While the average is
appropriate to use at the population level, the IQ
of any individual taken from that population could
be higher or lower than the average. It would be
a fallacy to assume that each individual had
exactly the average IQ measured for the entire
population.
All of the above study designs are subject to
a variety of biases that can distort the relationship
between the exposure and disease. One such bias
is random error, which can arise when data tend
to be randomly biased in one direction, and thus
bias final results. A solution to this type of bias is
to either measure variables more precisely in
order to minimize random noise or to increase
the number of participants or samples to the point
where small random fluctuations are unlikely to
alter the final results significantly.
Another type of bias is selection bias, which
occurs when exposure or disease status influence
participation in a study. For example, if
researchers want to recruit children with ASD
into a study, and advertise on TV and the Internet
for participants, they may likely get a biased
sample. More educated, financially well-off indi-
viduals may be more likely to see those adver-
tisements and participate. Results from that study
may differ greatly than a study conducted using
a random sample from a comprehensive registry
of children diagnosed with ASD.
Confounding is another bias and may arise
when there are systematic differences between
exposed and unexposed groups. These differ-
ences may lead investigators to falsely conclude
that exposure alone caused differences in health
outcomes. Confounders are typically factors
that cause exposure as well as disease.
A simple example of this would be a study that
Epidemiology
investigated whether or not use of a mood-
stabilizing medication among men with
Asperger’s syndrome could cause autism in
their child. A naı̈ve analysis examining the rela-
tionship between medication and the child’s
ASD status could find a strong association, but
it is likely that much if not all of the associations
could be explained by the genetic history of the
father. Attributing all cases of ASD to the med-
ication would be a biased conclusion, one that is
often referred to as “confounded.”
Another important source of bias is informa-
tion bias. Information bias generally refers to the
circumstance when data collected on an individ-
ual is not completely accurate. If a study partici-
pant reported having a relative with autism when
that relative actually was diagnosed with obses-
sive compulsive disorder, that would be an exam-
ple of information bias. Information bias is often
broken into two categories: differential and
nondifferential. Nondifferential bias refers to
inaccurate measurement of either exposure or
disease status, but the inaccuracy is the same in
both the control and comparison groups. For
instance, in a case-control study examining
ASD as an outcome and maternal flu vaccina-
tion as an exposure, if mothers of children with
ASD incorrectly reported their vaccination his-
tory in a similar fashion to mothers of children
without ASD, then that “recall bias” would be
referred to as nondifferential. However, if
mothers of children without ASD underreported
their flu vaccination history while mothers of
children with ASD overreported their flu vacci-
nation history, then that inaccurate measure-
ment of exposure would be called differential
(different recall in the case and comparison
groups). Nondifferential misclassification is
less concerning than differential misclassi-
fication. While both forms of bias typically
give answers that differ from the truth,
nondifferential misclassification gives answers
that are biased consistently toward the null (no
association), while differential misclassification
can bias results either toward or away from the
null. This unpredictability is undesirable and
makes it difficult to interpret the results with
any confidence.
Epigenetic Mechanisms
Future Directions
Historically, epidemiology has been used to
discover associations between exposures and
disease. In fact, according to US law, epidemiol-
ogy cannot be used by itself to prove causative
relationships between exposure and disease in
a particular individual; rather, it can only make
a probabilistic statement about whether an expo-
sure could have caused an outcome in an individ-
ual (National Research Council, 2011). However,
the science of epidemiology has always
attempted to explore and identify causal relation-
ships. With the advent of computers, develop-
ments in genetics, and availability of
sophisticated measurement tools, epidemiolo-
gists have been able to better explore causal rela-
tionships between various exposures and
diseases. Modern technology, including sophisti-
cated statistical tools and electronic recording of
data, has greatly improved the feasibility of
conducting large, rigorous studies of health and
analyzing large quantities of data. As the field of
epidemiology continues to develop, there is great
hope that previously untreatable diseases and
health conditions will be better understood and
that each successive generation will enjoy better
health than those that came before.
See Also
▶ Incidence
▶ Prevalence
References and Readings
Amaral, D., Geschwind, D., & Dawson, G. (2011). Autism
spectrum disorders (1st ed.). Oxford, USA: Oxford
University Press.
Breslow, L., & Cengage, G. (Eds.). (2006). Encyclopedia
of public health. eNotes.com. Retrieved from http://
www.enotes.com/public-health-encyclopedia/history-
public-health
Chess, S. (1971). Autism in children with congenital
rubella. Journal of Autism and Childhood Schizophre-
nia, 1(1), 33–47. doi:10.1007/BF01537741.
Doll, R., & Hill, A. B. (1950). Smoking and carcinoma of
the lung; Preliminary report. British Medical Journal,
2(4682), 739–748.
1135 E
Doll, R., & Hill, A. B. (1956). Lung cancer and other
causes of death in relation to smoking; A second report
on the mortality of British doctors. British Medical
Journal, 2(5001), 1071–1081.
Friedman, L., Furberg, C., & DeMets, D. (2010).
Fundamentals of clinical trials (4th ed.). New York:
Springer.
Hammond, E. C., & Horn, D. (1954). The relationship
between human smoking habits and death rates. Jour-
nal of the American Medical Association, 155(15),
1316–1328. doi:10.1001/jama.1954.03690330020006.
Jadad, A. R., & Enkin, M. W. (2007). Randomised con-
trolled trials: Questions, answers and musings E
(2nd ed.). London: BMJ Books.
Koepsell, T. D., & Weiss, N. S. (2003). Epidemiologic
methods: Studying the occurrence of illness (1st ed.).
Oxford, USA: Oxford University Press.
Merril, R. M., & Timmreck, T. C. (2006). Introduction to
epidemiology. Sudbury, MA: Jones & Bartlett
Learning.
National Research Council. (2011). Reference Manual on
Scientific Evidence-Third Edition. Washington, D.C.:
National Academies Press.
Rothman, K. J., Greenland, S., & Lash, T. L. (2008).
Modern epidemiology (3rd ed.). Philadelphia:
Lippincott Williams & Wilkins.
Snow, J. (1855). On the mode of communication of chol-
era. London: John Churchill.
Szklo, M., & Nieto, J. (2006). Epidemiology: Beyond the
basics (2nd ed.). Sudbury, MA: Jones and Bartlett.
Epigenetic Mechanisms
Thomas Fernandez
Yale Child Study Center, Yale University School
of Medicine, New Haven, CT, USA
Definition
Means by which gene expression is regulated
without altering the underlying DNA sequence.
Epigenetic mechanisms result in heritable anno-
tations or modifications to DNA and associated
histones which include the following: methyla-
tion, acetylation, ubiquitylation, phosphoryla-
tion, and sumoylation.
Historical Background
Coining of the term “epigenetics” is often attrib-
uted to Conrad H. Waddington, a developmental
E 1136
biologist, geneticist, and philosopher who
established foundations for systems biology. In
1942, predating knowledge of the physical nature
of genes and their role in heredity, he used the
term to refer to the study of the “causal mecha-
nisms” by which “the genes of the genotype bring
about phenotypic effects” (Waddington, 1942).
Early on, “epigenetics” was a vaguely understood
idea that was often invoked to explain phenom-
ena when basic genetic principles fell short.
Despite an absence of direct scientific evidence,
Holliday and Pugh (1975) and Riggs (1975) inde-
pendently proposed the idea that methylation was
a heritable epigenetic process that played an
important role in regulating gene expression.
Subsequently, a large amount of direct evidence
accumulated which validated these ideas, and
epigenetics began to evolve into a field of science
whose molecular underpinnings were clarified.
Holliday’s review of “the inheritance of epige-
netic defects” (Holliday, 1987) initiated wide-
spread use of the term “epigenetic” during the
1990s. Today, molecular biologists define epige-
netics as “the study of mitotically and/or meioti-
cally heritable changes in gene function that
cannot be explained by changes in DNA
sequence” (A.D. Riggs, 1996).
Current Knowledge
Overview
Two predominant mechanisms provide the
molecular basis for epigenetic regulation of
gene expression: DNA methylation and histone
modifications (which include methylation, acety-
lation, ubiquitylation, phosphorylation, and
sumoylation of histone tails). These alterations
are thought to alter the shape of chromatin, the
complex of DNA wrapped around an octamer
structure of histone proteins in the cell nucleus,
and thereby affect gene transcription. Epigenetic
mechanisms are active in both the germ line and
somatic tissues; they are influenced by both
genetic and environmental factors. The resulting
epigenetic alterations can be conceptualized as
comprising an “epigenotype” that is heritable
between mother and daughter cells (meiotic
Epigenetic Mechanisms
inheritance) and between generations (mitotic
inheritance). Epigenetic modifications yielding
differing epigenotypes are one explanation for
how cells or organisms with otherwise identical
DNA sequence may display different pheno-
types. With regard to autism spectrum disorders
(ASD), epigenetic modifications in several genes
and genomic regions have been reported in both
syndromic and nonsyndromic forms of ASD and
may represent an important pathway in pathogen-
esis. Understanding the role of epigenetic
changes in ASD is of particular interest, as their
reversal may represent a potential target of novel
therapeutic strategies.
DNA Methylation
Methylation is a well-characterized epigenetic
modification that involves the covalent addition
of a methyl group to cytosine bases at the carbon-
5 position of a CG dinucleotide sequence of DNA
(CpG dinucleotide) (Fig. 1). Regions of the
genome rich in CG dinucleotide sequence are
known as CpG islands and exist in the promoter
regions of approximately half of all known
genes. Methylation occurs on both strands of
a CpG dinucleotide via DNA methyltransferase
(DNMT) enzymes and the methyl donor
S-adenosyl-L-methionine (SAM). There is no
known enzyme with DNA demethylating activ-
ity. Highly methylated regions are associated
with a closed chromatin conformation state (het-
erochromatin), displaying less transcriptional
activity and therefore less gene protein expres-
sion. DNA methylation may inhibit gene expres-
sion by direct interaction with factors that repress
transcription, or indirectly through recruitment
of methyl-CpG-binding proteins complexed
with enzymes that modify histone proteins,
transforming chromatin from an active to
a repressed state. Alternatively, lack of methyla-
tion is associated with an open chromatin confor-
mation state (euchromatin), leading to more
transcriptional activity and gene expression.
Tumor growth has been associated with a state
of hypomethylation, increasing the rate of
mitotic recombinations from baseline and
leading to genomic instability (e.g., structural
rearrangements).
Epigenetic Mechanisms
METHYL GROUP
CHROMOSOME
DNA
GENE
HISTONE
DNA hidden, gene turned off
Epigenetic Mechanisms, Fig. 1 Epigenomic marks.
The epigenome can mark DNA in two ways, both of
which play a role in turning genes off or on. The first
occurs when certain chemical tags called methyl groups
attach to the backbone of a DNA molecule. The second
Histone Modifications
Another type of epigenetic mechanism which has
the potential to modify gene expression involves
chromatin remodeling via reversible covalent
posttranslational modifications to histone pro-
teins (Fig. 1). Two copies of four histone proteins
(H2A, H2B, H3, and H4) form an octamer struc-
ture around which DNA is wrapped. The flexible
N-terminus tails of histone proteins, H3 and H4,
are most likely to carry numerous modifications
of amino acids, including acetylation, methyla-
tion, phosphorylation, ubiquitylation, and
sumoylation. Histone acetylation (via histone
acetyltransferase enzymes) and phosphorylation
is associated with an open or relaxed chromatin
conformation state (euchromatin), facilitating
transcriptional activity and gene protein expres-
sion. Conversely, histone deacetylation (via his-
tone deacetylase enzymes) or sumoylation is
associated with a closed or compact chromatin
1137 E
CHEMICAL
TAG
E
HISTONE TAIL
HISTONE TAIL
DNA accessible, gene turned on
occurs when a variety of chemical tags attach to the tails of
histones, which are spool-like proteins that package DNA
neatly into chromosomes. This action affects how tightly
DNA is wound around the histones (Courtesy of National
Human Genome Research Institute)
conformation state (heterochromatin), repressing
transcription and gene protein expression. Other
histone modifications may facilitate or repress
transcription, depending on which amino acid
residue is altered.
Epigenetic Syndromes and ASD
With respect to ASD, there are several examples
of known epigenetic syndromes associated with
increased risk. With the important caveat that
intellectual disability in these syndromes may
account for some of the observed phenotypic
overlap in ASD, it is also possible that shared
genes and epigenetic mechanisms may confer
risk for ASD as well.
Rett Syndrome and Methyl-CpG-Binding
Proteins
Many features of Rett syndrome (language
impairments, stereotypic behaviors, seizures,
E 1138
sleep abnormalities, age of onset) are shared in
common with autism, and both disorders are
classified as pervasive developmental disorders
in DSM-IV-TR. Approximately 80% of Rett syn-
drome patients (almost exclusively females) and
a small number of patients with autism (without
Rett syndrome) have been reported with rare
and common mutations in the MECP2 gene
on the X chromosome. This transcript codes for
a methyl-CpG-binding protein with functional
domains for methyl binding and transcription
repression via inhibition of transcription factor
binding; it may also facilitate histone modifica-
tions. Studies of MECP2 in autism have shown
decreased brain expression relative to matched
controls, and expression levels have been corre-
lated with rare variants and hypermethylation in
the gene’s promoter (Nagarajan, Hogart, Gwye,
Martin, & LaSalle, 2006).
Fragile X Syndrome
Fragile X syndrome (FXS) is linked to the expan-
sion of a CGG repeat sequence in the 50
untranslated region of the FMR1 gene on chro-
mosome Xq27. These repeat expansions lead to
increased methylation, decreased acetylation,
and therefore decreased expression of FMR1,
a gene whose protein product is involved with
RNA processing. Such epigenetic modifications
appear to be crucial to the development of FXS,
as a normal phenotype in the presence of the
CGG repeat allele is observed if
hypermethylation is absent. ASD risk for full-
mutation (>200 CGG repeats) males and females
range from 60% to 67% and 10% to 23%, respec-
tively, based on studies using the Autism Diag-
nostic Interview (ADI) and Autism Diagnostic
Observation Schedule (ADOS) (Clifford et al.,
2007). Shared ASD features include repetitive
behaviors, language impairments, and eye-gaze
aversion.
Prader-Willi and Angelman Syndromes
Both Prader-Willi syndrome (PWS) and Angelman
syndrome (AS) have an increased risk for ASD
(19–37% for PWS and 42–100% for AS) (Hogart,
Wu, LaSalle, & Schanen, 2010). These syndromes
result from a specialized epigenetic mechanism
Epigenetic Mechanisms
called imprinting, a phenomenon by which each
parent contributes different “epigenotypes” via
their germ cells for specific genomic loci. DNA
methylation or histone acetylation marks one allele
of an imprinted gene and prevents its transcription/
expression. This yields monoallelic expression of
an imprinted gene. PWS and AS are caused by
epigenetic errors or chromosomal rearrangements
at an imprinting cluster on chromosome 15q11-13
(e.g., AS results from loss of UBE3A expression,
a gene that is normally expressed exclusively from
the maternal chromosome) (Nicholls & Knepper,
2001). Increased risk for ASD in PWS and AS and
an increased risk for ASD with maternal duplica-
tions of 15q11-13 (with and without PWS and AS)
suggest that a loss of imprinting may increase
susceptibility to ASD (Veltman, Craig, & Bolton,
2005).
Epigenetic Modifications in ASD Candidate
Genes
In addition to one report of ASD association with
increased MECP2 methylation, as mentioned
above, there is some evidence that other
(nonimprinted) ASD candidate genes may be
epigenetically regulated. One study found
increased DNA methylation in the promoter of
the oxytocin receptor gene (OXTR) in blood and
temporal cortex (Gregory et al., 2009). Similarly,
the long allele of the reelin gene (RELN) has been
associated with ASD and appears to cause
decreased gene expression via epigenetic mech-
anisms (Persico, Levitt, & Pimenta, 2006). Sero-
tonin transporter genes and BDNF (brain-derived
neurotrophic factor) are included among other
candidate genes which are being investigated
for evidence of epigenetic regulation
(Rumajogee, Madeira, Vergé, Hamon, & Miquel,
2002). While these genes have not been defini-
tively demonstrated to play a role in ASD, they
are one line of evidence that epigenetic mecha-
nisms could contribute ASD pathogenesis.
Environmental Influences on Epigenetic
Modifications
There is some evidence that certain environmen-
tal exposures may cause epigenetic changes
which can lead to increased risk for ASD. One
Epigenetic Mechanisms
example is prenatal exposure to valproate. The
risk of ASD to children of mothers taking this
drug during pregnancy has been estimated up to
15 times the general population risk (Rasalam
et al., 2005). Two possible mechanisms of
valproate teratogenicity include interference
with folate metabolism, which can modify gene
expression in certain metabolic pathways, and
inhibition of histone deacetylases, which can
result in increased expression of multiple genes
(Phiel et al., 2001). Furthermore, decreased
expression of an autism candidate gene,
NLGN3, has been reported in mice treated with
valproate (Kolozsi, Mackenzie, Roullet,
deCatanzaro, & Foster, 2009).
Future Directions
Epigenetic mechanisms that regulate gene
expression have emerged as a fundamental mech-
anism in developmental biology and the patho-
genesis of disease. New technologies allowing
high-throughput and whole-genome screening
for DNA methylation and chromatin modifica-
tions hold great promise for the identification of
epigenetic determinants in ASD. Given that epi-
genetic modifications to DNA are potentially
influenced by environmental factors, elucidating
the epigenetics of ASD could lead to the devel-
opment of a new era of therapeutics.
See Also
▶ Angelman/Prader-Willi Syndromes
▶ Deoxyribonucleic Acid
▶ Fragile X Syndrome
References and Readings
Clifford, S., Dissanayake, C., Bui, Q. M., Huggins, R.,
Taylor, A. K., & Loesch, D. Z. (2007). Autism spec-
trum phenotype in males and females with fragile
X full mutation and premutation. Journal of Autism
and Developmental Disorders, 37(4), 738–747.
Grafodatskaya, D., Chung, B., Szatmari, P., & Weksberg,
R. (2010). Autism spectrum disorders and epigenetics.
1139 E
Journal of the American Academy of Child and
Adolescent Psychiatry, 49(8), 794–809.
Gregory, S. G., Connelly, J. J., Towers, A. J., Johnson, J.,
Biscocho, D., Markunas, C. A., et al. (2009). Genomic
and epigenetic evidence for oxytocin receptor
deficiency in autism. BMC Medicine, 7, 62.
Hamilton, J. P. (2011). Epigenetics: Principles and
practice. Digestive Diseases, 29(2), 130–135.
Hogart, A., Wu, D., LaSalle, J. M., & Schanen, N. C.
(2010). The comorbidity of autism with the genomic
disorders of chromosome 15q11.2-q13. Neurobiology
of Disease, 38(2), 181–191.
Holliday, R. (1987). The inheritance of epigenetic defects. E
Science, 238(4824), 163–170.
Holliday, R., & Pugh, J. E. (1975). DNA modification
mechanisms and gene activity during development.
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Kolozsi, E., Mackenzie, R. N., Roullet, F. I., deCatanzaro,
D., & Foster, J. A. (2009). Prenatal exposure to
valproic acid leads to reduced expression of synaptic
adhesion molecule neuroligin 3 in mice. Neuroscience,
163(4), 1201–1210.
Nagarajan, R. P., Hogart, A. R., Gwye, Y., Martin, M. R.,
& LaSalle, J. M. (2006). Reduced MeCP2 expression
is frequent in autism frontal cortex and correlates with
aberrant MECP2 promoter methylation. Epigenetics,
1(4), e1–e11.
Nicholls, R. D., & Knepper, J. L. (2001). Genome organi-
zation, function, and imprinting in Prader-Willi and
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and Human Genetics, 2, 153–175.
Persico, A. M., Levitt, P., & Pimenta, A. F. (2006). Poly-
morphic GGC repeat differentially regulates human
reelin gene expression levels. Journal of Neural
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Phiel, C. J., Zhang, F., Huang, E. Y., Guenther, M. G.,
Lazar, M. A., & Klein, P. S. (2001). Histone
deacetylase is a direct target of valproic acid,
a potent anticonvulsant, mood stabilizer, and terato-
gen. The Journal of Biological Chemistry, 276(39),
36734–36741.
Rasalam, A. D., Hailey, H., Williams, J. H., Moore,
S. J., Turnpenny, P. D., Lloyd, D. J., et al.
(2005). Characteristics of fetal anticonvulsant
syndrome associated autistic disorder. Develop-
mental Medicine and Child Neurology, 47(8),
551–555.
Riggs, A. D. (1975). X inactivation, differentiation, and
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Riggs, A. D. (1996). Introduction. In V. E. A. Russo (Ed.),
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Cold Spring Harbor, NY: Cold Spring Harbor Labora-
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Waddington, C. H. (1942). The epigenotype. Endeavour,
1, 18–20.
Epilepsy
Gregory Barnes1, Reet Sidhu2 and
Roberto Tuchman3
1
Department of Neurology, School of Medicine,
Vanderbilt University, Nashville, TN, USA
2
Department of Pediatric Neurology,
Columbia University, New York, NY, USA
3
Department of Neurology, Miami Children’s
Hospital, Weston, FL, USA
Synonyms
Seizure disorder
Short Description or Definition
Epilepsy is operationally defined as more than
one unprovoked seizure of any type. Recent
definitions of epilepsy have emphasized the neu-
rologic, cognitive, psychological, and social con-
sequences of this group of disorders (Fisher et al.,
2005). Epilepsy, like autism, is not one disorder
and is best conceptualized as the epilepsies.
Seizures are clinical events characterized by
paroxysmal, stereotyped, relatively brief inter-
ruptions of ongoing behavior, associated with
electrographic seizure patterns (ILAE, 1981).
The term “subclinical or nonconvulsive seizure”
is used to refer to electrographic patterns
without clinically recognizable cognitive, behav-
ioral, or motor functions or apparent impairment
of consciousness and requires concurrent electro-
encephalogram (EEG) during behavioral testing.
Seizures are differentiated into those that are
provoked secondary to an acute event such as
fever, infection, trauma, or metabolic illness and
those that are unprovoked (i.e., seizures that are
Epilepsy
likely to be genetic). There are two peaks of
seizure onset in autism. The early peak of seizure
onset in autism occurs in the first 5 years of life
and is commonly associated with epileptic
encephalopathies (see below). The second peak
of seizure onset starts in adolescence and con-
tinues into adulthood. This secondary peak of
seizure onset may be more common in individ-
uals with ASD than early onset seizures and as
such may represent a different distribution of
seizure onset than in the general population (Bol-
ton et al., 2011).
Interictal epileptiform discharges and epilep-
tiform activity are terms used interchangeably to
describe abnormal electroencephalogram (EEG)
activity, specifically referring to spikes alone or
accompanied by a slow wave, occurring either
singly or in bursts and lasting at most 1 or 2 s.
The association of epileptiform activity with an
epileptic disorder is variable. The term “subclin-
ical or nonconvulsive seizure” has also been
used to refer to electrographic patterns without
clinically recognizable cognitive, behavioral, or
motor functions or any apparent impairment of
consciousness. Studies on the prevalence of epi-
leptiform activity in individuals with ASD and no
clinical history of seizures range from 6% to 31%
(Kagan-Kushnir, Roberts, & Snead, 2005).
There is significant controversy regarding the
specificity of these findings to the ASD pheno-
type, and it is likely that the high prevalence of
epileptiform activity in ASD is secondary to path-
ophysiological processes common to autism and
other neurodevelopmental disorders. The treat-
ment of intertical epileptiform discharges in chil-
dren with autism remains controversial with little
evidence that suppression of spikes accounts for
behavioral improvement, except in rare clinical
scenarios (see below under epileptic encephalop-
athies) (Tuchman, Alessandri, & Cuccaro, 2010).
Epidemiology
The prevalence of epilepsy in ASD is highly
variable and depends on the cohort studied, with
rates ranging from 5% to 46% (Spence &
Schneider, 2009). The reported rates of epilepsy
in ASD are several fold higher than the 0.5–1%
Epilepsy
prevalence of epilepsy in the general population
but are similar to the prevalence of epilepsy in
a population of children with intellectual disabil-
ity, with the highest rates of epilepsy in those
with severe cognitive impairments (Tuchman,
Cuccaro, & Alessandri, 2010).
Natural History, Prognostic Factors, and
Outcomes
A consistent finding across multiple studies of
autism and epilepsy is that severity of intellectual
disability is a significant risk factor for the devel-
opment of epilepsy in children with ASD (Amiet
et al., 2008). Individuals with ASD and epilepsy
are, as a group, significantly impaired as young
adults (Danielsson, Gillberg, Billstedt, Gillberg,
& Olsson, 2005), and children with autism and
epilepsy have worse cognitive (lower IQ),
adaptive, behavioral, and social outcomes than
children with autism without epilepsy (Hara,
2007; Turk et al., 2009).
Clinical Expression and
Pathophysiology
Clinical Expression
Epilepsy syndromes are differentiated based on
clinical findings, etiology, and patterns of EEG
abnormalities. The most common epilepsy syn-
dromes associated with autism spectrum disor-
ders, especially those in which the epilepsy
begins in the first 3 years of life, are the epileptic
encephalopathies.
Epileptic encephalopathy is defined as “a con-
dition in which the epileptiform abnormalities
themselves are believed to contribute to the pro-
gressive disturbance in cerebral function” (Berg
et al., 2010; Engel, 2001). As a group, the epilep-
tic encephalopathies are associated with regres-
sion or slowing of cognitive, language, or
behavioral development; the hypothesis is that
the seizures or the interictal epileptiform activity
are responsible for the deterioration (Dulac,
1141 E
2001; Nabbout & Dulac, 2003, 2008). Among
these epileptic encephalopathies, West syndrome
or infantile spasms (IS), Landau-Kleffner syn-
drome (LKS), and epilepsy with continuous
spike waves during slow-wave sleep (CSWS) are
most commonly associated with an ASD pheno-
type (Ballaban-Gil & Tuchman, 2000). However,
it should be noted that the ASD phenotype might
not be exclusive to these three encephalopathies;
the ASD phenotype may be under-recognized or
E
under-investigated in other epileptic encephalop-
athies such as Dravet syndrome (Wolff, Casse-
Perrot, & Dravet, 2006).
Infantile spasms are associated with multiple
etiologies and represent a distinct subgroup of
epilepsies with poor cognitive and social out-
comes. Infantile spasms is an age-specific epi-
lepsy syndrome that occurs between 3 and
18 months with a peak age of presentation
between 4 and 8 months of age (Zupanc, 2009).
The seizure consists of a sudden flexion or
extension of the proximal and truncal muscles
which lasts for approximately 0.2–2 s. They are
more prolonged than a myoclonic jerk (<100 ms)
but less sustained than a tonic seizure (few
seconds to minutes). Frequently, they are associ-
ated with high-voltage abnormalities on the
interictal EEG that have been called
hypsarrhythmia. Coincident intellectual retarda-
tion or regression of neurodevelopment in infan-
tile spasms is common. The risk of developing
autism after having infantile spasms is approxi-
mately 46% but can be as high as 69% in those
with infantile spams and significant associated
brain lesions.
Dravet syndrome is a genetically determined
infantile epileptic encephalopathy mainly caused
by de novo mutations in the SCN1A gene
(Scheffer, Zhang, Jansen, & Dibbens, 2009). Pro-
gressive decline or plateau in development occurs
by 1–4 years of age with intellectual disability
and an autism phenotype commonly present
especially in those with greater than five seizures
per month (Wolff et al., 2006). There is emerging
evidence that vaccine encephalopathy, character-
ized by the appearance of seizures and regression
in infants following vaccination, may be second-
ary to SCNA1 gene mutations in these infants,
E 1142
suggesting that vaccine encephalopathy could,
in fact, be a genetically determined epileptic
encephalopathy (Berkovic et al., 2006).
A controversial example of an epileptic
encephalopathy that has been linked to ASD is
Landau-Kleffner syndrome (LKS), an acquired
aphasia in association with an epileptiform EEG
with spikes, sharp waves, or spike and wave
discharges that are usually bilateral and occur
predominantly over the temporal regions (Lan-
dau & Kleffner, 1998). On a continuum with
Landau-Kleffner syndrome is continuous spike
waves during slow-wave sleep (CSWS), an epi-
leptic encephalopathy associated with the EEG
pattern of electrical status epilepticus during
slow-wave sleep (ESES), various seizure types,
and cognitive, motor, and behavioral distur-
bances (Tassinari et al., 2009). Continuous spike
waves during slow-wave sleep and Landau-
Kleffner syndrome are sleep-related epileptic
encephalopathies with common clinical features
including seizures, regression, and epileptiform
abnormalities that are activated by sleep (Nickels
& Wirrell, 2008). In continuous spike waves
during slow-wave sleep, there is a regression in
global skills, while in Landau-Kleffner syn-
drome, the primary clinical manifestation is
a regression of language. Autistic regression
with an epileptiform EEG is the terminology
used to describe the association of an epilepti-
form EEG in children with autistic regression,
e.g., those in whom both language and social
skills are lost. This group of children should be
differentiated from those with LKS. In this group
of children, the language and social skill loss
occurs earlier, before the age of 2, as compared
to those with LKS in which it occurs usually after
age 3 years. In addition, the children with autistic
regression and an epileptiform EEG usually do
not have frequent spikes on the EEG and rarely
have the ESES EEG pattern common in LKS.
The importance of differentiating children with
autism, regression in language and social skills,
and epileptiform EEG from those with LKS is
that there is no evidence that the treatments used
in LKS, such as the use of steroids or surgical
interventions, are effective interventions for this
group of children (Tuchman, 2009).
Epilepsy
Pathophysiology
The word “epileptogenesis” in pediatrics refers to
dynamic processes which constitute the appear-
ance and natural history of epilepsy. The appear-
ance of autism in epilepsy patients and epilepsy
in autism patients suggests that a final common
set of neural pathways and molecular processes
are shared by both autism patients and epilepsy
patients. The understanding of the development
of epilepsy, progression of epilepsy, and interac-
tion between epileptic seizures and cerebral mat-
uration will be critical to our knowledge of
epileptogenesis in autism epilepsy patients.
Mechanisms responsible for epileptogenesis
of partial seizures may be shared among autism
and nonautism patients. Models of partial epi-
lepsy reveal a characteristic course in the devel-
opment of isolated epileptogenic lesions (Thom,
Mathern, Cross, & Bertram, 2010). Children
under 10–11 years of age tend to have epilepti-
form discharges focally in the centrotemporal or
centroparietal regions (Chez et al., 2006). Thus,
mechanisms responsible for focal epilepsy may
be applicable to younger children with autism/
epilepsy. First, a localized structural or molecular
change occurs in the region of brain tissue which
in itself may not cause seizures. Reorganization
of synaptic inputs with altered neural integration
ensues, which, in many cases, change the
regional balance to excessive excitation and path-
ologic synchronization of action potential firing.
Localized interictal EEG spikes occur in this
region, and later, in most cases, spontaneous
seizures are seen emanating from the site.
The kindling model of epilepsy demonstrates
the process of partial epileptogenesis. Kindling is
a process by which initially subconvulsive elec-
trical stimulus to a brain region, such as the
amygdala, is repeated once a day for 21 days.
An initial subconvulsive electrical stimulus may
only evoke an electrographic discharge with little
change in the animal’s behavior (Racine, Tuff, &
Zaide, 1975). The repeated electrical stimulus will
evoke first a behavior arrest (class I seizure) and
then stepwise at day 21 evoke a secondarily gener-
alized tonic-clonic seizure (class V seizure).
An animal is considered fully kindled when the
same stimulus evokes a secondarily generalized
Epilepsy
tonic-clonic seizure over three consecutive days.
Electrophysiologic and structural analyses of kin-
dled animals suggest permanent alterations to
rodent limbic cortex which parallels changes seen
in human temporal lobe epilepsy (Morrell, 1999).
The genetic program activated over a period of
time includes three phases: (1) expression of
immediate early genes and apoptosis genes,
(2) expression of secondary transcriptional regula-
tory proteins, and (3) expression of tertiary or
quaternary target genes (neurotrophins, guidance
cue genes, etc.) in response to transcriptional reg-
ulatory proteins and electrical activity. The end
result of this genetic reprogramming is synaptic
reorganization and epileptogenesis. The final com-
mon pathway here seems to be recurrent excitatory
networks. Kindling causes epileptogenesis by
a variety of possible mechanisms including
(1) reorganization of axons/synaptic connections,
(2) alterations in AMPA and NMDA receptors,
(3) enhanced release of glutamate by neurosecre-
tory mechanisms, and (4) alteration of inhibition
via kainic acid receptor activation (Wang, Smith,
Murphy, & Cook, 2010).
Shared Molecular Pathophysiology Between
Autism and Epilepsy
Genetic Components
The standard hypothesis to explain the overlap of
autism and epilepsy is that an altered balance
between excitation and inhibition is one biological
mechanism for both diseases; thus, the disturbance
in the development of either cortical projection
neurons or interneuron maturation would tip over
this delicate balance. Giving the fact that autism
co-occurs with numerous neurodevelopmental dis-
orders and the complexity of synaptogenesis and
function, it is not surprising that there are multiple
molecules and signaling pathways associated with
the pathogenesis of autism. Subtle perturbations or
alterations in any of these molecules critical in
neurodevelopment, synaptogenesis, and synaptic
function may cause defects in the downstream
common biological pathways within brain circuits
contributing to ASD pathogenesis (Geschwind &
Levitt, 2007).
The genetic architecture of autism includes at
least two distinct genetic mechanisms: rare,
1143 E
private (de novo) single-gene mutations that
may have a large effect in causing ASD and
inherited, common functional variants of
a combination of genes, each having a small to
moderate effect in increasing ASD risk (Abra-
hams & Geschwind, 2008; O’Roak & State,
2008; Veenstra-VanderWeele & Cook, 2004;
Weiss et al., 2009). Rare point mutations range
from ASD risk genes encoding numerous synap-
tic proteins (such as contactin-associated protein-
E
like 2, CNTNAP2; SH3 and multiple ankyrin
repeat domains 3, SHANK3; and neuroligin-3,
NLGN3) to gains or losses of DNA segments,
termed copy number variation (e.g., 16p11.2
and 15q11-q13), and to gross chromosomal
rearrangements that are estimated to occur in
about 7% of autism cases (Abrahams &
Geschwind, 2008).
In epilepsy, genetic advances have identified
ion channel genes as the major category of
epilepsy susceptibility genes, although nonion
channel genes have also been identified to be
associated with epilepsy (Suzuki et al., 2004).
These ion channels include both voltage-gated
and ligand-gated ion channels. The voltage-gated
ion channels include sodium channels like SCN1A,
SCN2A, and SCN1B; potassium channels like
KCNQ2 and KCNQ3; and calcium channels like
CACNA1A (Glasscock, Qian, Yoo, & Noebels,
2007) and CACNB4 (Escayg et al., 2000). The
ligand-gated ion channels include GABAA recep-
tors (Kang & Macdonald, 2009) and nicotinic ace-
tylcholine receptors (Steinlein & Bertrand, 2010).
Mutations of these ion channel genes that either
directly or indirectly enhance excitatory neuro-
transmission or reduce inhibitory neurotransmis-
sion increase brain hyperexcitability and thereby
predispose patients to seizures. Rare copy number
variations, already implicated in ASD (Weiss,
2009), have been noted in patients with idiopathic
generalized epilepsy (IGE) (Carmona-Mora &
Walz, 2010; Sisodiya & Mefford, 2011). IGEs are
a well-defined group of epilepsies, accounting for
a third of all cases of epilepsy in the general
population and an even higher proportion in chil-
dren (1). IGEs usually begin in childhood, are
genetically determined, and have no structural or
anatomic cause (Benbadis et al., 2005). However,
E 1144
the prevalence of this genetic mechanism in IGEs
remains to be established.
There are a number of mutations or variants
in GABAA receptors that have been associated
with epilepsies of various phenotypes (Kang &
Macdonald, 2009; Macdonald, Kang, &
Gallagher, 2010). These mutations/variants
associated with epilepsies have been reported
in a1, b3, g2, and d subunits. Most of the muta-
tions have autosomal dominant inheritance and
have been associated with epilepsy syndromes
comprised of pure febrile seizures (FS), mixed
afebrile and febrile seizures such as CAE and
FS, generalized epilepsy with febrile seizures
plus (GEFS+) syndrome, Dravet syndrome, and
juvenile myoclonic epilepsy (JME). These
mutations include missense, nonsense, and
intronic splice donor site mutations. Most of
the mutations are associated with fairly mild
phenotypes like simple febrile seizures and
CAE which are outgrown with age. In summary,
defects in multiple genes and molecules may
lead to alterations in the final common neural
pathways involved in the pathogenesis of epi-
lepsy and autism. Among all these genetic
and molecular pathways, impaired GABAergic
signaling is a prominent pathology underlying
the pathogenesis of both autism and epilepsy.
Abnormal Brain Development
Both autism and epilepsy have abnormal brain
development. But there are many more studies on
brain development of autism than on epilepsy.
Cross-sectional magnetic resonance imaging
(MRI) studies have long hypothesized that the
brain in children with autism undergoes an abnor-
mal growth trajectory that includes a period of
early overgrowth. The abnormalities in autism
could be broad including frontal and temporal
lobes, amygdala, basal ganglia, corpus callosum,
parietal lobe, and cerebellum (Allen &
Courchesne, 2003). In addition to the identifica-
tion of brain overgrowth in autistic brains
(Courchesne, 2002; Courchesne, Carper, &
Akshoomoff, 2003), Courchesne and his group
also demonstrated the first direct evidence with
Epilepsy
MRI study that anatomic abnormalities within the
limbic system exist from the earliest years of
autism and change throughout development and
up through middle age. It is worth noting that
cerebellar abnormality is repeatedly reported in
most specimens examined, thus challenging the
view that the function of cerebellum is exclu-
sively motor coordination (Allen & Courchesne,
2003). Interestingly, gene mutations in GABRA6
(Dibbens et al., 2009) were also associated with
epilepsy. The transcript of a6 subunit was
reported to be confined to the postnatal cerebel-
lum (Laurie et al., 1992). This may suggest that
this subunit may exist in other unknown brain
areas or argue against the role of cerebellum
simply being motor coordination.
There are shared neuropathologies underlying
ASD and epilepsy (Taylor, Neville, & Cross,
1999; Wegiel et al., 2010). SPECT/PET scans
of autism/epilepsy patients and pediatric patients
with medication-resistant focal epilepsy caused
by focal cortical dysplasia show similar areas of
abnormalities in the frontal or temporal cortex
(Sasaki et al., 2010). The discrete focal areas of
hypometabolism suggest similar cellular abnor-
malities in the cortices of both types of patients
(Sasaki et al., 2010; Taylor et al., 1999; Wegiel
et al., 2010). The initial overgrowth in autism
patients is associated with focal developmental
abnormalities. The focal abnormalities include
subependymal nodular dysplasias, subcortical
and periventricular heterotopias, dysplasias
including either cell loss or increased numbers
of poorly differentiated neurons with disturbed
lamination in neocortex, archicortex, dentate
gyrus, cornu ammonis, and cerebellar cortex
(Taylor et al., 1999; Wegiel et al., 2010). In
autism brain, tuber-like structures as seen in
tuberous sclerosis are detected in cortical and
subcortical regions such as the basal ganglia
(Numis et al., 2011). Older autopsy specimens
tend to be associated with cell loss and disturbed
cortical minicolumns. Posterior regions of the
corpus callosum are also reduced in size in autism
in a study of 3- to 42-year-olds (Schumann et al.,
2010). MRI studies of older ASD children
suggested that altered volumes of caudate nuclei,
hippocampi, amygdale, and corpus callosum are
Epilepsy
associated with higher rates of epilepsy and lower
sensory response rates (Bloss & Courchesne,
2007; Brambilla et al., 2003; Schumann et al.,
2004, 2010). In conclusion, these recent MRI
and neuropathology observations suggest abnor-
mal regulation of brain growth in autism: over-
growth early in life followed by abnormally
slowed growth in some regions, but premature
arrest of growth/poor differentiation followed
by cell loss in others.
The role of pathologic neural activity such as
interictal epileptiform discharges (IEDs) and sei-
zures in the developing brain of children with
ASD is less clear. Evidence from human epilepsy
and ASD patients indicates that there is abnormal
and equivalent histology in human mesial tempo-
ral sclerosis and ASD hippocampi (Blumcke
et al., 2009). These changes include substantial
granule cell loss and architectural abnormalities
like granule cell dispersion, ectopic neurons or
clusters of neurons in the molecular layer, or
bi-lamination (Blumcke et al., 2009). However,
the contribution of abnormal brain development
and neural activity in IGEs has just started to draw
attention. For example, the knock-in mice harbor-
ing GABRG2 (R43Q) is a mutation associated
with febrile seizures and childhood absence epi-
lepsy. Activation of the mutant allele GABRG2
(R43Q) during early development increased the
seizure susceptibility, and inactivation of the
mutant allele would decrease the seizure suscepti-
bility. These data suggest that disruption of the
physiological effects of GABAA receptors during
the sensitive developmental epochs in fetal and
neonatal/infantile life may compromise the devel-
opmental processes that are crucial for normal
brain development and facilitate the development
of epilepsy (Chiu et al., 2008). This may underlie
why patients carrying GABAA receptor subunit
mutations have mental compromise ranging from
mild learning difficulty to mental retardation in
addition to seizures and autism such as those
seen in Dravet syndrome (Li et al., 2011).
Abnormal GABA Receptor and Excitatory
Receptors in Autism
The balance of excitatory and GABA neurotrans-
mission throughout brain development determines
1145 E
the final trajectory of neural pathways responsible
for cognitive and behavioral output in autism and
epilepsy patients. Although it is unknown of
how exactly GABAA receptor function affects
neurodevelopment, a recent study demonstrated
that activation of GABAA receptors leads to
hyperpolarization, increased cell volume, and
accumulation of stem cells in S phase, thereby
causing a rapid decrease in cell proliferation
(Andang et al., 2008). Any subtle change in stem
E
cells may have profound impact in neuronal
function and leave imprint on later brain network
activity. In addition to altered interneuron and
excitatory neuronal numbers, studies on brain
specimen of both autism and epilepsy from multi-
ple investigators have consistently demonstrated
that the expression of GABAA receptors and
ionotropic glutamate receptors is altered in both
disorders (Fetami et al., 2010, Jansen, Peugh,
Roden, & Ojemann, 2010).
In the case of GABA, the alterations extend to
multiple GABAA receptor subunits instead of
single GABAA receptor subunit. This aberrant
profile of GABAA receptors is consistent with
the complex GABAA receptor assembly and
dynamic expression patterns in the brain. In
normal brain, expression of GABAA receptor
subunits varies regionally and temporally. For
example, a1 and g2 subunits have low expression
in early brain but increase over development and
then stabilize through adolescence and adult-
hood, whereas a4 subunit expression is higher in
infants than in older children. But based on
a recent study in epilepsy patient brains, the nor-
mal expression pattern of GABAA receptor
subunit is absent in those with focal cortical dys-
plasia and in those with gliosis (Jansen et al.,
2010). Brain specimens of autism patients have
demonstrated that systematic changes in GABAA
subunit expression (Fatemi et al., 2010; Fatemi,
Reutiman, Folsom, & Thuras, 2009). Oblak dem-
onstrated reduction of GABAA receptors and
benzodiazepine binding sites in both the anterior
and posterior cingulate cortices and fusiform
gyrus in autism (Oblak, Gibbs, & Blatt, 2009,
2011). Given the fact that GABAA receptor traf-
fics and functions as pentamer at the cell surface
and synapse and the receptor stoichiometry of 2a
E 1146
(x)2b(x)1g, 2a(x)2b(x)1d or 2a(x)3b(x)/3a(x)2b
(x), it is not surprising that multiple GABAA
receptor subunits are reduced. The brain regions
that displayed different distribution include supe-
rior frontal cortex, parietal cortex, and cerebel-
lum of subjects with autism (Fatemi et al., 2009,
2010). The fact that multiple regions are
affected suggests the comprehensiveness of
neurodevelopment abnormalities. There are also
multiple mechanisms underlying the GABAA
receptor subunit protein reduction: (1) altered
GABAA receptor mRNA levels or stability,
(2) altered posttranslational modifications which
reduce subunit maturation and receptor forward
trafficking, (3) reduced neuronal numbers due
to cell death of presynaptic interneurons, and
(4) altered epigenetic regulations of GABAA recep-
tor subunits (Samaco, Hogart, & LaSalle, 2005).
Further research is needed to more fully
understand how glutamate receptor and trans-
porter biology is affected in autism and how it
may contribute to epilepsy as a comorbidity in
ASD. The core features of autistic brain develop-
ment suggest that alterations of excitatory neuro-
nal numbers may, in themselves, account for
changes in excitatory receptor concentrations. In
addition to abnormal minicolumnar structure in
the frontal, temporal, and anterior cingulate cor-
tices, Courchesne et al. (2011) recently reported
that neuronal counts in the dorsolateral prefrontal
cortex and the medial prefrontal cortex in autistic
brains were increased by 79% and 29%, respec-
tively, compared to similar young age-matched
males (Casanova, 2006). The idea of increased
proliferation or reduced apoptosis in autistic
brains leading to excessive production of excit-
atory neurons may explain the increases in many
axonal tracts of autistic brains and increased local
functional connectivity (Allen & Courchesne,
2003). Studies of the blood have shown either
increases or decreases in blood glutamate or
blood glutamine (Lam, Aman, & Arnold, 2006).
Gene expression studies have shown
upregulation of several glutamate receptors or
linked genes including EAAT1, GluR1, GluR2,
and GluR3 mRNAs in the cerebellum and hippo-
campus of autistic individuals (Purcell, Jeon,
Epilepsy
Zimmerman, Blue, & Pevsner, 2001). Surpris-
ingly, few actual glutamate receptors or trans-
porters are among identified ASD-associated
genes including kainate receptor GluR6,
metabotropic GluR8 (GRM8), NMDA receptor
GRIN2A, and AMPA receptor-associated protein
GRIP1 (Barnby et al., 2005; Choudhury, Lahiri,
& Rajamma, 2012; Mejias et al., 2011). Many
of these associations are significant since these
proteins control interneuron excitability (GluR6,
GRIN2A), gamma oscillations from parvalbumin
interneurons, critical periods (GRIN2A), and
AMPA/GABA receptor expression (GRIP1 vari-
ants) in synapses (Endele et al., 2010; Fisahn
et al., 2004; Kocsis, 2011; Mejias et al., 2011;
Zhang & Sun, 2011).
Abnormal Neurotransmitter Signaling in
Neurodevelopmental Disorders with Autism
and Epilepsy as a Phenotype
Epilepsy and autism are comorbid in several
neurodevelopmental disorders which, at their
core, have impaired synaptic homeostasis.
These disorders include, but are not limited to,
Dravet syndrome, tuberous sclerosis, Angelman
syndrome, fragile X syndrome, and Rett
syndrome. GABA signaling could participate in
neurodevelopmental disorders because GABA
occupies a central role in development. Patients
with these syndromes often suffer from
autism, intellectual disabilities, and epilepsy.
GABAergic function impairment may be
a common pathway for many neurodeve-
lopmental disorders including autism and epi-
lepsy. It is not surprising given the essential role
of GABA signaling in brain development. The
exact mechanism of the concurrent epilepsy and
autism in these neurodevelopmental disorders
remains unclear. However, from both animal
and genetic studies, altered GABAergic signaling
is consistently observed in these disorders. In
Angelman syndrome, a maternally inherited
deletion of 15q11-13 locus is identified in the
majority of cases. The deletion includes the
UBE3A gene (ubiquitin-protein ligases E3A) as
well as three GABAA receptor subunit genes: the
GABRB3, GABRA5, and GABRG3 (Hogart,
Epilepsy
Nagarajan, Patzel, Yasui, & Lasalle, 2007; Knoll
et al., 1989; Wagstaff, Chaillet, & Lalande,
1991). UBE3A signaling controls EphB-EphrinB
regulation of glutamate synapse development
(Margolis et al., 2010). Conversely, increased
dosage of UBE3A results in mice with autistic-
like behavior and decreased glutamate neuro-
transmission (Smith et al., 2011).
In fragile X syndrome, GABAA receptor sub-
units are downregulated, possibly due to lack of
translational regulation by FMRP1 (D’Hulst
et al., 2006; Fatemi, Folsom, Kneeland, & Liesch,
2011). Studies on fragile X syndrome indicate
that the increased activation of metabotropic
glutamate receptor 5 (mGluR5), a member of
the group I mGluR family, contributes to
a predisposition for the development of epilepsy,
autism, and other neuropsychiatric disorders
(Bianchi et al., 2009). The major neuropsychiat-
ric features of fragile X syndrome are caused by
unchecked activation of mGluR5 (Bear et al.,
2004), and downregulation of postsynaptic
mGluR5 signaling can correct developmental
disorders in the disease (Dolen et al., 2007).
Depolarized firing states of neurons are driven
by recurrent local excitation and inhibition in
a given cortical region which underlies the so-
called slow oscillation neocortical rhythm
(<1 Hz). Aberrant postsynaptic mGluR5 signal-
ing in neocortex of FXR1 KO mice alters this
slow oscillation and inhibitory dendritic cur-
rents from somatostatin interneurons (Hays,
Huber & Gibson, 2011; Paluszkiewicz,
Olmos-Serrano, Corbin, & Huntsman, 2011).
Additionally, transient local hyperconnectivity
of prefrontal cortex during development and
abnormal presynaptic short-term plasticity con-
tributes to slower synaptic responses and inte-
gration of informational processing in the FXR
KO mice (Deng, Sojka, & Klyachko, 2011;
Testa-Silva et al., 2011). All these mechanisms
contribute to the aberrant maturation and func-
tion of synchronized cortical rhythmic activity
needed for behavioral and cognitive output of
neural networks.
In FXR KO mice, increased mTOR signaling
and increased protein synthesis is associated with
1147 E
the above described synaptic pathology and sei-
zures (Carson, Van Nielen, Winzenburger, &
Ess, 2012). In contrast, recent advances in TSC
KO mouse studies show increased synaptic
mTOR signaling, and decreased protein synthe-
sis is associated with reductions in glutamate and
GABA neurotransmission (Auerbach, Osterweil,
& Bear, 2011). In tuberous sclerosis (TSC),
there is altered transcription of genes encoding
glutamatergic and gamma-aminobutyric acid
E
(GABA)-ergic receptors. GABRA1 and
GABRA2 mRNA levels were reduced in both
dysplastic neurons and giant cells compared to
control neurons (White et al., 2001). In Rett syn-
drome, the recent study by Zoghbi et al., (2010)
demonstrated that MeCP2 is critical for normal
function of GABA-releasing neurons and that
subtle dysfunction of GABAergic neurons alone
can recapitulate the numerous neuropsychiatric
phenotypes and epilepsy common to Rett syn-
drome patients (Chao et al., 2010). In addition
to this comprehensive list of neurodevelopmental
disorders, impaired GABAergic signaling is
frequently identified in other ASD- and
epilepsy-associated genes too. For example,
genetic disruption of the autism spectrum disor-
der risk genes MET, PLAUR, and neuropilin-2
induces the alteration of GABAA receptor sub-
units and defects in GABAergic and excitatory
circuitry which lead to autistic-like traits and
epilepsy (Brooks-Kayal, 2010; Eagleson et al.,
2010; Gant et al., 2009; Powell et al., 2003).
In summary, the phenotypical and genomic
heterogeneity of both autism and epilepsy still
remains a challenge. These findings suggest that
the genetic heterogeneity of both autism and
epilepsy may produce similar deficits by bidirec-
tional deviation from normal synaptic homeosta-
sis at GABAergic or excitatory synapses. Future
work using human neuropathology specimens
and models especially those associated with
neurodevelopmental abnormalities will further
elucidate the molecular pathophysiological
mechanisms of aberrant neurotransmitter recep-
tors and their effects on signaling in autism alone,
epilepsy alone, or patients with the autism and
epilepsy phenotype.
E 1148
Treatment
See ▶ Neurologist
See Also
▶ Seizure
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Epilepsy and Autism
▶ Psychomotor Epilepsy
Epinephrine
Alex Bonnin
Keck School of Medicine, University of Southern
California, Los Angeles, CA, USA
Synonyms
Adrenaline; L-Epinephrine; L-Adrenalin;
L-Epinehphrine; Levo-Methylaminoethanol-
catechol; Levoreninum; Lyodrin
Definition
Epinephrine is a catecholamine transmitter and
hormone, generated from the amino acid tyrosine
(or phenylalanine) in a common biosynthetic
pathway with dopamine and norepinephrine.
The enzyme tyrosine hydroxylase converts tyro-
sine to L-dihydroxyphenylalanine (L-DOPA).
L-DOPA is then decarboxylated to dopamine
Epilepsy and Autism
by DOPA decarboxylase (DDC). Dopamine
b-hydroxylase converts dopamine to norepi-
nephrine. Finally, epinephrine is generated
by N-methylation of norepinephrine,
a process catalyzed by phenylethanolamine
N-methyltransferase (E.C. 2.1.1.28, PNMT;
Axelrod, 1962), utilizing S-adenosylmethionine
as the methyl donor.
The adrenal medulla is the major site of
peripheral epinephrine production. Once released
in the blood, it causes systemic vasoconstriction
and gastrointestinal relaxation, stimulates the
heart, and dilates bronchi and cerebral vessels.
In the brain, epinephrine-producing (adrener-
gic) neurons were identified by their expression
of PNMT. Immunohistochemical studies in ani-
mals have established several groups of adrener-
gic neurons (PNMT+) in the medulla oblongata:
ventrolateral A1 and C1 cell groups, dorsomedial
A2 and C2 groups, a rostral midline C3 group,
and an additional unnumbered compact group in
the dorsolateral portion of the nucleus tractus
solitarii (nTS). PNMT-positive neurons have
also been mapped in the human medulla.
Epinephrine exerts its actions via three distinct
types of adrenergic receptors: a1, a2, b. The a1
receptor class (a1A, a1B, and a1D receptors) is
coupled to Gq-type G-proteins. The a2 class
(a2A, a2B, and a2C) of receptors is coupled
to Gi-type G-proteins. The b class of receptors
(b1, b2, and b3) couples to Gs-type G-proteins.
Epinephrine is catabolized to the inactive
compound L-metanephrine through the action of
catecholamine-O-methyltransferase (COMT).
See Also
▶ Catecholamine System
▶ Catechol-O-Methyltransferase
References and Readings
Gai, W. P., et al. (1993). Loss of C1 and C3 epinephrine-
synthesizing neurons in the medulla oblongata in
Parkinson’s disease. Ann Neurol, 33, 357–367.
IUPHAR database. http://www.iuphar-db.org/DATA-
BASE/LigandDisplayForward?ligandId¼509)
Epistasis
Wong, D. L. (2006). Epinephrine biosynthesis: Hormonal
and neural control during stress. Cell Mol Neurobiol,
26(4–6), 891–900.
Wurtman, R. J., & Axelrod, J. (1965). Adrenaline synthe-
sis: Control by the pituitary gland and adrenal gluco-
corticoids. Science, 150, 1464–1465.
Episodic Memory
Diane M. Lickenbrock
Human Development and Family Studies,
The Pennsylvania State University,
University Park, PA, USA
1153 E
References and Readings
Lind, S. E., & Bowler, D. M. (2010). Episodic memory
and episodic future thinking in adults with autism.
Journal of Abnormal Psychology, 119, 896–905.
Toichi, M., & Kamio, Y. (2003). Long-term memory in
high-functioning autism: Controversy on episodic
memory in autism reconsidered. Journal of Autism
and Developmental Disorders, 33, 151–161.
Tulving, E. (1983). Elements of episodic memory. Oxford,
UK: Clardendon Press.
Tulving, E. (1985). How many memory systems are there?
American Psychologist, 40, 385–398.
E
Wheeler, M. A., Stuss, D. T., & Tulving, E. (1997).
Toward a theory of episodic memory: The frontal
lobes and autoneoetic consciousness. Psychological
Bulletin, 3, 331–354.

Synonyms
Epistasis
Autobiographical memory
Kai Wang
Dept of Psychiatry and Dept of Preventive
Definition Medicine, The Zilkha Neurogenetic Institute,
Keck School of Medicine, University of Southern
A subtype of the declarative memory system California, Los Angeles, CA, USA
which stores personally experienced events
(e.g., a memory of a specific place or time).
Episodic memory is often associated with autobio- Definition
graphical context (e.g., remembering what
happened on one’s tenth birthday). This specific In genetics, epistasis refers to the interaction
type of memory is assessed using a free recall task. between two or more genes, such that the pheno-
Research has shown that individuals with type differs from what would be expected if the
Autism Spectrum Disorder can have impairments genes exert their effects independently. The
in episodic memory. importance of epistasis has been increasingly
recognized in human genetics in recent years,
since it may be partially responsible for the
See Also “missing heritability” observed for complex dis-
eases, that is, the aggregation of the marginal
▶ Declarative Memory effects from genetic variants associated with
▶ Explicit Memory a disease do not completely explain the heritabil-
▶ Free Recall ity of the disease.
▶ Memory
▶ Memory Assessment
▶ Memory Development Historical Background
▶ Recognition Memory
▶ Retrieval of Information The term “epistasis” was first used by the English
▶ Rote Memory geneticist William Bateson in 1909 in his book
▶ Semantic Memory “Mendel’s Principles of Heredity.” It was used to
▶ Short-Term Memory describe deviations from Mendelian inheritance
E 1154
patterns due to one gene masking the effects of
another gene, that is, a particular variant in one
locus prevents a variant at another locus from
manifesting its effects. The book also popular-
ized Mendel’s Law of Segregation and Law of
Independent Assortment, originally conceived by
Gregor Mendel in the eighteenth century and
rediscovered in 1900. Bateson was also the first
person to use the word “genetics” to describe the
study of inheritance and the science of variation,
and he codiscovered genetic linkage with
Reginald Punnett.
There are many well-known examples of epis-
tasis in genetics. One of the oldest examples
described in humans is on the expression of the
ABO blood group system. Some individuals have
a rare condition where they lack a protein called
the H antigen. The H antigen is used to form
A and B antigens, so these individuals cannot
make A antigen or B antigen, and this scenario
is often referred to as the “Bombay phenotype.”
Individuals with Bombay phenotype can only be
transfused with blood from other Bombay pheno-
type individuals. Even though these individuals
with Bombay phenotype may have A or B genes,
they cannot express the A or B blood group, and
instead they appear to be blood group O. In this
example, the H antigen masks the effect of the
A or B genes, resulting in epistasis.
Another well-known example of epistasis is
on genetics of coat color in mice. Two coat-color
loci are involved in the control of coat color. At
the first locus, having color (allele A) is dominant
over lack of color (allele a). At the second locus,
having the coat color agouti (allele B) is domi-
nant over black (allele b). Consider a mouse that
has homozygous aa alleles in the first locus: it
will show no coat color, regardless of its geno-
type at the second locus (BB or Bb or bb). Thus,
the variants at the first locus mask the effect of the
second locus, and there is epistasis between the
two loci.
It is important to emphasize that Bateson’s
simple form of epistasis, as illustrated by the two
well-known examples above, is merely a limited
form of epistasis that works on Mendelian trait and
is intuitively appealing to most biologists.
However, a broader form of epistasis – from
Epistasis
a population genetics perspective – involves
more sophisticated statistical modeling and is
more relevant for complex traits genetics. For
example, two alleles at two different loci may
each increase adult height by 1 cm on average,
but when these two alleles occur together in the
same individual, they may increase the height by
4 cm, which is more than what would be expected
if the two alleles exert their effects independently.
This broader form of epistasis is what typically
emerges from current literature and is one of the
hotly researched areas in genetics of complex dis-
eases and traits.
Current Knowledge
Contribution of Epistasis to “Missing
Heritability”
Genome-wide association studies (GWASs) have
been very successful in identifying and replicat-
ing disease susceptibility loci for common and
complex human diseases. These studies assay
whole-genome SNP markers (typically 500,000
or more) for individuals grouped by different
phenotypes (such as patients and control sub-
jects) then test the statistical association between
each marker and the phenotype. Top findings
showing strong evidence of statistical signifi-
cance are then replicated in another set of sam-
ples. As of December 2010, over 1,200 human
GWASs have examined over 200 diseases and
traits and found almost 4,000 SNP associations.
A question that often arises in GWAS is
“where is the missing heritability?” The question
refers to the fact that the collection of variants
discovered in GWAS only explains a minor frac-
tion of the heritability when simply added
together, even for diseases or traits that are highly
heritable. Multiple reasons have been proposed to
explain the missing heritability, including (1) rare
variants at known loci that act independent of
common causal variants, (2) rare mutations in
many thousands of loci, (3) copy number vari-
ants, (4) gene-gene interactions, (5) hidden envi-
ronmental factors and epigenetic changes, and
(6) wrong diagnosis of “common diseases.”
Among these possible explanations, epistasis or
Epistasis
gene-gene interactions could play a major role in
contributing to “missing heritability,” since if the
effect of one locus is masked by effects at another
locus, power to detect the first locus is likely to be
reduced and elucidation of the joint effects at the
two loci will be hindered. If more than two loci
are involved, complex multiway interactions may
be present, further complicating the situation. For
complex traits, given the known involvement of
many contributing loci detected in GWAS, it is
quite likely that epistasis will have to play a role.
Therefore, it is reasonable to suspect that epista-
sis is a ubiquitous component of the genetic
architecture of complex traits and diseases, such
as neuropsychiatric and neurodevelopmental
disorders.
Epistasis in Autism
Although several syndromes with single-gene
causes, such as Rett syndrome and fragile
X syndrome, share some phenotypic features
with autism, it is widely recognized that autism
is not a single-gene disease. Instead, the molecu-
lar pathophysiology of autism perhaps requires
many genes in multiple biological pathways.
However, the exact underlying genetic architec-
ture for autism is still not well understood, and
less is known on how different genetic compo-
nents interact with each other. It is possible that
rare, highly penetrant variants play a major role in
each individual patient (oligogenic model), or it
is also possible that thousands of variants, each
with moderate effect sizes, contribute to autism
pathogenesis. The first argument is supported by
the observation that many highly penetrant muta-
tions, especially large-scale deletions, have been
enriched in patients with autism, although each
patient may have different combinations of rare
variants. The second argument is supported by
the observation that sophisticated statistical
approaches that utilize information from whole-
genome markers, each with small effect sizes,
can explain a large fraction of schizophrenia sus-
ceptibility. Besides these standing hypotheses, it
is also possible that epistatic interactions play
a major role in autism pathogenesis and that
genetic variants with moderate effects sizes,
when present in particular combination, will
1155 E
lead to much higher effect sizes that ultimately
results in autism pathogenesis.
There are sporadic reports in literature on
observed epistasis in autism susceptibility. For
example, Coutinho et al. have tested for epistasis
between loci with marginal effects in autism. In
addition to the significant independent effects,
evidence for interaction between SLC6A4 and
ITGB3 markers was also found. The overall
results implicate SLC6A4 and ITGB3 gene inter-
E
actions in both autism etiology and in serotonin
level determination, providing evidence for
a common underlying genetic mechanism and
a molecular explanation for the association of
platelet hyperserotonemia with autism. With the
wider application of GWAS and copy number
variation studies, more epistasis may be observed
in autism in the future.
Physical Interaction Versus Statistical
Interaction
The word “interaction” is sometimes used to infer
epistasis; however, there are two types of inter-
actions in the contexts of genetics: physical inter-
action versus statistical interaction. Proteomics
techniques, such as yeast two-hybrid systems,
are now available to locate proteins that interact
with one another in a protein complex. In these
cases, proteins bind to each other, resulting in
molecular functions that cannot be performed
by each components of the protein complex. In
contrast, statistical interaction summarizes geno-
type-phenotype relationships using population-
level data rather than proteomic data. In fact,
genes with statistical interactions do not have to
physically bind to each other.
Statistical Methods to Detect Epistasis from
Genetic Data
Mathematically, the quantitative genetic concept
of epistasis may be represented for two loci by the
linear model
y ¼ u þ a1 x1 þ a2 x2 þ d1 z1 þ d2 z2 þ iaa x1 x2
þ iad x1 z2 þ ida z1 x2 þ idd z1 z2
where y is a quantitative phenotype and xi and zi
are dummy variables related to the underlying
E 1156
genotype at locus i. The coefficients m, a1, d1, a2,
and d2 represent genetic parameters that may
be estimated corresponding to the mean effect,
additive effect, and dominance effects at the
two loci; iaa, ida, ida, and idd correspond to
epistatic interaction effects. Lack of epistasis
in this model implies that all interaction
coefficients are zero. In this case, the resulting
model is
y ¼ u þ a 1 x1 þ a 2 x2 þ d1 z 1 þ d2 z 2
where each allele exerts their effect indepen-
dently with the effect size of a1, a2, d1, and d2,
respectively.
In practice, it is more typical to assume
a simple additive model where the effect sizes
of a homozygote doubles that of a heterozygote.
Therefore, it is convenient to use a single variable
x or z to denote the number of copies of the allele
2 present at the locus. The linear model can then
be simplified as
y ¼ u þ ax þ dz þ iad xz
In this case, lack of epistasis in this model
implies that iad is zero, that is, model will
simply be
y ¼ u þ ax þ dz
For binary traits, a logit function is typically
used to model the response variable:
logitðpÞ ¼ logðp=ð1  pÞÞ
¼ u þ ax þ dz þ iad xz
where the outcome of interest (such as probability
of disease) is defined to be p.
It is important to note that besides these simple
parametric linear models, other forms of model-
ing strategies also exist. There are unique advan-
tages for using linear models as it is intuitively
simple to interpret and it is relatively easy to
implement. However, they may have limitations
for detecting nonlinear patterns of interactions.
For example, when many genes are involved in
explaining complex diseases or traits, the number
Epistasis
of predictor variables (genotype combinations)
grow exponentially as each SNP is added to the
model. Estimation of parameters in such linear
models can be unstable and may easily result in
overfitting the data. Additionally, linear models
generally assume that genetic factors involved in
interaction also exhibit independent marginal
effects, but this may not be the case in reality
(although it is not known how common it is for
interaction to be present in the absence of any
marginal effects). Nonparametric approaches,
especially those involving modern machine-
learning approaches, may have their unique
advantages in specifically addressing these issues
(see below).
Future Directions
The Role of Epistasis in Genetic Susceptibility
to Autism
Despite the recent discovery of multiple com-
mon and rare genetic variants that confer
autism susceptibility with different effect
sizes, whether and how these genetic factors
interact with each other is currently not
known. Furthermore, the form of epistasis
involved in autism pathogenesis may include
both gene-gene and gene-environment interac-
tions. Many environmental factors, such as air
pollution and paternal age, have been linked to
autism susceptibility in recent years, but
whether these environmental risk factors func-
tion independently of genetic risk factors is an
unexplored area of research. On the other hand,
it is well known that certain environmental
factors, including radiation, smoking, and
older age, can increase the possibility of de
novo genetic alterations, such as de novo copy
number variants (CNVs). Given the known
involvement of de novo variants in autism, it
is highly reasonable to suspect that there may
be gene-environment interactions that play
a role in increasing genetic susceptibility to
autism. This hypothesis needs to be tested in
future larger scale genetic studies that also col-
lect various aspects of environmental variables.
Epistasis
Testing Epistasis in Genome-Wide Level
In recent years, a large collection of methods
have been developed to detect the presence of
epistasis from population-level genetic data. By
allowing for epistatic interactions between can-
didate disease loci, it may be possible to succeed
in identifying genetic variants with weak mar-
ginal effects that may otherwise evade detection.
In addition, some statistical or computational
models for modeling genome-wide epistasis
(such as support vector machine approaches and
penalized regression approaches) can be easily
adapted for prediction of phenotypes from geno-
types, enabling the implementation of personal-
ized disease risk predictions.
Although the importance of epistasis has been
increasingly recognized, one may argue that it
has never really received the attention that it
deserves in genetic association studies, especially
in GWAS. The major reason is not the lack of
methods to test epistasis per se, but the need to
adjust the enormous burden of multiple testing,
and the lack of appropriate biological interpreta-
tion to significant results. In typical GWAS with
500,000 SNP markers, testing genome-wide epis-
tasis implies the need to test for approximately
250 billion hypotheses, even when considering
only two-way interactions. The situation
becomes worse when three-way or multiway
interactions are considered. With the availability
of massively parallel computational platform,
this may no longer be a computational issue, but
how to appropriately calculate the effective num-
ber of independent tests and accordingly adjust
multiple testing is a problem without consensus
on solution.
The Development of Bioinformatic
Approaches
Although sophisticated approaches based on var-
ious forms of linear models have been used to
detect epistasis in genome-wide scale, they may
have some intrinsic limitations as discussed
above. Therefore, novel approaches from
1157 E
the computational science arena, including
machine-learning approaches such as random
forests (RFs) and multifactor dimensionality
reduction (MDR), have been developed to
address these issues. Some of these approaches
represent “black-box” modeling strategies: rather
than fitting the data into a prespecified statistical
model that the investigators believes in, these
methods aim to let the data tell us what the appro-
priate model is. This is a rapidly growing area
E
for methods development, and several recent
reviews highlighted the advantage of these
methods.
Biological Interpretation of Epistasis
When significant epistasis is found, the next nat-
ural question is how to interpret the results and
how to leverage this information to better under-
stand the genetic architecture of complex dis-
eases. Unfortunately, there is no easy answer to
these questions. Many factors may blur the seem-
ingly straightforward interpretation of the epi-
static effects. For example, many modern
genetic association studies use SNP markers,
which rely on linkage disequilibrium to detect
indirect associations. Since the marker allele
most likely may not be the true disease allele,
the detected epistatic effects could be due to the
artifact of the imperfect tagging of the disease
allele. Even worse, if the marker allele, being
a common allele, is merely a proxy for multiple
rare functional alleles (so-called synthetic asso-
ciation), then it will not be possible to tell which
rare allele has epistasis with variants at another
loci or whether the observed epistasis merely
reflects a “synthetic epistasis” on multiple rare
alleles. Therefore, significant statistical results
may not always lead to a biologically sound
explanation, and it is important not to
overinterpret the statistical results.
In summary, direct biological inference from
the results of analysis on epistasis can be very
difficult. Compared to marginal effects of indi-
vidual markers in association tests, the biological
knowledge gained from investigation of epistasis,
E 1158 Equinus Gait

even in the presence of strong statistical evi-

dence, can be quite limited. The most effective ER
interpretation of epistasis probably depends on
some levels of prior biological knowledge on ▶ Emotional Regulation
the genes under investigation, as well as addi-
tional molecular evidence, rather than a pure sta-
tistical exercise on P values and effect sizes.
ERN

▶ Error-Related Negativity
See Also

▶ Genetics
▶ Genome-Wide Association Error of Measurement
▶ Modifier Genes and Autism Susceptibility
▶ Measurement Error

References and Readings

Bateson, W. (1909). Mendel’s principles of heredity. Error Correction

Cambridge: Cambridge University Press.
Carlborg, O., & Haley, C. S. (2004). Epistasis: Too often
neglected in complex trait studies? Nature Reviews
Genetics, 5(8), 618–625.
Cordell, H. J. (2002). Epistasis: What it means, what it
doesn’t mean, and statistical methods to detect it
in humans. Human Molecular Genetics, 11(20),
2463–2468.
Coutinho, A. M., Sousa, I., Martins, M., Correia, C.,
Morgadinho, T., Bento, C., Marques, C., Ataı́de, A.,
Miguel, T. S., Moore, J. H., Oliveira, G., &
Vicente, A. M. (2007). Evidence for epistasis between
SLC6A4 and ITGB3 in autism etiology and in the
determination of platelet serotonin levels. Human
Genetics, 121(2), 243–256.
Moore, J. H., Asselbergs, F. W., & Williams, S. M. (2010).
Bioinformatics challenges for genome-wide associa-
tion studies. Bioinformatics, 26, 445–455.
Moore, J. H., & Williams, S. M. (2009). Epistasis and its
implications for personal genetics. American Journal
of Human Genetics, 85(3), 309–320.
Phillips, P. C. (2008). Epistasis–the essential role of gene
interactions in the structure and evolution of genetic
systems. Nature Reviews Genetics, 9(11), 855–867.
Wolf, J. B., Brodie, E. D., & Wade, M. J. (2000). Epistasis
and the evolutionary process (1st ed.). New York:
Oxford University Press.
Equinus Gait
▶ Toe Walking
Josh Pritchard1 and Mark Malady2
1
Applied Behavior Analysis, Florida Institute of
Technology, Orlando, FL, USA
2
Florida Institute of Technology, Melbourne,
FL, USA
Definition
In the applied autism literature, error correction is
a procedure that details what a trainer or program
implementer does when the learner engages in an
incorrect response during a teaching opportunity.
Error correction aims to enhance learning by teach-
ing the learner the appropriate response and
increasing the learner’s contact with reinforcement
contingencies rather than simply extinguishing
errors. This procedure is intended to help learners
acquire skills much faster and with less frustration
than simply allowing trial and error. In other words,
it teaches the learner what to do instead of just
allowing them to make mistakes and try to deter-
mine the correct response on their own.
There are three types of procedures for error
correction. All three types are presented after the
learner engages in a defined incorrect response
(including no response within a specific amount
Error-Related Negativity
of time) and are combined with a differential
reinforcement procedure. Each of the three is
defined independently below:
1. A procedure consisting of a series of response
prompts following a learner’s error to increase
the probability of the learner immediately
engaging in the target response.
2. A series of repetitions of the target response
contingent on a learner’s error, typically com-
bined with a differential reinforcement proce-
dure (Worsdell et. al., 2005).
3. Manipulation of the stimulus or addition of
a stimulus contingent on the learner engaging
in an error, typically combined with
a differential reinforcement procedure (Cata-
nia, 2007).
The type of error correction in teaching
approaches can vary substantially. For instance,
some approaches use an “errorless” approach,
in which they provide the correction (in the
form of prompts) before or as soon as the
incorrect response occurs. Other approaches
utilize the “no-no prompting” correction in
which they gradually increase the amount of
error correction. Often these are chosen and
tailored on the basis of the learner’s skill level
and learning goals.
See Also
▶ Differential Reinforcement
▶ Hand-Over-Hand Assistance
▶ Modeling
▶ Prompt Hierarchy
▶ Prompt System
▶ Prompting
References and Readings
Catania, C. (2007). Learning. New York: Sloan.
Gena, A., Couloura, S., & Kymissis, E. (2005). Modifying
the perspectives of preschoolers with autism using in-
vivo or video modeling and reinforcement contingen-
cies. Journal of Autism and Developmental Disorders,
35, 545–556.
Rodgers, T. A., & Iwata, B. A. (1991). An analysis of
error-correction procedures during discrimination
training. Journal of Applied Behavior Analysis, 24,
775–781.
1159 E
Error-Related Negativity
Michael J. Crowley
Developmental Electrophysiology Laboratory,
Yale Child Study Center, New Haven,
CT, USA
Synonyms
E
ERN
Definition
The error-related negativity, or ERN, is an
electrical brain signal measured with an electro-
encephalogram. Detectible at the scalp via the
event-related potential (ERP), the ERN occurs
when an individual makes a behavioral error.
The ERN is typically evoked with simple
cognitive tasks when an individual responds
incorrectly or responds when a response should
be withheld. The ERN manifests as a negative
deflection in the ERP at approximately
80–150 ms following error commission, time-
locked to an individual’s response. The ERN is
largest at central to frontal-central scalp regions.
The most likely neural generator of the ERN is
the anterior cingulate cortex, with converging
evidence coming from fMRI (Ito, Stuphorn,
Brown, & Schall, 2003), EEG source modeling
(Luu, Tucker, Derryberry, Reed, & Poulsen,
2003), and brain lesion research (Stemmer,
Segalowitz, Witzke, & Schönle, 2004).
See Also
▶ Anterior Cingulate
▶ Cingulate Cortex
▶ Feedback-Related Negativity
References and Readings
Ito, S., Stuphorn, V., Brown, J. W., & Schall, J. D. (2003).
Performance monitoring by the anterior cingulate
cortex during saccade countermanding. Science,
302(5642), 120–122.
E 1160
Luu, P., Tucker, D. M., Derryberry, D., Reed, M., &
Poulsen, C. (2003). Electrophysiological responses to
errors and feedback in the process of action regulation.
Psychological Science, 14, 47–53.
Stemmer, B., Segalowitz, S. J., Witzke, W., & Schönle,
P. W. (2004). Error detection in patients with lesions
to the medial prefrontal cortex: An ERP study.
Neuropsychologia, 42(1), 118–130.
Escalante’s Syndrome
▶ Fragile X Syndrome (FXS)
Escape Extinction
▶ Escape Training
Escape Training
John Molteni
Institute for Autism and Behavioral Studies,
University of Saint Joseph, West Hartford, CT,
USA
Synonyms
Escape extinction
Definition
Escape training/extinction is a behavioral
procedure that is generally used to treat escape
or avoidance maintained behaviors. Utilization
of escape extinction procedures includes
discontinuing the escape contingency upon the
occurrence of the behavior. That is, when
a behavior that is reinforced by negative rein-
forcement (removal of a stimulus contingent on
a response that leads to an increase in that
Escalante’s Syndrome
behavior), preventing escape contingent on that
behavior will lead to a reduction in that behavior.
Escape extinction has been demonstrated as
being effective alone and as part of a treatment
package for a variety of escape maintained
behaviors. One area of emphasis in the research
literature where escape extinction has been
widely used is feeding interventions for individ-
uals with selective feeding or food refusal.
Escape extinction in the form of non-removal of
the spoon (i.e., presenting the bolus of food
within close proximity to the mouth of the par-
ticipant until the food is accepted) is one example
of escape extinction. Extinction procedures have
several potential side effects including the extinc-
tion burst – an immediate increase in the fre-
quency or intensity of behavior following the
discontinuation of reinforcement – extinction-
induced aggression-an escalation in aggressive
behavior and spontaneous recovery, that
is, a return to higher levels of the target behavior
after a behavior has been reduced to low levels. In
order to address the potential side effects of
extinction, use of reinforcement-based proce-
dures (e.g., reinforcement of food acceptance in
the above example) is strongly recommended.
Behaviors can demonstrate resistance to extinc-
tion, meaning that the behavior will persist even
when the reinforcement for that behavior has
been removed. There are several factors that
may contribute to this resistance including the
level of motivation for the reinforcer (i.e.,
the higher the value of the reinforcer, the more
resistant it is to extinction), the schedule of rein-
forcement, the alternative sources of reinforce-
ment for the same behavior, the amount of effort
required to emit the behavior (i.e., the higher the
effort the less resistant to extinction), and
whether the behavior has been under extinction
before with rapid decreases with each application
of extinction. Use of extinction is not
recommended when the individual engages in
high-intensity behavior such as dangerous
aggressive and self-injurious behavior as an
increase in the intensity of behavior would lead
to risk of injury to the individual or others.
Escitalopram
See Also
▶ Differential Reinforcement
▶ Negative Reinforcement
References and Readings
Ahearn, W. H., Kerwin, M. L., Shantz, J., & Swearingin,
W. (1996). An alternating treatments comparison of
two intensive interventions for food refusal. Journal of
Applied Behavior Analysis, 29, 321–332.
Cooper, J. O., Heron, T. E., & Heward, W. L. (2007).
Applied behavior analysis (2nd ed.). Upper Saddle
River, NJ: Pearson Education.
Lalli, J. S., Casey, S., Goh, H., & Merlino, J. (1994).
Treatment of escape-maintained aberrant behavior
with escape extinction and predictable routines.
Journal of Applied Behavior Analysis, 27, 705–714.
Piazza, C. C., Patel, M. R., Gulotta, C. S., Sevin, B. M., &
Layer, S. A. (2003). On the relative contributions of
positive reinforcement and escape extinction in the
treatment of food refusal. Journal of Applied Behavior
Analysis, 36(3), 309–324.
Zarcone, J. R., Iwata, B. A., Hughes, C. E., & Vollmer, T. R.
(1993). Momentum versus extinction effects in the treat-
ment of self-injurious escape behavior. Journal of
Applied Behavior Analysis, 26, 135–136.
Escitalopram
Carolyn A. Doyle1 and Christopher McDougle2
1
Indiana University School of Medicine,
Indianapolis, IN, USA
2
Lurie Center for Autism/Harvard Medical
School, Lexington, MA, USA
Synonyms
Brand names: Anxiset E (India); Cipralex
(Canada); Lexam; Lexamil; Lexapro; Seroplex
Indications
According to the official prescribing information,
escitalopram is FDA-approved to treat major
1161 E
depressive disorder (MDD) in adults and in ado-
lescents aged 12–17 years old, both acutely and
as maintenance therapy (Forest Pharmaceuticals,
2011). It is also approved for the acute treatment
of generalized anxiety disorder (GAD) in adults.
It is not approved for children under the age of
12 years.
Escitalopram is not approved for the treatment
of autism spectrum disorders (ASDs). ASDs
include the DSM-IV-TR diagnoses of autistic
E
disorder, Asperger’s disorder, and pervasive
developmental disorder, not otherwise specified
(PDD-NOS). The decision to use escitalopram in
the treatment of established clinical indications
that may co-occur with ASDs, as mentioned
above, or for commonly observed symptoms of
ASDs, such as hyperactivity, inattention, irrita-
bility, aggression, repetitive behaviors, and social
impairment, can be made on an individual basis
by the treating practitioner. This will be discussed
in more detail in the “Clinical Uses” section.
Mechanisms of Action
Escitalopram is a selective serotonin reuptake
inhibitor (SSRI). Normally, serotonin is released
from the presynaptic axon terminal to travel
across the synaptic cleft and attach to the post-
synaptic axon terminal. Any excess serotonin
remaining in the cleft is picked up by the seroto-
nin reuptake transporter in the presynaptic axon
to be degraded and recycled. It is hypothesized
that a depletion of serotonin available to act on
the postsynaptic axon results in symptoms expe-
rienced in some mood and anxiety disorders,
including sadness, nervousness, guilt, loneliness,
apathy, and avolition. Escitalopram attaches
itself to the serotonin reuptake transporter and
prevents whatever serotonin remains in the cleft
from being taken back up in the presynaptic
neuron. The excess serotonin is free to attach to
postsynaptic receptors and exert its intended
effects.
Escitalopram begins acting immediately to
inhibit serotonin reuptake, but like other SSRIs,
E 1162
its antidepressant and anxiolytic effects are often
not experienced for up to 6–8 weeks. This is
thought to be due to gradual changes SSRIs
make on serotonin receptor sensitivity. It is
believed that the decreased amounts of serotonin
found in mood and anxiety disorders cause the
postsynaptic axon to upregulate the number of
postsynaptic axonal receptors expressed. In
other words, a decreased amount of serotonin in
the synaptic cleft results in an increased amount
of receptors at the ready. When escitalopram
enters the picture, the level of serotonin in the
cleft rises. Postsynaptic receptors respond to the
serotonin increase and send messages to the axon
nucleus about the changes in the synaptic cleft.
The nucleus begins downregulating the amount
of serotonin receptors ready to receive serotonin.
These changes are gradual and are believed to
take 6–8 weeks before being fully completed,
reflecting the amount of time before many
patients begin feeling relief from their symptoms.
Like other SSRIs, escitalopram’s antagonism
of the postsynaptic 5-HT2C receptor results in
some of its unique therapeutic effects. When
serotonin attaches to the 5-HT2C receptor, it
blocks the release of neurotransmitters norepi-
nephrine and dopamine in the brain. When
escitalopram blocks the postsynaptic 5-HT2C
receptor, norepinephrine and dopamine are
instead released and exert their effect in the pre-
frontal cortex. The effect is activating, often lead-
ing patients to feel more energized and less
fatigued, with improved concentration and atten-
tion. Escitalopram’s effects can also be described
as anxiolytic, and it is currently FDA-approved
for the treatment of GAD. Escitalopram is often
considered the “quintessential SSRI” as it only
contains the S enantiomer, unlike the related
compound citalopram (Celexa), whose racemic
makeup includes both R and S enantiomers.
(Enantiomers are a pair of chemical structures
that exist as mirror images and subsequently
exert different effects.) Escitalopram’s lone
S enantiomer yields a “purer” serotonin reuptake
inhibition response and removes some side
effects that exist in the racemic (mixed) com-
pound. This unique property allows for
Escitalopram
escitalopram to be more efficacious at lower
doses given the absence of a potentially interfer-
ing R enantiomer. The lack of CYP450 enzyme
interactions makes escitalopram one of the best
tolerated of the SSRIs, although it is not yet
generic and therefore can be expensive.
Specific Compounds and Properties
(S)-1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-
1,3-dihydroisobenzofuran-5-carbonitrile
Clinical Use (Including Side Effects)
FDA-Approved Clinical Uses
In adults, escitalopram is FDA-approved to treat
MDD, both acutely and as maintenance therapy,
and for the acute treatment of GAD (Forest Phar-
maceuticals, 2011). Per the official prescribing
information, escitalopram is typically started at
10 mg once daily for the treatment of MDD with
a recommended maximum of 20 mg daily. If the
dose is increased to 20 mg once daily, it should
occur after a minimum of 1 week. For GAD in
adults, the recommended starting and target dose
is 10 mg once daily. The goal of treatment is
complete remission of symptoms and prevention
of future relapses, so escitalopram is taken both
throughout and in between clinical relapses
(Stahl, 2009). Although escitalopram can elimi-
nate symptoms while being taken, it does not cure
MDD or GAD, and symptoms can reoccur after
the medicine has been stopped. If escitalopram is
to be discontinued, a gradual dose reduction is
recommended (Forest Pharmaceuticals, 2011).
After the first episode of depression in the treat-
ment of adults with MDD, escitalopram should
be taken for 1 year following symptom relief
(Stahl, 2009). After the second or any subsequent
episodes of depression, treatment with
escitalopram may be indefinite to avoid relapse
of symptoms. Treatment of GAD may also
require indefinite treatment.
Regarding the pediatric population,
escitalopram is FDA-approved for the treatment
Escitalopram
of MDD in adolescents aged 12–17 years (Forest
Pharmaceuticals, 2011). There are no clinically
approved uses of escitalopram for children under
the age of 12 years. In the treatment of adolescent
MDD, escitalopram is typically started at 10 mg
once daily with a recommended maximum of
20 mg daily (Forest Pharmaceuticals, 2011). Per
the official prescribing information, if the dose is
increased to 20 mg once daily, it should occur
after a minimum of 3 weeks.
Clinical Uses of Escitalopram in Autism
Spectrum Disorders
Regarding pediatric populations, there is minimal
evidence to suggest the effectiveness of
escitalopram in children and adolescents with
autism. Interestingly, antidepressants have been
the most commonly prescribed psychotropic
medications in treating symptoms associated
with ASDs (Aman, Lam et al., 2005). Given the
frequent use of SSRIs in autism, it is imperative
that prescribing clinicians balance the benefit of
such medications in lieu of their side effects. In
2004, the FDA released safety warnings about the
increased risk of suicide-related behaviors in
children and adolescents taking SSRIs, which
subsequently curtailed the prescribing of SSRIs
to this population (Nemeroff, Kalali et al., 2007).
The decision to use escitalopram in the treatment
of established clinical indications that may co-
occur with autism should therefore be made on an
individual basis by the treating practitioner after
careful consideration of the available data.
There are currently no published randomized,
placebo-controlled trials examining the use of
escitalopram in treating symptoms associated
with ASDs. Therefore, minimal conclusions can
be drawn about the efficacy of escitalopram in
treating both adults and children with ASDs.
Among the available research, a study by
Owley, Walton et al. (2005) attempted to shed
light on this subject. This prospective, open-label
study included 28 children (25 males, 3 females)
diagnosed with an ASD (71% with autistic disor-
der) between the ages of 6 and 17 years. They
received escitalopram over the course of
10 weeks, which was increased to a maximum
1163 E
dose of 20 mg/day as tolerated. This study con-
cluded that escitalopram was “useful in treating
some difficulties associated with pervasive devel-
opmental disorders (PDDs)” as evidenced by
a 61% response rate, improvement in the areas
of irritability (the most improvement), hyperac-
tivity, lethargy, stereotypy, and inappropriate
speech, and “significant improvement” via the
Clinical Global Impressions scale. Again,
a prescriber should be cautious in generalizing
E
these results to the larger population of patients
with ASDs given the study’s design and small
sample size which limit its interpretation.
Side Effects
Escitalopram is often considered the most toler-
ated of the SSRIs due to its simplified chemical
structure, which potentially results in “purer”
inhibition of the serotonin transporter and fewer
cytochrome P450 enzyme-mediated drug interac-
tions (Stahl, 2008). Stimulation of serotonin
receptor subtypes (5-HT2A, 5-HT2C, 5-HT3, and
5-HT4) in various parts of the brain likely causes
many of the SSRIs’ observed side effects.
A small amount of increased synaptic serotonin
shortly after initiating therapy is often enough to
cause some side effects, even if the clinical ben-
efit is not yet apparent to the patient. Therefore, it
is possible that side effects may be experienced
earlier than symptom relief when first starting
treatment with escitalopram (Stahl, 2008). Side
effects experienced may also be dose dependent
(i.e., they increase as the dose increases) or time
dependent (i.e., they start right after taking the
medication but diminish with time) (Stahl, 2009).
Patients who are treated for MDD are at
increased risk for experiencing suicidal thinking
and behavior. Antidepressants as a class have
been shown to increase the risk of suicidal think-
ing and behavior in children, adolescents, and
young adults (ages 18–24) with MDD and other
psychiatric disorders (Forest Pharmaceuticals,
2011). Such risk should be carefully considered
when prescribing escitalopram in the pediatric
and young adult population. Escitalopram is cur-
rently not approved for use in children younger
than age 12 years. According to Stahl (2009),
E 1164
gastrointestinal side effects are common and can
include decreased appetite, nausea, diarrhea, con-
stipation, or dry mouth. Sexual dysfunction is
a common side effect in both males and females
and is due to the effect of increased serotonin in
both the brain and the region of the spinal cord
regulating sexual response. In males, this
includes delayed ejaculation, erectile dysfunc-
tion, and decreased sexual desire. In women,
this includes decreased sexual desire and
anorgasmia. Central nervous system side effects
include insomnia or sedation, agitation, tremors,
headache, and dizziness or lightheadedness.
Patients with undiagnosed bipolar or psychotic
disorders may be vulnerable to the activating prop-
erties of escitalopram, resulting in hypomania,
mania, or psychosis. Patients may also experience
vasodilatation, dry mouth, diaphoresis, or abnor-
mal vision. Increased serotonin can lead
to diminished dopamine release, which may lead
to emotional flattening, apathy, and cognitive
slowing in some patients. Escitalopram has not
been shown to result in clinically important body
weight changes (Forest Pharmaceuticals, 2011).
Of note, SSRIs have been found to yield side
effects in people with ASDs, particularly agita-
tion, hyperactivity, aggression, and insomnia
(Posey, Erickson et al., 2006). Extrapyramidal
symptoms (Sokolski, Chicz-Demet et al., 2004)
and hypomania (Damore, Stine et al., 1998) have
also been observed in case reports. These results
are limited by a lack of placebo-controlled stud-
ies, although there is some evidence to suggest
that children with ASDs may be more likely to
develop such side effects relative to adults with
ASDs (Posey, Erickson et al., 2006).
See Also
▶ Antidepressant Medications
▶ Anxiolytic Drugs
▶ Anxiolytics
▶ Citalopram
▶ Depressive Disorder
▶ Dopamine
▶ Generalized Anxiety Disorder
▶ Norepinephrine
ESCS
▶ Repetitive Behavior
▶ Serotonin
▶ Serotonin Reuptake Inhibitors (SRIs)
▶ Stereotypic Behavior
References and Readings
Aman, M. G., Lam, K. S., et al. (2005). Medication pat-
terns in patients with autism: Temporal, regional, and
demographic influences. Journal of Child and Adoles-
cent Psychopharmacology, 15(1), 116–126.
Damore, J., Stine, J., et al. (1998). Medication-induced
hypomania in Asperger’s disorder. Journal of the
American Academy of Child and Adolescent Psychia-
try, 37(3), 248–249.
Forest Pharmaceuticals prescribing information. 2011.
Retrieved from http://www.frx.com/pi/lexapro_pi.pdf
Nemeroff, C. B., Kalali, A., et al. (2007). Impact of pub-
licity concerning pediatric suicidality data on physi-
cian practice patterns in the United States. Archives of
General Psychiatry, 64(4), 466–472.
Owley, T., Walton, L., et al. (2005). An open-label trial of
escitalopram in pervasive developmental disorders.
Journal of the American Academy of Child and
Adolescent Psychiatry, 44(4), 343–348.
Posey, D. J., Erickson, C. A., et al. (2006). The use of
selective serotonin reuptake inhibitors in autism and
related disorders. Journal of Child and Adolescent
Psychopharmacology, 16(1–2), 181–186.
Sokolski, K. N., Chicz-Demet, A., et al. (2004). Selective
serotonin reuptake inhibitor-related extrapyramidal
symptoms in autistic children: A case series. Journal
of Child and Adolescent Psychopharmacology, 14(1),
143–147.
Stahl, S. M. (2008). Stahl’s essential psychopharmacol-
ogy: Neuroscientific basis and practical applications
(3rd ed., pp. 522–539). New York: Cambridge Univer-
sity Press.
Stahl, S. M. (2009). Stahl’s essential psychopharmacol-
ogy: The prescriber’s guide (3rd ed., pp. 171–179).
New Delhi: Cambridge University Press.
ESCS
▶ Early Social-Communication Scales (ESCS)
ESP
▶ Evaluation of Sensory Processing
Establishing Operations 1165 E
Keller and Schoenfeld (1950) who first coined the
Establishing Operations term “establishing operations” (Vargas, 2009).
Establishing operations have been discussed
Susan A. Mason extensively in the literature on verbal behavior
Services for Students with Autism Spectrum and are independent variables that have been
Disorders, Montgomery County Public Schools, present in the study of applied behavior analysis
Silver Spring, MD, USA since its inception. Experimental analysis of
behavior and applied behavior analysis have
both been concerned with complex ways of
Definition
arranging reinforcers to change behavior (Bailey
E
& Burch, 2002).
Establishing operations (EOs) are “events that
alter the value of a reinforcer” (Michael, 1982).
EOs are sometimes called motivating operations
Rationale or Underlying Theory
(see MOs) (Vargas, 2009). EOs can be condi-
tioned or unconditioned. They may exist in
As stated earlier, EOs change the value of
many forms and often are reliant on states of
a reinforcer. In a classroom situation, this is
deprivation; however, it is important to note that
especially important as we want learners to
just as deprivation is experienced throughout the
acquire new skills. Ensuring specific states of
day, aversive stimulation is also common in our
deprivation, or altering the value of a reward
environment. Vargas (2009) noted, “Aversive
such that it functions as a powerful reinforcer,
situations are establishing operations for avoid-
enhances the potential for positive learning
ance/escape behaviors.” Another form of
outcomes. In the field of autism, establishing oper-
establishing operation is known as “value alter-
ations play an important part for increasing verbal
ing.” In this situation, a stimulus or set of stimuli
behavior, especially when teaching manding
function to make the reinforcer more reinforcing.
(requesting). When there is a strong establishing
For example, effective advertising increases the
operation in place, there is an increased likelihood
desire to have the product being advertised;
that the target behavior will be demonstrated in
advertising is not reliant on a state of deprivation,
order to access the reinforcer. Accessing the rein-
and in a sense, it may create an aversive situation
forcer, in turn, strengthens the response and
if everyone else has the item that is advertised and
increases the likelihood that it will occur again
the person who does not have the item stands out
under the same or similar conditions.
because they are “different.” Key components of
EOs are that an establishing operation “precedes
the response it is functionally related to and it
Goals and Objectives
increases the effectiveness of a particular stimu-
lus change as reinforcement” (Peterson, 1978). In
As noted previously, the goal of using EOs is to
sum, an establishing operation determines what
alter the value of a reinforcer such that the target
a person wants at any given time, and it is
response will be more likely to occur. Use of
dynamic in nature because establishing opera-
EOs increases the effectiveness of a particular
tions are always changing (Cooper, Herron, &
stimulus change as reinforcement. EOs play an
Heward, 2007).
important role in behavior change.

Historical Background
Historically, Skinner (1953) introduced the con-
cept of EOs in his first publications when he
wrote about a “third variable”; however, it was
Treatment Participants
Studies that examine the effects of EOs have been
executed and replicated for years and have
E 1166
focused on many different populations in the
research from animals to human beings.
The examination of EOs has been particularly
prevalent in the research conducted on verbal
behavior and, of late, has included studies
focused on teaching persons with autism spec-
trum disorders to request desired items. Research
has also focused on aberrant behaviors of persons
with severe disabilities who engage in self-injury,
aggression, and pica (McGill, 1999).
Treatment Procedures
EOs have been included in such treatment
procedures as (a) extinction, (b) noncontingent
reinforcement, (c) multicomponent treatment
packages, (d) social attention (behavioral
momentum), (e) functional communication train-
ing, (f) naturalistic/incidental language training,
and (g) social-positive, social-negative, and auto-
matic reinforcement (McGill, 1999).
Efficacy Information
Large quantities of research exist to point to the
efficacy of EOs within the context of reinforcer
delivery. Researchers have demonstrated the
salience of student choice in increasing the
value of a reinforcer (Mason & Egel, 1995;
Mason, McGee, Farmer-Dougan, & Risley,
1989; Lerman et al., 1997), varying the presenta-
tion of the reinforcer (Egel, 1980, 1981), states of
deprivation versus satiation (Volmer & Iwata,
1991), and properties of sensory stimuli as rein-
forcers (Ferrari & Harris, 1981; Rincover &
Newsom, 1985). Each of these studies has dem-
onstrated that EOs are intimately linked to what
a person wants at any given time and in so doing,
establishing operations affect the potency of the
reinforcer.
Outcome Measurement
Current outcome measures for EOs support
their importance across a variety of research
Establishing Operations
applications. Quantitative data collected during
research regarding EOs has repeatedly proven
that EOs have an impact on behavior change.
EOs have been examined in the context of teach-
ing language and communication to students with
autism as well as other disabilities. They also
have been examined within the context of other
studies of verbal behavior as well as reduction of
aberrant behaviors such as self-injury, pica, and
aggression. Although the bulk of research that
has been conducted involves single-subject
research design, the quantity of replication across
behaviors, subjects, and settings speaks to the
validity of EOs in the context of examining rein-
forcers and reinforcement.
Qualifications of Treatment Providers
Although not explicitly stated in the research,
persons who provide reinforcers in the context
of teaching and/or behavior change projects
should be knowledgeable in the field of
applied behavior analysis and/or experimental
analysis of behavior. Careful examination of
the effects of any behavior change procedure
should be closely monitored through data
collection and analysis; modifications should
be implemented according to data analysis.
As such, qualified behavior analysts are pro-
viders that can use EOs within the context of
educational procedures and behavior change
procedures. Special education and general
education teachers and paraprofessionals are
capable of implementing reinforcement
procedures under the guidance of a qualified
behavior analyst.
References and Readings
Bailey, J. S., & Burch, M.R. (2002). Research methods in
applied behavior analysis (p. 182). Thousand Oaks,
CA: Sage Publications.
Cooper, J. O., Heron, T. E., & Heward, W. L. (2007).
Positive reinforcement. In Applied behavior analysis
(2nd ed., pp. 263–365). Upper Saddle River, NJ: Pear-
son, Merrill Prentice Hall.
Ethics
Egel, A. L. (1980). The effects of constant vs varied
reinforcer presentation on responding by autistic chil-
dren. Journal of Experimental Child Psychology, 30,
455–463.
Egel, A. L. (1981). Reinforcer variation: Implications for
motivating developmentally disabled children. Jour-
nal of Applied Behavior Analysis, 14, 345–350.
Ferrari, M., & Harris, S. L. (1981). The limits and moti-
vating potential of sensory stimuli as reinforcers for
autistic children. Journal of Applied Behavior Analy-
sis, 14, 339–343.
Keller, F. S., & Schoenfeld, W. N. (1950). Principles of
psychology. New York: Appleton.
Lerman, D. C., Iwata, B. A., Rainville, B., Adelinis, J. D.,
Crosland, K., & Kogan, J. (1997). Effects of reinforce-
ment choice on task responding in individuals with
developmental disabilities. Journal of Applied Behav-
ior Analysis, 30, 411–422.
Mason, S. A., McGee, G. G., Farmer-Dougan, V., &
Risley, T. R. (1989). Client selected rewards:
A practical strategy for ongoing assessment of stimu-
lus preference in the classroom. Journal of Applied
Behavior Analysis, 22, 171–179.
Mason, S. A., & Egel, A. L. (1995). What does Amy like?:
Using a mini reinforcer assessment to increase student
participation in instructional activities. Teaching
Exceptional Children, 28, 42–44.
McGill, P. (1999). Establishing operations: Implications
for the assessment, treatment, and prevention of prob-
lem behavior. Journal Applied Behavior Analysis, 32,
393–418.
Michael, J. (1982). Distinguishing between discriminative
and motivational functions of stimuli. Journal of the
Experimental Analysis of Behavior, 37, 149–155.
Peterson, N. (1978). Establishing operations. In An intro-
duction to verbal behavior (pp. 19–21). Michigan:
Behavior Associates.
Rincover, A., & Newsom, C. D. (1985). The relative
motivational properties of sensory reinforcement
with psychotic children. Journal of Experimental
Child Psychology, 24, 312–323.
Skinner, B. F. (1953). Science and human behavior.
New York: Macmillan.
Vargas, J. S. (2009). Verbal behavior. In Behavior analy-
sis for effective teaching (pp. 245–258). New York:
Routledge.
Volmer, T. R., & Iwata, B. A. (1991). Establishing oper-
ations and reinforcement effects. Journal of Applied
BehaviorAnalysis, 24, 279–291.
Wilder, D. A., & Carr, J. E. (1998). Recent advances in the
modification of establishing operations to reduce aber-
rant behavior. Behavioral Interventions, 13, 43–59.
Estrogens (Female Sex Hormones)
▶ Sex Hormones
1167 E
ESY
▶ Extended School Year (ESY) Services
Ethics
Pat Walsh
E
Centre of Medical Law and Ethics, Dickson Poon
School of Law, Somerset House East Wing,
Kings College London, London, UK
Definition
Broadly speaking, ethics is the philosophical
study of how we ought to live and what kinds of
people and societies we ought to be or become.
While the term sometimes refers to the system-
atic study of reasoning about how we ought to act
often called moral philosophy, ethics is also
concerned with matters of the most fundamental
practical import. Central among its questions are
those to do with how, as individuals and societies,
we ought to treat others, why we ought to treat
them in that way, how we should evaluate the
motives underlying actions, and our responsibil-
ity for the predictable consequences of our
actions and policies. Variations in answers to
questions of this sort often depend on different
general viewpoints drawn from moral theories
such as deontology or consequentialism or from
various religious perspectives, all with their dif-
ferent meta-ethical and ontological assumptions.
In addition to this philosophical input, reflection
on many ethical issues, such as those raised by
autism spectrum disorders, should be informed
by empirical research to a large extent.
However, a continuing lack of knowledge
about the biological causes of autism and its
neurobiological bases means that there is
a corresponding uncertainty about the identifica-
tion and resolution of the moral issues specific to
autism and about how much illumination can be
drawn from more general and established ethical
discourses such as those concerning disability
E 1168
rights or reproductive ethics. Given the current
state of knowledge about autism, there are actual
and emergent ethical issues relating to its diag-
nosis and categorization, its prevention and cure,
its treatment, and its associated research practices
and agenda. All of these ethical concerns tend to
have both conceptual and empirical aspects.
Historical Background
As a neurobiological developmental condition,
autism has almost certainly always existed in
the human population. However, it was only rec-
ognized as a distinct condition in the mid-
twentieth century. Hence the concept of autism
has a relatively short history. From the 1940s
until the 1980s, autism was understood as
a categorical condition affecting a relatively
small number of people and characterized by
a distinctive set of behavioral features such as
severe delays in language, impaired cognitive
skills, and a profound lack of emotional contact
with others. The goal of therapy was largely to
“free” the child from the shell of isolation
imposed by autism. Later, the idea of autism as
a psychological problem was replaced by the idea
of it as a biologically based problem. Treatment
and research strategies changed accordingly
while preserving the ultimate goal, assumed to
be ethically straightforward, of its remediation. In
the last three decades, a new body of knowledge
has emerged from studies documenting the com-
plex pattern of strengths as well as weaknesses
present in autism and from autobiographical writ-
ings by people with autism, such as Temple
Grandin. The introduction in the 1980s of the
idea that autism is best understood as
a spectrum condition was an attempt to capture
the heterogeneity of autism and the many ways it
is experienced by those affected and remains
hugely influential in thinking about autism
(Wing, 1981). Clearly, then, while autism is not
a new condition (or range of conditions), the
understanding and concept of autism are rela-
tively new, still evolving, and currently quite
contested – all of which reservations enter into
the ethical debate about autism.
Ethics
Current Knowledge
One of the major difficulties in identifying and
clarifying the ethical issues raised by autism is
the sheer range of ways in which the condition
manifests itself. People with autism are located
somewhere on a broad spectrum from low to high
functioning, reflected by, for example, the range
in IQ from severe intellectual impairment to high
IQ or in communication styles from no speech or
language use to high, often eccentric, articulacy,
associated with the condition. The concept of
a spectrum also captures the variabilities in
health, in developmental difficulties, and in sen-
sory problems that also contribute to the different
profiles of people affected by autism.
The general public remains largely unaware of
this level of complexity. An increasing current
cultural fascination with autism is fed by repre-
sentations of it established by books like The
Curious Incident of the Dog in the Night-Time
and iconic films like Rainman, where the
savantism of the main autistic character has led
many people to believe that people with autism
generally possess similarly unusual talents. In
reality, of course, the majority of diagnosed indi-
viduals sit at points along the spectrum rather
than at or near its extreme ends. Among the
possibilities, he or she may be a person who is
profoundly intellectually impaired and nonver-
bal; or someone who is extremely disabled but
has unique strengths in an area such as art, music,
or mathematics; or an individual who works
effectively in solitude but is overcome by serious
social difficulties when asked to work in direct
contact with others. Moreover, the position of
individuals on the spectrum is not fixed through
the course of their life, because the condition is
developmental and because they may learn social
and adjustment skills that may minimize their
symptoms. The withdrawn and nonverbal child
with autism, for instance, may grow into a “high-
functioning” adult. Furthermore, it seems that in
any given period of time, an individual with
autism may fit behavioral descriptions of both
high and low functioning, in different respects
and even in different settings. In comparison
with other recognized disabilities then – both
Ethics
those which are categorical such as cerebral palsy
or being wheelchair-bound, and those like deaf-
ness, blindness, and Down’s syndrome where
people may be affected to different degrees –
autism seems unique in the sheer range of its
symptoms and behaviors, in the relatively plastic
nature of its symptoms (especially early in life)
and in the possibility of movement along a wide
spectrum through the course of life. The hetero-
geneity of autism – perhaps more effectively
captured by the notion of a “landscape” than
a “spectrum” – has led some scientists to suggest
that rather than one unique phenomenon, there
may be different “autisms,” with different under-
lying biological processes and developmental
pathways (Happe, Ronald, & Plomin, 2006).
The fact of heterogeneity presents obvious dif-
ficulties for identifying appropriate medical and
educational interventions but it also hugely com-
plicates ethical questions about how we should
regard those affected by autism and how we should
respond to and intervene in their lives. Hence it is
to be expected that any appropriate ethical judg-
ment about autism will tend to be cautious, provi-
sional, and open to much qualification.
One example of this is provided by the process
of diagnosis. Initial diagnosis may provide the
occasion whereby individuals and their families
come to understand for the first time the reason
for the problems they have been experiencing
and, importantly, it may serve as the mechanism
through which they can access the range of inter-
ventions and supports that are available. On the
other hand, it currently confirms someone as
a person with a neurologically based disorder,
with all the implications of that for how the indi-
viduals view themselves, how others view them,
and how they are viewed by services, teachers,
employers, and so on. The clear moral serious-
ness of this is compounded by difficulties in mak-
ing the diagnosis secure. First, in not a few cases,
there will be the difficulty, implicit in the notion
of a spectrum, of establishing a nonarbitrary cut-
off point between behavior considered “normal”
or “mildly eccentric” and behavior considered
“disordered.” Second, in many more cases, the
general difficulty of applying the accepted
criteria with confident objectivity will be felt.
1169 E
The diagnosis of autism currently involves
assessing an individual’s developmental history
and patterns of behavior against purely behav-
ioral criteria as set out in the internationally rec-
ognized diagnostic manuals, the Diagnostic and
Statistical Manual of Mental Disorders
(DSM-IV, 2000) and the International Classifica-
tion of Diseases (ICD-10, 2010). Though mini-
mal, these criteria are arrayed in complex ways
such that there is no behavior or set of behaviors
E
that unequivocally denote autism. Because the
genetic and neurobiological bases of autism are
as yet largely unknown, no more objective phys-
ical tests are available to the diagnostician. That
lack has led to an intensive search for biological
markers, which in addition to shedding light on
the causes of autism, might also be clinically
useful in complementing and improving its
behavioral diagnosis and in enabling its earlier
detection. To date, comparatively little has been
achieved in identifying biomarkers with clinical
utility – though if and when they are found they
may well pose new ethical challenges in the field
of autism (Walsh, Elsabbagh, Bolton, & Singh,
2011). Third, there is the undermining effect of
the uncertainty noted earlier as to how well
autism is established as a cohesive syndrome.
The Medical Research Council of Great Britain
puts this uncertainty this way: “Whilst it is well
known that autism involves impaired social com-
munication, language impairment, and repetitive,
stereotyped interests, it is still unknown whether
this constellation of impairments is inherent in
a cohesive syndrome (usually called Autism
Spectrum Disorder or ASD), or whether it is an
artefact of diagnostic practice” (MRC, 2010).
The question raised is whether there is such
a thing as autism in the natural biological world
(Timimi, Gardner, & McCabe, 2011). It is clearly
morally important that diagnostic dialogues
should acknowledge these various serious diffi-
culties and uncertainties to all concerned.
Asking whether those dialogues should not
also include references to the positive aspects of
autism brings a fundamental and profound ques-
tion into focus: what value should be placed on
autism as a condition, and on different aspects of
the condition? Is it enough, or even correct, to
E 1170
characterize autism solely as a disability and, as
such, something to be prevented or cured where
medically and ethically possible? The challenge
here is to the prevailing “deficit model” of autism.
So, the exclusively negative character of the
criteria in the diagnostic manuals – the “impair-
ment” is characterized by examples of “failure,”
“lack,” and “stereotyped,” “repetitive,” and
“abnormal” behaviors – evokes the response
that this characterization is implicitly evaluative
and question-begging, rather than scientific. The
challenge is also to many forms of treatment and
intervention that, following the reasoning that
guides diagnosis, focus strongly on counteracting
behaviors taken to be undesirable. Whether in
diagnosis or in treatment, there seems to be
a good case for emphasizing the more positive
aspects of autism such as the presence of strong
persistent interests, attention to detail, and
unusual memory, as well as the heightened skills
that are associated with some forms of autism,
such as great visual acuity, perfect musical pitch,
and remarkable mathematical prowess (Walsh,
2010).
The idea that autistic behavior could be under-
stood in terms of a “triad of impairments” in
communication, imagination, and social interac-
tion, which emerged in the late 1970s, became the
impetus for many influential theoretical develop-
ments (Wing & Gould, 1979). Psychologists have
attempted to explain each of these fundamental
deficits, with the aim of clarifying the forms of
treatment that could ameliorate and compensate
for them. According to one theory, people with
autism lack a “theory of mind” in being unable to
understand the perspectives and points of view of
other people (Baron-Cohen, 1995). A second
“executive function” theory explains some
aspects of the repetitive behaviors seen in autism
as an inability to plan sequences and actions
(McGregor, Nunez, Cebula, & Gomez, 2008).
A third “weak central coherence” theory is
based on the idea that people with autism cannot
process differences in a manner that makes them
cohere into a general pattern (Frith, 1989). Some
philosophers have taken the first of these theories
in particular, that people with autism are
“mindblind,” as posing at least a legitimate
Ethics
query as to whether they have the full moral
status of “persons” (Barnbaum, 2008). The argu-
ment draws on a putative distinction between the
concepts “human being” and “person” which
gained currency in bioethical debates about the
moral permissibility of abortion in the 1970s.
Being genetically human, it was (and is) argued,
is a morally irrelevant fact, while the term “per-
son” identifies those morally important features
of beings, including human beings, that should
guide our estimate of their moral status and,
thereby, our thinking and decision-making in
their regard. Features of persons said to provide
reasons for regarding them as subjects of moral
concern and bearers of the fundamental protec-
tion of rights vary, but centrally include con-
sciousness, self consciousness, a capacity for
rational decision-making, and a capacity to com-
municate. In possessing none of these character-
istics, it was argued that a human fetus is not
a person in this sense and that abortion may
therefore be morally permissible. The same dis-
tinction has since been sometimes considered in
relation to people in a persistent vegetative state,
and the severely demented. In regard to autism, it
is suggested that the lack of a functioning theory
of mind means people with autism are unable to
recognize that others have beliefs, preferences,
emotions and desires independent of their
own. The resulting lack of empathy leads to an
inability to relate to others as persons in their own
right and to enter into meaningful reciprocal rela-
tionships with them. Even more fundamentally,
they may not be able to reflect on their own
mental states. On this view of the matter, at
least some autistic people fail on two of the
criteria of personhood. Though undoubtedly
conscious, they may not be conscious of other
people in the meaningful ways central to human
relationships, and they may not be self-conscious
in the ways necessary to qualify for moral
personhood.
The more general question of the value to
place on autism is also seen as having to engage
with philosophical discussions of the conditions
necessary for a good or flourishing human life.
Most accounts of these conditions give a central
place to the emotions, including particularly
Ethics
having personal relationships and a sense of affil-
iation with other people (Nussbaum, 2006).
Many of us (including many autistic people)
would agree that friendship, for example, is an
essential contributor to our well-being and recog-
nize that autistic people have particular difficul-
ties in this area. However, it is sometimes argued
that individuals who lack a theory of mind, like
those with autism, simply cannot live a full
flourishing human life because their inability to
empathize compromises their friendships and
their sense of affiliation with others.
What might be said in response to these
suggestions of the severe limits on the value of
autistic life, said to follow from their
“mindblindness”? First of all, if this deficit
hypothesis is not valid – not correct, or only
partly correct – none of the ethical implications
described would follow. And in fact there are
many problems about the precise status of the
mindblindness hypothesis, to do with its explan-
atory power and specificity to the case of autism,
how it interacts with the other two “fundamental
deficit” theories, and, crucially, whether it can
incorporate and reflect the idea of a spectrum of
abilities. At present, it may be best viewed as
a description rather than an explanation of autis-
tic behavior, or as a step on the way to a full and
coherent psychological explanation of autism.
But, second, even if the “mindblindness” theory
is correct, neither of the claims said to follow,
about the moral status of people with autism and
the possibility of a flourishing autistic life, would
necessarily follow. It is extremely important to
remember that the notion of a moral person at
play here is highly stipulative, a matter of moral
argument and decision rather than an empirical
discovery of facts about human beings. Indeed,
the long history of the idea that those who are
“different from us” should thereby be placed
outside the circle of our moral concern or
assigned a diminished level of moral status
is an ignominious one. Again, accounts of
a flourishing human life that assign so central
a place to friendship and the emotional life may
be seen as simply begging the question when it
comes to people with autism. Even for non-
autistic people, the need for friendship and
1171 E
socialization fluctuates and may be quite mini-
mal. To assume that socialization with others is
so important that we cannot have well-being
without it may be to buy far too much into
a contemporary culture which values extrovert
behavior. Furthermore, it can be seen as danger-
ous, for the future if not the present. Arguing that
autistic people alive today have a less flourishing
life than the rest of us may be a more or less
serious problem for them, but its implications
E
may be much more fateful for a future context
in which emergent genetic technologies will play
a major role in reproductive decisions about
whether to prevent the birth of disabled
individuals.
The advent of a “neurodiversity” movement
led by, and giving a voice to, people on the
autistic spectrum and their families and sup-
porters has brought a sharp political edge to this
ethical question of value. Drawing on a wider
political debate about disabilities and disability
rights, and paralleling campaigns by other disad-
vantaged groups to change societal perspectives
of their condition, it forces attention on to the
complexities and contested nature of the concept
“normality,” the positive aspects of autistic spec-
trum conditions, and the advantages as well as the
justice of respect for cognitive differences. For
this movement, autism is simply a neurologically
atypical, but not abnormal, human variation.
A distinction between “neurodiverse” and
“neurotypical” functioning displaces the concep-
tually and morally problematic distinction
between “normal” and “abnormal” functioning,
with the implication that we should no longer
think of autism as a condition requiring funda-
mental treatment, correction, or prevention. Sup-
port for this stance is sometimes drawn from the
list of famous people – including Isaac Newton,
Albert Einstein, Carl Jung, Immanuel Kant,
Vincent Van Gogh, Bill Gates, and Andy Warhol,
among others – who are deemed to have had, or to
have, autistic traits. Whatever their case to case
legitimacy, these attributions have been suffi-
ciently plausible to contribute to a shift in the
perception and representation of autism, from
outright “disability” toward “difference,” while
also encouraging those with autism to celebrate
E 1172
the distinctive strengths of their historical com-
munity. There is a risk to be guarded against,
however, that emphasis on a biological basis of
“difference” – a still unidentified, but presumed
to be “deep,” basis – may inadvertently reinforce
queries regarding the moral status of people with
autism.
On the other side of the debate about how to
value autism, an equally vocal lobby regards
autism as a serious disability and supports
funding of the kind of scientific research that
might lead to prevention and cure. It should be
noted that these objectives are shared by many
carers of autistic people and many autistic people
themselves. This lobby claims that the
neurodiversity movement underestimates the
grave effects autism has on the lives of everyone
involved. It does not, and cannot, represent those
so severely disabled by autism that they are inca-
pable of speaking for themselves, or the families
and carers of those with severe cognitive impair-
ments, or even those high functioning individuals
who often experience acute isolation and loneli-
ness. Clearly, this conflict, among other things,
reflects and trades on the many ways autism
impacts on peoples’ lives, sometimes terribly –
or terribly at some times – sometimes positively,
by virtue of its spectrum nature and general
heterogeneity.
The autism research agenda is a major focus of
the conflict. In spite of the growing influence of
the neurodiversity movement, early detection,
prevention, and cure seem to be the main impetus
and the overriding goals of biomedical research
into autism. The National Institute of Mental
Health in the United States, for example, pro-
claims its vision to be “a world in which mental
illnesses are prevented and cured” and names
autism as one of a group of “serious, often life-
threatening illnesses for which we need reliable
diagnostic tests, new treatments, and effective
strategies for prevention” (National Institute of
Mental Health [NIMH], 2008). One of the largest
autism charities in the world, Autism Speaks,
declares itself “dedicated to funding research
into the causes, prevention, treatment and a cure
for autism,” and has donated $160 million to such
research since its inception in 2005 (Autism
Ethics
Speaks, 2012). The official mission statements
of such research agencies also include research
support for those who have to live with autism –
and they and their supporters are not necessarily
opposed to respecting cognitive difference. It
remains, however, that these seem not to be
their priorities. One of the main bones of conten-
tion in this area is about whether research funding
should be directed toward improving the lot of
autistic people living now rather than be for the
benefit of future generations of those with autism:
proponents of the neurodiversity approach have
little trouble suggesting research projects that
would have objective practical benefit for those
who live with autism, if only funds were more
equitably allocated.
However, the more basic criticism from the
neurodiversity perspective is that the goals of
prevention, radical treatment, and cure are funda-
mentally misguided. The value issues here are
complex. They include, but go well beyond,
interpretations of the key terms. A “cure,” to
start with it, ought to be rather more than some-
thing that would ameliorate the negative impacts
of autism on affected individuals. But taken to
mean something that “gets rid” of the autism, it
faces two distinguishable challenges. The first,
relating to identity, is captured in a website state-
ment of a view that is often expressed by those in
the neurodiversity movement: “To ‘cure’ some-
one of autism would be to take away the person
they are, and replace them with someone else”
(Aspies for Freedom, 2010). The obliteration of
the condition is seen here as amounting to the
destruction of an identity. That this view is per-
suasive owes much to two features of autism, first
that by its cognitive nature it impacts more or less
pervasively on a person’s life, and second that it
is an early-onset condition and is, indeed,
assumed to be a preexperiential and pre-social
“given,” though not manifesting itself in the
very earliest years. In combination, these features
imply that autism by its nature is truly deep set in
those who have it and live with it. However, it
seems pertinent to observe that identity, in one
important sense, is something that is acquired,
built up, and defined progressively. So, while
curing, as opposed to ameliorating, an adult’s
Ethics
autism may be a destructive project, if indeed it is
not an incoherent one, the case is less clear where
infants are the likely recipients of the cure.
The second challenge is to the “cost-benefit”
analysis that the project of curing a person of his
or her autism would seem to assume. From the
neurodiversity perspective, autism is not of
itself “a cost” and there is no “benefit” in prin-
ciple from engineering a switch to neurotypical.
That stance is obviously harder to maintain,
however, in regard to those destined to be at
the low-functioning end of the spectrum. It is
not known whether science will ever enable
very early reliable identification, not only of
autism, but of broad spectrum position – with-
out which cost-benefit analyses could only be
crude affairs.
A question noted earlier is in the background
here: to what degree are the common positive (or
positively described) features and the common
negative (or negatively described) features of
autism independent of each other, as opposed to
always shadowing each other? Hans Asperger,
for one, presented them as two sides of the same
coin when he wrote of one of his patients: “this
boy’s positive and negative features are two nat-
urally necessary, connected aspects of one really
homogenously laid out personality. . . the diffi-
culties this boy has with himself as well as his
relationship to the world, are the price he has to
pay for his special gifts” (Asperger, 1938). To
the extent that they are independent of each
other, however, it would be possible in principle
to seek interventions that enhanced or protected
the positive while reducing or minimizing the
negative. A similar theoretical possibility is
interventions that would shift the balance
between features and their shadows toward
more positive forms of interaction, for example,
to reduce a suffocating attentiveness to detail
sufficiently to allow attention to patterns to
develop. These kinds of interventions, however,
would count better as “treatments” of autism
than as cures.
“Prevention,” to come to it, does not have to
mean “eradication” inasmuch as its primary ref-
erence may be symptoms rather than the condi-
tion itself. So, a major goal of research programs,
1173 E
whether biological or psychological, may be to
identify interventions that “prevent” the more
severe cognitive, behavioral, and social chal-
lenges that are often associated with autism and
impact negatively on autistic individuals and
their families. This prevention may be by early
treatment that forestalls the significant develop-
ment of these challenges or by interventions that
reduce or limit their impact when they have
already developed, by restoring function as
E
much as is possible. Regarding the latter, the
neurodiversity lobby object to particular research
and interventions aimed at “normalizing” certain
autistic behaviors, such as prolonging eye contact
or reducing “stimming,” where that is done for no
more objectively important reason than to make
the person with autism less visible by encourag-
ing them to fit in with contemporary cultural
norms.
The Future
Lack of a clear scientific, medical, and public
consensus on the definition, causes, diagnosis,
and treatment of autism means that many ethical
issues pertaining to autism are probably still to
emerge. Two that have emerged for discussion,
but depend on future scientific and medical
development, may be identified here.
One is the issue of gender in autism. Currently
autism is seen as a predominantly male condition.
The ratio of approximately four males being
diagnosed to every female has even led to
a theory that autism is an example of extreme
maleness, more specifically of the extreme male
brain. It is a question whether or not this view is
unconsciously influenced by stereotypes to
accept too readily the idea of differences between
male and female brain functioning. Alternative
explanations of the diagnostic imbalance suggest
that many females with autism may present dif-
ferently from males and so never be referred for
diagnosis, or that the diagnostic criteria as cur-
rently set are based on the more noticeably
disruptive behavioral characteristics of boys
(Gould & Ashton-Smith, 2011). The possible
injustice of large numbers of females not receiv-
ing a diagnosis and the assistance that goes with it
gives added moral importance to ongoing
E 1174
scientific investigation into how the biology of
sexual difference does, and does not, impact on
behavior (Timimi et al., 2011).
A second issue probably causes most conster-
nation in many parts of the autism community, as
well as being a concern to others. It is the pros-
pect of a future range of genetic technologies
capable of indicating levels of risk of autism for
use in the context of reproductive decision-
making. If and when they are developed, the
availability of such technologies, it is feared,
will lead to an avoidance of having children by
those identified as at risk of conceiving autistic
offspring and, beyond that, to large-scale elective
abortion of fetuses deemed to be at some – per-
haps even quite small – level of risk. Such worries
are tempered by the realization that the current
state of science does not face us with such choices
today; no “autism gene” or autism set of genes
have been discovered, and if and when discovery
happens, its practical import might turn out to be
modest. Nevertheless, it seems likely that future
developments in this area will confront us with
difficult ethical choices for which we should be
preparing ourselves.
Supporting the fears of proponents of
neurodiversity about an agenda to eradicate
autism, there is evidence to suggest that
preventing the birth of individuals with disabil-
ities that can be diagnosed prenatally seems to
many an obvious step to take, and is encouraged
by medical professionals and bioethicists alike.
Some bioethicists have even argued that there is
a moral obligation to prevent the births of dis-
abled individuals where possible, and regardless
of the level and kind of disability (Harris, 2001).
As parental decision-making is likely to be
influenced by available genetic information, it
will be important to offer parents counseling
about genetic and nongenetic risk factors; poten-
tial social, educational, and developmental out-
comes; and treatment options (Walsh et al.,
2011). It will also be crucial precisely how
genetic counselors communicate the probabilistic
and uncertain picture derived from genetics as
well as the complex and contested nature of the
Ethics
autistic spectrum itself, since this is also likely to
have a huge impact on what parents decide. This
presents a problem for genetic counselors since
even the existence of a screening process, or
a testing technology or the offer of prenatal test-
ing can easily be taken by parents as some kind of
recommendation. There is a clear need that
genetic counselors should provide fair, support-
ive, evidence-based information to prospective
parents.
Professional guidelines for genetic counselors
display a strong commitment to patient autonomy
particularly in regard to reproductive decisions
because of a belief that parents are in the best
position to know what they should do and have
a right to choose (and also, no doubt, to distance
the practice of genetic counseling from questions
of eugenics and the promotion of abortion). And
indeed many would agree that the final moral
decision appropriately lies with the choosers
among the available options – that is, the parents
of the actual or potential child at risk of autism –
with the hope that important ethical consider-
ations regarding, for example, the morality of
abortion or how we should think about disability
and disabled lives would continue to weigh
heavily in the choices people make. Even this
seemingly moderate point of view may be chal-
lenged however. It could be argued that just as
our autonomous decisions affecting others
including our children after birth are restricted
by considerations of harm to others, so should
they be similarly restricted before birth. Should
parents decide to abort a fetus identified as at risk
for autism (if and when that becomes possible),
their choice, it may be claimed, harms the fetus in
that from the fetus’s point of view it is better to be
born autistic than not born at all. Hence the harm
criterion suggests abortion in such cases is wrong
(Barnbaum, 2008). It is unclear whether propo-
nents of this view think abortion is wrong in all
circumstances, wrong in all cases of disability, or
wrong because it is the abortion of people with
autism. However, if living an autistic life is less
good than living a non-autistic life, consider-
ations of harm would not serve to restrict those
Evaluation of Sensory Processing
parental choices aimed at preventing the exis-
tence of autistic children (through pre-
implantation genetic diagnosis, for example).
What this brief discussion of the complexity of
reproductive decision-making as it pertains to
autism indicates is how necessary it has become
to think about how autism is and should be
characterised: it seems winning the battle of
words about the value of autism is not only
important for setting and reorienting the research
agenda but is likely to be crucial in life and death
decision-making in the context of future repro-
ductive choices.
References and Readings
American Psychiatric Association. (2000). Diagnostic
and statistical manual of mental disorders (4th ed.,
text rev.). Arlington, VA: Author.
Asperger, H. (1938). The mentally abnormal child.
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Aspies for Freedom. (2010). Retrieved from http://www.
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Autism Speaks. (2012). Retrieved from http://www.
autismspeaks.org
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Baron-Cohen, S. (1995). Mindblindness: An essay on
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Frith, U. (1989). Autism: Explaining the enigma. Oxford:
Blackwell.
Gould, J., Ashton-Smith, J. (2011, May). The diagnosis
and education of girls and women with autism. Good
Autism Practice.
Happe, F., Ronald, A., & Plomin, R. (2006). Time to give
up on a single explanation for autism. Nature Neuro-
science, 9, 1218–1220.
Harris, J. (2001). One principle and three fallacies of
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383–387.
McGregor, E., Nunez, M., Cebula, K., & Gomez, J.-C.
(Eds.). (2008). Autism: An integrated view from
neurocognitive, clinical and intervention research.
Oxford: Blackwell Publishing/E. L. Hill.
Medical Research Council of Great Britain. (2010). MRC
autism forward look and review. Retrieved from http://
www.mrc.ac.uk/Utilities/Documentrecord/index.htm?
d¼MRC007354
National Institute of Mental Health. (2008). NIMH strate-
gic plan. Retrieved from http://www.nimh.gov/about/
strategic-planning-reports/index.shtml
1175 E
Nussbaum, M. (2006). Frontiers of justice: Disability,
nationality, species membership. Cambridge: Harvard
University Press.
Timimi, S., Gardner, N., & McCabe, B. (2011). The myth
of autism. London: Palgrave Macmillan.
Walsh, P. (2010). Asperger syndrome and the supposed
obligation not to bring disabled lives into the world.
Journal of Medical Ethics, 36, 521–524.
Walsh, P., Elsabbagh, M., Bolton, P., & Singh, I. (2011).
In search of biomarkers for autism: Scientific, social
and ethical challenges. Nature Reviews Neuroscience,
12, 603–612.
Wing, L. (1981). Language, social and cognitive E
impairments in autism and severe mental retardation.
Journal of Autism and Developmental Disorders,
11(1), 31–44.
Wing, L., & Gould, J. (1979). Severe impairments of
social interaction and associated abnormalities in chil-
dren: Epidemiology and classification. Journal of
Autism and Developmental Disorders, 9, 11–29.
World Health Organisation. (2010). International Classi-
fication of Diseases (ICD-10). Geneva: Author.
Ethnography
▶ Qualitative Versus Quantitative Approaches
Evaluation of Sensory Processing
Tara J. Glennon
Occupational Therapy, Quinnipiac University –
Hamden, CT Center for Pediatric Therapy,
Fairfield & Wallingford, CT, Hamden, CT, USA
Synonyms
ESP
Definition
In 2000, Diane Parham and Cheryl Ecker formally
shared their work called the Evaluation of Sensory
Processing (ESP). This parent questionnaire,
whose development was originally initiated by
E 1176
LaCroix in 1993, was intended to identify behav-
iors thought to be indicative of sensory processing
problems. The unpublished test, produced at the
University of Southern California, was ultimately
included in the 2002 (Parham & Ecker, 2002) text
titled Sensory Integration: Theory and Practice
(2nd ed.) for occupational therapy clinician’s to
utilize in practice. After many years of research on
the utility of the tool, the authors signed an agree-
ment with Western Psychological Services (WPS)
to complete the standardization and normative
sampling. Simultaneously, WPS was also working
with a group of researchers currently undertaking
the task of developing a similar testing instrument
for use within the school environment called the
School Assessment of Sensory Integration (SASI;
Miller Kuhaneck, Henry, & Glennon,
unpublished). The two assessment tools, one for
parents and one for educational staff, were ulti-
mately combined for standardization to create the
Sensory Processing Measure (Parham, Ecker,
Kuhaneck, Henry, & Glennon, 2007) and the Sen-
sory Processing Measure - Preschool (Miller
Kuhaneck, Ecker, Parham, Henry, & Glennon,
2010).
See Also
▶ Sensory Processing Measure
References and Readings
LaCroix, J. E. (1993). A study of content validity using the
sensory history questionnaire. Unpublished
master’s thesis, University of Southern California,
Los Angeles.
Miller Kuhaneck, H., Ecker, C. E., Parham, L. D.,
Henry, D. A., & Glennon, T. J. (2010). Sensory
processing measure-preschool (SPM-P): Manual.
Los Angeles, CA: Western Psychological Services.
Parham, L. D., & Ecker, C. (2000). Evaluation of sensory
processing. Unpublished test, University of Southern
California, Los Angeles, CA.
Parham, L. D., & Ecker, C. (2002). Evaluation of sensory
processing. In A. Bundy, S. Lane, & E. Murray’s
(Eds.), Sensory integration: Theory and practice
(2nd ed.). Philadelphia: F A. Davis.
Event-Related Functional Magnetic Resonance Imaging (MRI)
Parham, L. D., Ecker, C., Miller Kuhaneck, H., Henry,
D. A., & Glennon, T. J. (2007). Sensory processing
measure (SPM): Manual. Los Angeles, CA: Western
Psychological Services.
Event-Related Functional Magnetic
Resonance Imaging (MRI)
Kevin A. Pelphrey
Child Study Center, Yale University School of
Medicine, New Haven, CT, USA
Synonyms
Blood-oxygen-level-dependent (BOLD) contrast;
fMRI; Functional MRI
Definition
Functional magnetic resonance imaging (fMRI)
is a brain imaging technique that uses a standard
magnetic resonance imaging scanner, a high rate
of image acquisition, and specialized pulse
sequences to measure localized brain activity. In
most cases, fMRI takes advantage of the endog-
enous blood-oxygen-level-dependent (BOLD)
contrast to image brain activity without the use
of ionizing radiation. As such, this technique is
ideal for studying the developing brain in chil-
dren. The technique is now the dominant tech-
nique for the study of brain function and its
disruption in autism.
See Also
▶ Functional MRI
References and Readings
Malisza, K. L., Clancy, C., Shiloff, D., Foreman, D.,
Holden, J., Jones, C., et al. (2011). Functional
evaluation of hidden figures object analysis in children
Evoked Potentials
with autistic disorder. Journal of Autism and
Developmental Disorders, 41(1), 13–22.
Pitskel, N. B., Bolling, D. Z., Hudac, C. M., Lantz, S. D.,
Minshew, N. J., & Pelphrey, K. A. (2011). Brain
mechanisms for processing direct and averted gaze in
individuals with autism. Journal of Autism and
Developmental Disorders, 41(12), 1686–1693.
Event-Related Potential
Benjamin Aaronson
Psychiatry and Behavioral Sciences, UW Autism
Center, University of Washington, Seattle,
WA, USA
Synonyms
Evoked potentials
Definition
An event-related potential is an electrical brain
response, recorded via electroencephalography,
time-locked to a particular stimulus or event.
External visual and auditory stimuli are com-
monly used in ERP research. In order to isolate
the response to the particular stimulus being
studied, multiple trials of responses to similar
stimuli are averaged together to produce
a composite waveform, ultimately reducing the
potential influence of extraneous factors.
See Also
▶ Electroencephalography
▶ Evoked Potentials
▶ Mismatch Negativity
References and Readings
Coles, M. G. H., & Rugg, M. D. (1996). Event-related
brain potentials: An introduction. Electrophysiology of
Mind, 1(6), 1–27.
Fabiani, M., Gratton, G., & Federmeier, K. D. (2007).
Event-related brain potentials: Methods, theory, and
1177 E
applications. In J. T. Cacioppo, L. G. Tassinary, &
G. G. Berntson (Eds.), Handbook of psychophysiology
(3rd ed., pp. 85–119). Cambridge, UK: Cambridge
University Press.
Luck, S. J. (2005). An introduction to the event-related
potential technique. Cambridge, MA: MIT Press.
Otten, L. J., & Rugg, M. D. (2005). Interpreting
event-related brain potentials. In T. C. Handy (Ed.),
Event-related potentials: A methods handbook
(pp. 229–259). Cambridge, MA: MIT Press.
E
Event-Related Potential (ERP)
▶ Evoked Potentials
Evoked Potentials
Benjamin Aaronson
Psychiatry and Behavioral Sciences, UW Autism
Center, University of Washington, Seattle, WA,
USA
Synonyms
Brainstem Evoked Response (BER); Event-
Related Potential (ERP); Evoked Response;
Visual Evoked Potential (VEP)
Definition
Evoked potentials refer to electrical activity
generated by a biological system in response to
an event. Events triggering electrical potentials
classically include responses in the visual system,
auditory system, motor system, and nervous
system.
See Also
▶ Electroencephalography
▶ Event-Related Potential
E 1178
References and Readings
Andreassi, J. L. (2007). Psychophysiology: Human
behavior & physiological response (5th ed.).
Mahwah, NJ: Lawrence Erlbaum Associates.
Coles, M. G. H., & Rugg, M. D. (1996). Event-related
brain potentials: An introduction. Electrophysiology of
Mind, 1(6), 1–27.
Fabiani, M., Gratton, G., & Federmeier, K. D. (2007).
Event-related brain potentials: Methods, theory, and
applications. In J. T. Cacioppo, L. G. Tassinary, &
G. G. Berntson (Eds.), Handbook of psychophysiology
(3rd ed., pp. 85–119). Cambridge, UK: Cambridge
University Press.
Otten, L. J., & Rugg, M. D. (2005). Interpreting
event-related brain potentials. In T. C. Handy (Ed.),
Event-related potentials: A methods handbook
(pp. 229–259). Cambridge, MA: MIT Press.
Evoked Response
▶ Evoked Potentials
EVT-2
▶ Expressive Vocabulary Test II
Exactingness
▶ Perfectionism
Example, Demonstration
▶ Modeling
Exceptionality
Michael Miklos
Pennsylvania Training and Technical Assistance
Network, Harrisburg, PA, USA
Synonyms
Abnormality; Atypical; Disability; Extraordinary
Evoked Response
Definition
Having some degree of difference from an
established norm in a specific skill area. Excep-
tionalities may include characteristics including
disabilities as well as special gifts and talents. An
individual with a noted exceptionality may pre-
sent a need for special education or supports in
relation to a disabling condition or due to special
talents or abilities such as mental giftedness.
Individuals with autism spectrum disorder may
present exceptionalities that are below what
would be normally expected in some areas of
function and may also present exceptional
abilities above the norm in others. The term
“exceptionality” is often used interchangeably
with the terms “disability” and “special need.”
Many state statutes use the term “exceptionality”
to denote categories of disability. Autism is one
example of a category of exceptionality.
See Also
▶ Disability
▶ Giftedness
▶ Special Needs
References and Readings
Assistance to States for the Education of Children with
Disabilities and Preschool Grants for Children with
Disabilities; Final Rule, 2004, 4000-01-U Department
of Education 34 CFR Parts 300 and 301, Part II.
Individuals with Disabilities Education Act of 2004, 20 U.
S. C., et. seq.
Executive Function (EF)
Marjorie Solomon
Department of Psychiatry and Behavioral
Sciences, UC Davis M.I.N.D. Institute,
Sacramento, CA, USA
Definition
“Executive functions” is a broad term used to
describe the set of cognitive processes required
Executive Function (EF)
to prepare for and execute goal-directed
behaviors. Various theoretical models propose
that executive functions are executed by slightly
different component processes. However, in gen-
eral terms, these components are thought to
include:
• Goal (or rule) representation, which also may
be referred to as working memory
• Inhibition
• Cognitive flexibility, which also may be
referred to as set shifting or task switching
• Planning
Some also consider “higher level” cognitive
processes like problem solving and abstract rea-
soning to be forms of executive functioning.
Other terms such as controlled (versus automatic)
processing; selective attention; and supervisory
attention, which originate in different theoretical
models, may be used to describe the properties of
executive functions.
Historical Background
Impairments in executive functions are among
the most consistently reported deficits in
individuals with autism spectrum disorders or
“ASD” (see Hill, 2004; Ozonoff, Pennington, &
Solomon, 2006; Pennington & Ozonoff, 1996).
Many early studies of executive functions in
autism used the Wisconsin Card Sorting Test
(WCST), which requires participants to figure
out a sorting rule, derived from one of the cards’
three dimensions (color, quantity, or design),
based on minimal feedback. Once the participant
has demonstrated that they understand the sorting
rule by executing it properly multiple times, the
rule unexpectedly changes. Studies using the
WCST find that persons with autism tend to per-
severate on incorrect responses (i.e., are unable to
stop sorting using the old rule when it is no longer
correct) more than matched controls. Interest-
ingly, these impairments appear to be reduced
when the task is administered on a computer.
Given that patients with focal frontal lobe
lesions have difficulty in planning future actions
and in inhibiting habitual responses, executive
functions traditionally are associated with the
1179 E
prefrontal cortex (PFC). Many clinical neuropsy-
chology assessment batteries and tasks like the
WCST are premised on this assumption and are
designed to test what are believed to be the spe-
cific components of executive functioning based
on studies of patients with brain lesions. How-
ever, more contemporary research suggests that
executive functions cannot be localized to one
brain region or process.
Executive functions deficits are not specific to
E
autism spectrum disorders. They are present in
many other forms of developmental psychopa-
thology including attention deficit hyperactivity
disorder (ADHD). However, it is important to
study executive functions in persons with ASD
because longitudinal studies show that executive
functions deficits have a parallel influence across
social, language, and other domains of function-
ing. Furthermore, they are related to cognitive
abilities that have a very strong relationship
with long-term outcomes, and can serve as
a treatment target.
Current Knowledge
Consistent with findings about perseveration on
the WCST in persons with ASD, the most com-
mon perspective on executive functions deficits is
that they are related to cognitive flexibility. More
specifically, many studies have shown that indi-
viduals with ASDs have difficulty in shifting their
frame of reference in thinking about problems
(shifting cognitive set); in shifting how they con-
ceptualize options that are not presented in the
immediate environment (extra-dimensional set
shifting); in shifting the focus of their visual
attention; in shifting their attention between sen-
sory modalities, like seeing and hearing; and in
shifting between sets of rules they have learned.
Another component of executive function that
is consistently found to be impaired is planning.
This commonly is measured using the Tower of
Hanoi or the Tower of London tasks which
require participants to move disks of various
sizes across three pegs. They are given
a starting position and a picture of an ending
position and must reproduce the ending position
E 1180
using the fewest moves. The task grows progres-
sively harder over trials, and task rules prevent
self-correction. The Tower task requires that the
participants think through (or plan) disk moves in
their heads before executing them. This is
a relatively difficult task, and some have criti-
cized the use of this type of task because it is
unclear exactly what it assesses.
Several executive functions are thought to be
intact in ASDs. The first of these is inhibition,
which once was thought to differentiate persons
with ASDs from those with ADHD. However,
a growing body of research suggests that individ-
uals with ASDs also have difficulty inhibiting
prepotent response tendencies. It is unclear why
there has been this shift in the literature. Some
have suggested that there have been changes in
diagnostic conventions since the early 1990s and
that individuals formerly diagnosed with ADHD
now are diagnosed with ASDs – a trend referred
to as diagnostic substitution. Another possibility
is that tasks that have been used to assess inhibi-
tion are not directly comparable and that gener-
ally harder tasks produce greater deficits.
A second executive function traditionally thought
to be intact is working memory. Here too, results
have become less clear as various versions of the
task have been used.
Following one study that showed that high
functioning persons with autism perform better
on the intelligence tests that involve more visuo-
spatial versus verbal reasoning – the Raven’s
Progressive Matrices test (Dawson, Soulières,
Gernsbacher, & Mottron, 2007), there now have
been several that show that aspects of conditional
and analogical reasoning are relatively preserved
in persons with ASDs.
As all parents and clinicians know, the con-
tention that executive functions deficits create
problems for persons with ASDs in everyday
life would appear to be true. Individuals with
ASDs have difficulty maintaining reciprocal
social relationships, having two-sided conversa-
tions, transitioning between activities, and
disengaging from idiosyncratic interests. They
also have difficulty inhibiting old behaviors in
favor of new, more appropriate ones. At school,
they struggle to stay organized. They lose or
Executive Function (EF)
forget to turn in homework. They have difficulty
reading for meaning and writing clearly. They
may be unable to organize information well
enough to correctly answer math story problems.
However, despite the fact that deficits in execu-
tive functions would appear to map directly
related to these inflexible everyday behaviors, it
has been challenging to demonstrate this link
empirically using clinical neuropsychology mea-
sures (see Geurts, Corbett, & Solomon, 2009). It
has been suggested that we need better measures
that tap “real-world” inflexible behaviors.
Another focus of current research is on how
executive functions develop. Adolescent devel-
opment of executive functions has become an
area of active scrutiny given that profound brain
changes occur during normative adolescent
development, leading to maturation, and provid-
ing a window of opportunity for intervention.
During adolescence, reductions in cortical gray
matter, and increases in white matter volume,
result in the refined calibration of the excitatory-
inhibitory balance in the PFC, and the strength-
ening of networks governing cognitive
processing. In typical development, most execu-
tive functions mature by age 15, although reac-
tion times and performance on more complex
tasks and combinations of tasks improve into
the 20s.
Future Directions
Fortunately, the advent of new technologies
including functional magnetic resonance imaging
is helping to advance what we know about brain
functioning beyond what could be learned by
lesion models. “Cognitive control” is a term
evolving in the field of cognitive neuroscience
to describe the cognitive processes that tradition-
ally have been thought of as executive functions
(Miller & Cohen, 2001). The newer cognitive
control-based model of PFC function suggests
that (1) the PFC is specialized for the representa-
tion and maintenance of context information;
(2) that context information is maintained in the
PFC as a pattern of neural activity; and (3) that
Executive Function (EF)
context representations mediate cognitive control
through interactions that modulate the flow of
information in other brain systems that more
directly support task performance. Proper func-
tioning of this system is required for (a) effective
allocation of attention, (b) inhibition of irrelevant
responses, (c) appropriate shifting of frame of
reference, (d) relating information appropriately
over time and space, and (e) adjusting behavior
in relation to the evolving environment. For exam-
ple, when Americans visit London and attempt to
cross the street, cognitive control must be engaged
to avoid the customary practice of looking to the
left for oncoming traffic, in favor of looking to the
right. In sum, cognitive control must be engaged
when overcoming habitual responses, ignoring
irrelevant stimuli, or transforming representations.
Cognitive control is not required to perform sim-
ple or automatic behaviors, but must be engaged to
guide action in novel, difficult, or rapidly changing
conditions. This is especially important when
there is strong competition between the potential
responses (such as choosing between the ingrained
habit of looking left versus facing the prospect of
being run over!).
Specific brain regions thought to be involved
in the application of cognitive control include the
dorsolateral prefrontal cortex (DLPFC), medial
frontal cortex (including the anterior cingulate
cortex), and parietal cortex. In the cognitive con-
trol model, the DLPFC is believed to maintain
appropriate context for action. The anterior cin-
gulate cortex is thought to function as part of
a “control loop.” It detects response conflict and
signals the DLPFC to allocate more control-
related resources. The parietal cortex is activated
when it is necessary to switch attentional focus. It
also is thought to act as a repository of learned
stimulus-response associations from which the
DLPFC “selects” the appropriate response. In
another emerging model, a hierarchy of brain
regions is thought to implement cognitive con-
trol. The representation of the highest conceptual
level of a task is thought to rely on the anterior or
rostrolateral PFC.
In conclusion, it is an exciting time for exec-
utive functions research, and more work in this
area will help to advance the understanding of
1181 E
ASDs. Directions for future executive functions
research include:
1. The development of models and measures that
better capture what happens in the brain when
we are engaged in goal-directed activities.
This will include measures of connectivity
between different brain regions and neural
circuits.
2. Studies that compare these models and mea-
sures across other neurodevelopmental disor-
E
ders. This type of strategy may help us better
understand the genes involved in autism (and
other disorders involving similar problems).
3. Studies of executive functions/cognitive con-
trol in animals including rodents and
nonhuman primates. These studies can help
us tease apart the pathophysiology of disor-
ders. Animal models also can be used to test
promising drug treatments.
4. More ecologically valid measures might help
in forging associations between the observed
day-to-day behavior and models and measures
of goal-directed behavior.
5. Most experimental research has used data ana-
lytic models that focus on mean group differ-
ences. We need studies that consider the role
of individual differences in areas such as tem-
perament and personality, stress responsive-
ness, and motivation in studies of executive
functions.
6. Clinical trials of interventions that help us to
remediate executive functions deficits.
7. Studies that examine the development of exec-
utive functions/cognitive control through the
life span.
See Also
▶ Attention
▶ Memory
References and Readings
Dawson, M., Soulières, I., Gernsbacher, M. A., &
Mottron, L. (2007). The level and nature of autistic
intelligence. Psychological Science, 18, 657–662.
E 1182
Geurts, H., Corbett, B., & Solomon, M. (2009). The
paradox of cognitive flexibility in autism spectrum
disorders. Trends in Cognitive Science, 13(2), 74–82.
Hill, E. L. (2004). Executive dysfunction in autism.
Trends in Cognitive Science, 8(1), 26–32.
Miller, E. K., & Cohen, J. D. (2001). An integrative theory
of prefrontal cortex function. Annual Review of
Neuroscience, 24, 167–202.
Ozonoff, S. J., Pennington, B. F., & Solomon, M. (2006).
Neuropsychological perspectives on developmental
psychopathology. In D. Cicchetti (Ed.), Developmen-
tal psychopathology (2nd ed.). New York: Wiley.
Pennington, B. F., & Ozonoff, S. J. (1996). Executive
functions and developmental psychopathology.
Journal of Child Psychology and Psychiatry, 37(1),
51–87.
Executive Functions
▶ Frontal Lobe Findings in Autism
Experimental Research
▶ Qualitative Versus Quantitative Approaches
Explicit Memory
Diane M. Lickenbrock
Human Development and Family Studies,
The Pennsylvania State University,
University Park, PA, USA
Synonyms
Declarative memory; Fact memory
Definition
A specific type of memory that involves
intentional, conscious recollection. Explicit
Executive Functions
memory is often assessed by using tasks
that require recognition and recall. Research
has shown that individuals with Autism
Spectrum Disorder (ASD) have intact
explicit memory, although they use
a different memory retrieval process. Individ-
uals with ASD and intellectual disability
show greater impairments in explicit memory
compared to high-functioning individuals
with ASD.
See Also
▶ Declarative Memory
▶ Explicit Memory
▶ Free Recall
▶ Memory
▶ Memory Assessment
▶ Memory Development
▶ Recognition Memory
▶ Retrieval of Information
▶ Rote Memory
▶ Semantic Memory
▶ Short-Term Memory
References and Readings
Anooshian, L. J. (1997). Distinctions between implicit
and explicit memory: Significance for understanding
cognitive development. International Journal of
Behavioral Development, 21, 453–478.
Murphy, K., McKone, E., & Slee, J. (2003). Dissociations
between implicit and explicit memory in children:
The role of strategic processing and the knowledge
base. Journal of Experimental Child Psychology, 84,
124–165.
Renner, P., Klinger, L. G., & Klinger, M. R. (2000).
Implicit and explicit memory in autism: Is autism
an amnesic disorder? Journal of Autism and Develop-
mental Disorders, 30, 3–14.
Rovee-Collier, C. K., Hayne, H., & Columbo, M. (2001).
The development of implicit and explicit memory:
Advances in consciousness research. Philadelphia:
John Benjamins Publishing Company.
Squire, L. R. (1987). Memory and brain. New York:
Oxford University Press.
Expressive Language 1183 E
across the spectrum regardless of severity. Issues
Exploratory Factor Analysis noted specifically in children with ASD include
difficulties with word order in sentences (syntax),
▶ Latent Variable Modeling difficulties using appropriate word morphology
(word endings) and grammar (especially pro-
nouns), as well as noted difficulties in semantic
organization and word finding.
Exploratory Play

▶ Play See Also

E
▶ Broca’s Aphasia
▶ Childhood Aphasia
Expressive Communication
▶ Expressive Language
▶ Expressive Language Disorder
▶ Expressive Language

References and Readings

Expressive Dysphasia
De Hirsch, K. (1982). Differences in language acquisition:
Hope Morris Dysphasia-autism. Annals of Dyslexia, 32(1), 305–320.
Martos, J., & Ayuda, R. (2002). Communication and lan-
Communication Sciences and Disorders, guage in the autistic spectrum: Autism and dysphasia.
The University of Vermont, Burlington, Revista de Neurologia, 34(1), 58–63.
VT, USA Resnick, T., Allen, D., & Rapin, I. (1984). Disorders of
language development: Diagnosis and intervention.
Pediatrics in Review, 6, 85–92.
Tager-Flusberg, H., Paul, R., & Lord, C. (2005). Language
Synonyms and communication in autism. In F. R. Volkmar, A.
Klin, R. Paul, & D. J. Cohen (Eds.), Handbook
Developmental language disorder; Expressive of autism and pervasive developmental disorders
language disorder; Specific language impairment (Vol. I, pp. 335–364). Hoboken, NJ: Wiley.
Tuchman, R., Rapin, I., & Shinnar, S. (1991). Autistic and
dysphasic children. I: Clinical characteristics. Pediat-
rics, 88(6), 1211–1218.
Definition

In neurological contexts, language impairment is

identified as either acquired (aphasia) or devel- Expressive Language
opmental (dysphasia). An expressive dysphasia is
a language disorder linked to deviation or an Hope Morris
early injury to areas of the brain that are special- Communication Sciences and Disorders,
ized for language functions. In expressive dys- The University of Vermont, Burlington, VT,
phasia, children have difficulty with verbal USA
expression but have adequate language compre-
hension skills. Difficulties can be noted in putting
words into coherent sentences, using appropriate Synonyms
grammar, and recalling words. Expressive dys-
phasia is often observed in children with autism Expressive communication; Oral language;
spectrum disorders (ASD) and can be noted Spoken language
E 1184
Definition
Expressive language is a cognitive process that is
involved in the transmission of oral, symbolic, or
written language and allows for communicating
one’s ideas, desires, or intentions to others. Expres-
sive language is composed of form (grammar and
syntax), content (semantics or meaning), and use
(communicative function and intent). Expressive
language can take many forms including
verbalizations, sign language, gestures, pictures,
written words, and, in some cases, voice output
communication devices. Individuals with autism
spectrum disorders (ASD) can have difficulty
with expressive language in any of the aforemen-
tioned areas, especially in the area of language use.
See Also
▶ Communicative Functions
▶ Expressive Language Disorder
▶ Language
▶ Speech Morphology
References and Readings
Geurts, M., & Embrechts, M. (2008). Language profiles in
ASD, SLI, and ADHD. Journal of Autism and
Developmental Disorders, 38(10), 1931–1943.
Jarrold, C., Boucher, J., & Russell, J. (1997). Language
profiles in children with autism: Theoretical and meth-
odological implications. Autism, 1, 57–76.
Rescorla, L., & Schwartz, E. (1990). Outcomes of toddlers
with specific expressive language delay. Applied
PsychoLinguistics, 11, 393–407.
Tager-Flusberg, H., & Caronna, E. (2007). Language dis-
orders: Autism and other pervasive developmental
disorders. Pediatric Clinics of North America, 54(3),
469–481.
Tager-Flusberg, H., Paul, R., & Lord, C. (2005). Language
and communication in autism. In F. R. Volkmar,
A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook of
autism and pervasive developmental disorders (Vol. I,
pp. 335–364). Hoboken, NJ: Wiley.
Expressive Language Delay
▶ Expressive Language Disorder
Expressive Language Delay
Expressive Language Disorder
Hope Morris
Communication Sciences and Disorders,
The University of Vermont, Burlington,
VT, USA
Synonyms
Developmental language delay/disorder; Expres-
sive language delay; Specific language impairment
Definition
Expressive language disorder indicates an individ-
ual is likely to understand more than what he/she is
able to communicate. This means a person’s recep-
tive language (comprehension) is better than his/
her expressive language (use of language). This
disorder is often associated with a developmental
language delay. Expressive language disorders
can also be acquired (as a result of brain injury/
damage), as in aphasia. A developmental delay in
expressive language is more common in children
and can occur in a child with normal intelligence or
co-occur with cognitive impairment or other devel-
opmental disorders a child might experience.
Expressive language disorder can be observed in
both verbal and written communication forms.
Children with autism spectrum disorders (ASD)
often present with expressive language disorders.
Many children with ASD begin speaking later
than typically developing children and often dem-
onstrate a significantly slower development of
expressive language through the preschool years.
In particular, children with ASD present with dif-
ferences in the social use of language (pragmatics).
See Also
▶ Communication Disorder/Communication
Impairment
▶ Expressive Dysphasia
▶ Speech Delay
Expressive Vocabulary Test II
▶ Speech Impairment
▶ Speech/Communication Disabilities
References and Readings
American Psychiatric Association. (2000). Diagnostic
and statistical manual (4th ed.). Washington, DC:
APA Press. Text Rev.
Geurts, M., & Embrechts, M. (2008). Language profiles
in ASD, SLI, and ADHD. Journal of Autism and
Developmental Disorders, 38(10), 1931–1943.
Tager-Flusberg, H., & Caronna, E. (2007). Language
disorders: Autism and other pervasive developmental
disorders. Pediatric Clinics of North America, 54(3),
469–481.
Tager-Flusberg, H., Paul, R., & Lord, C. (2005). Language
and communication in autism. In F. R. Volkmar,
A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook of
autism and pervasive developmental disorders (Vol. I,
pp. 335–364). Hoboken, NJ: Wiley.
Toth, K., Munson, J., Meltzoff, A., & Dawson, G. (2006).
Early predictors of communication development in
young children with autism spectrum disorder: Joint
attention, imitation, and toy play. Journal of Autism
and Developmental Disorders, 36(8), 993–1005.
Expressive Vocabulary Test II
Maura Moyle and Steven Long
Speech Pathology & Audiology, Marquette
University, Milwaukee, WI, USA
Synonyms
EVT-2
Description
The Expressive Vocabulary Test, Second Edition
(EVT-2) is a quick, norm-referenced assessment
designed to measure expressive vocabulary and
word retrieval for Standard American English.
According to the author, additional applications
include screening for expressive language prob-
lems, screening for potential language delay in
young children, understanding reading difficul-
ties, monitoring growth in vocabulary, research,
1185 E
and evaluating the acquisition of English words.
Norms are provided for a wide age range (i.e.,
2 years 6 months to beyond 90 years of age).
Items require examinees to provide either labels
or synonyms. For each item, examinees are
shown a colored picture and prompted by the
examiner to provide a one-word response (e.g.,
“What is this animal?” or “Tell me another word
for jacket.”). The EVT-2 is co-normed with the
Peabody Picture Vocabulary Test, Fourth Edition
E
(PPVT-4; Dunn & Dunn, 2007), a measure of
receptive vocabulary (i.e., understanding of spo-
ken words). When both the PPVT-4 and EVT-2
are administered, direct comparisons can be
made between a client’s receptive and expressive
vocabulary. The EVT-2 has two parallel test
forms (A and B) so it may be used for progress
monitoring. EVT-2 materials include an exam-
iner’s manual, test easel (either form A or B), and
25 record forms (additional forms can be pur-
chased separately). Users can choose to purchase
ASSIST, a software program for electronic scor-
ing, which provides various types of group and
individual reports. Examiners administering the
EVT-2 must be trained and experienced in test
administration and scoring. Only qualified edu-
cational and psychological professionals should
interpret the test results.
The EVT-2 manual provides clear guidelines
for administration and scoring. Each form (A or
B) contains 190 test items presented in order of
increasing difficulty. In addition, two practice
items are presented to ensure the client under-
stands the procedure. The EVT-2 is administered
individually, and testing time is estimated to be
10–20 min, depending on age and ability (e.g.,
individuals with larger vocabularies tend to
require more testing time). Start points are
based on the client’s chronological age. The
basal rule is five consecutive correct responses,
and the ceiling rule is five consecutive incorrect
responses. A stimulus prompt and all possible
correct answers are provided for each item on
the score form. The most common incorrect
answers are also listed. Some incorrect answers
are tagged with a “P” indicating that the examiner
should provide an additional prompt to encourage
a correct response from the examinee. The
E 1186
manual does not provide an explanation as to why
some incorrect answers are prompted while
others are not. Although the test is officially
untimed, the manual suggests a 10-s limit for
responding to each item, especially if the EVT-2
is to be used as a measure of word retrieval. Items
are scored as incorrect (“0”) or correct (“1”) on
the score form during test administration. Space
is provided for examiners to write responses that
are not listed on the score form for later scoring.
The EVT-2 provides numerous options for
converting the data and guidelines for
interpreting the results. First, raw scores are cal-
culated by taking the highest item in the client’s
ceiling and subtracting errors for all items admin-
istered. Items below the basal are considered to
be correct. Raw scores are converted to standard
scores (mean ¼ 100, standard deviation ¼ 15)
based on either age or grade (fall or spring).
A raw score can also be converted to a growth
scale value (GSV) which is helpful for tracking
a client’s vocabulary development over time. The
GSV is an indicator of absolute level of perfor-
mance rather than a norm-referenced score.
If a client’s score increases on the EVT-2 upon
subsequent administrations, then his or her GSV
will also increase (versus norm-referenced scores
which may decrease over time if a client’s growth
is below average compared to his or her peers).
Tables are also provided for converting standard
scores to percentile ranks, normal curve equiva-
lents, and stanine scores. If the PPVT-4 was also
administered, tables are provided to determine
whether the absolute difference between the
EVT-2 and PPVT-4 scores is statistically
significant.
The EVT-2 also provides tools for conducting
various qualitative interpretations of a client’s
performance. These analyses include expressive
versus receptive vocabulary, home versus school
vocabulary, vocabulary by part of speech (i.e.,
noun, verb, attribute), vocabulary by tier using
a 3-tier model (i.e., tier 1 – vocabulary common
in conversation, tier 2 – vocabulary common in
school curricula, tier 3 – technical vocabulary;
Beck, McKeown, & Kucan, 2002), and crossover
vocabulary sampling between the EVT-2 and
PPVT-4 (i.e., comparing items common to both
Expressive Vocabulary Test II
assessments). Worksheets are provided in the
test manual to complete these qualitative
analyses by hand, or the ASSIST software will
compute them upon entering a client’s perfor-
mance item by item.
Historical Background
The previous edition of this assessment was the
Expressive Vocabulary Test (EVT; Williams,
1997). The first step in the 5-year revision process
was to survey and interview current users of the
EVT to gather ideas for improvements. In addi-
tion, a panel of ten consultants representing the
perspectives of several ethnic minorities was
formed to examine the test for cultural and lin-
guistic biases. Offensive items and items that
were potentially biased were eliminated. Several
updates were subsequently made to the EVT: two
parallel test forms were developed, more words
representing everyday vocabulary were included,
more words found in oral directions given in the
classroom were included, labeling-type items
were included throughout the range of difficulty
(versus just synonym types at the higher age
ranges), a specific stimulus question was included
for each item on the score form, several items
were dropped, all of the stimulus pictures were
updated, and the EVT-2 was co-normed with the
PPVT-4.
In order to create a parallel test form, many
new words needed to be added. Two guidelines
were followed for choosing which words were
included in the initial tryout pool. The first was
to choose words that represented Standard Amer-
ican English vocabulary encountered in typical
life experiences. The second guideline was to
choose words that occurred with relatively high
frequency (in order to measure word retrieval).
Several published lists of word frequencies were
consulted for the selection of new words (see the
test manual for the specific references). A set of
400 items were eventually chosen for the two
national tryout studies. Guidelines for scoring
were based on the results of the first tryout study
of 1,451 participants and also based on several
reference materials (e.g., dictionaries and
Expressive Vocabulary Test II
thesauruses). Specific details on choosing correct
and incorrect responses were not provided in the
manual. Items were subsequently analyzed in
terms of item difficulty, item discrimination
(i.e., ability to differentiate examinees with
lower and higher vocabulary levels), and item
bias (i.e., examining if an item was more difficult
for one group of examinees than another). The
items were reviewed by a second panel of 15
individuals representing various ethnic back-
grounds to examine cultural sensitivity and fair-
ness with inappropriate items subsequently
eliminated. Next, a second national tryout with
852 participants was conducted, and similar item
analyses were completed. Based on the two try-
out studies, the EVT-2 standardization versions
were created and norms were developed.
Psychometric Data
The sample used to standardize the EVT-2 and
create the test norms consisted of 3,540 individ-
uals at 320 sites nationwide ranging in age from
2 years, 6 months, to over 90 years of age. The
demographic characteristics of the participants
(i.e., gender, ethnicity, socioeconomic status,
geographic region, special education status)
closely resembled the larger population of the
United States according to the 2004 U.S. Census.
The sample was divided into 28 age groups, with
60 to 200 individuals within each group (all but
the two oldest groups contained at least 100 indi-
viduals). Grade norms are based on a subset of
2,003 cases with 100 to 233 students per grade.
Approximately half of the participants were
administered form A of the EVT-2 and half com-
pleted form B. A subset of 507 participants were
administered both forms. Mean scores across age
groups indicate no floor or ceiling effects for
either form. In addition, the test manual provides
evidence suggesting that the two forms are of
similar difficulty.
Reliability of the EVT-2 was assessed through
analyses measuring internal consistency (i.e.,
split-half and alpha reliabilities), alternate-form
reliability, and test-retest reliability. Measures of
internal consistency were calculated for the
1187 E
28 age groups and for both EVT-2 forms (A and
B). Split-half reliability coefficients were high,
ranging from .88 to .97, and alpha coefficients
were also high, ranging from .93 to .98, indicating
a high degree of internal consistency. Alternate-
form reliability resulted in correlations ranging
from .83 to .91 for the subset of participants who
were given both forms A and B, indicating that
the two forms provide similar results. Another
subgroup of 348 examinees across five age
E
groups was given the EVT-2 twice with an inter-
val of 2 to 6 weeks between administrations. The
resulting test-retest reliability was high, with
coefficients ranging from .94 to .97, suggesting
excellent stability of scores. Inter-rater reliability
was not reported.
The validity of the EVT-2 was assessed in
terms of content validity, its relationship to age,
and correlations to other tests (i.e., criterion-
related validity). In addition, its sensitivity to
measuring differences in various special
populations was examined. The author refers to
the process of item selection (discussed above) as
evidence for content validity. As stated earlier,
items were chosen if they were of moderate to
high frequency according to various published
resources and if they represented everyday expe-
riences. In addition, items were reviewed by con-
tent specialists and panels examining cultural and
linguistic biases. No more detail on the processes
of item generation or selection is provided. Also,
the manual does not report mean scores by race or
ethnicity which would provide additional evi-
dence for the cultural and linguistic fairness of
the test. EVT-2 mean test scores increase rapidly
in childhood, while growth is gradual in adoles-
cence and young adulthood. Scores plateau
through middle adulthood and then decline grad-
ually at older ages. This pattern of results is what
would be expected given what is known about
cognitive and linguistic development. Therefore,
the EVT-2 appears to be sensitive to age-related
changes in expressive vocabulary skill. In terms
of criterion-related validity, the relationships
between the EVT-2 and other measures of lan-
guage and reading were examined using subsets
of the norming sample (consisting mostly of chil-
dren and adolescents), including the PPVT-4, the
E 1188
Comprehensive Assessment of Spoken Language
(CASL; Carrow-Woolfolk, 1999), the Clinical
Evaluation of Language Fundamentals, Fourth
Edition (CELF-4), the Group Reading Assess-
ment and Diagnostic Evaluation (GRADE;
Williams, 2001), and the EVT. Results indicated
that the EVT-2 was moderately to highly corre-
lated with these other measures, providing evi-
dence that it is a valid measure of language skill.
The performance of 12 special populations on
the EVT-2 was also reported. These populations
included children or adults with speech impair-
ment, young children with language delay, chil-
dren or adults with language disorder, children
with hearing impairment (divided into those with
and without cochlear implants), and children with
either learning disability (reading), mental retar-
dation, emotional/behavioral disturbance, atten-
tion deficit disorder, or giftedness. Each group’s
mean score fell above, at, or below the mean as
would be expected based on group membership,
suggesting that the EVT-2 is a sensitive measure
of vocabulary skill in special populations. The
manual does not provide sensitivity or specificity
data for diagnostic classification, which is con-
sidered to be the gold standard when using assess-
ment tools for diagnostic purposes (Spaulding,
Plante, & Farinella, 2006). Moreover, the average
score for children with language delay or disorder
fell within one standard deviation of the mean.
Therefore, the results of the EVT-2 alone should
not be used for making diagnostic decisions about
language delay or disorder.
Clinical Uses
The EVT-2 is a quick assessment of expressive
vocabulary skill and word retrieval for children
and adults who speak Standard American
English. It can also be used for screening expres-
sive language delay or disorder, understanding
reading difficulties, monitoring vocabulary
growth, research, and evaluating the acquisition
of English words (although more evidence is
needed to support these applications of the
EVT-2). In addition, the EVT-2 is sensitive to
age-related changes in vocabulary skill and
Expressive Vocabulary Test II
discriminates among special populations. Several
qualitative interpretations are also available
(although no evidence for the validity of these
interpretations is provided). The EVT-2 was co-
normed with the PPVT-4, so comparisons
between expressive and receptive vocabulary
can be made if both assessments are adminis-
tered. The optional software program, ASSIST,
provides group and individual reports in addition
to evidence-based intervention ideas. Overall, the
EVT-2 appears to be a psychometrically sound
assessment of expressive vocabulary. However,
given that data on classification accuracy for
children with language delay or disorder were
not provided, caution should be taken in using
the EVT-2 for diagnostic classification.
The EVT-2 included 4 individuals with autism
in its norming sample, or 0.2%, which was reflec-
tive of the prevalence of autism in the 2004 US
population. It is unknown if individuals included
in the other special population groups (e.g., lan-
guage disorder, mental retardation) may have
been on the autism spectrum. If both the PPVT-
4 and EVT-2 are administered to a client, a higher
expressive than receptive vocabulary score (i.e.,
EVT-2 > PPVT-4) could be an indicator of ASD
(Paul, Chawarska, & Volkmar, 2008).
See Also
▶ Communication Assessment
▶ Expressive Language
▶ Expressive Language Disorder
▶ Language Tests
▶ Norm-Referenced Testing
▶ Peabody Picture Vocabulary Test
▶ Standardized Tests
References and Readings
Beck, I. L., McKeown, M. G., & Kucan, L. (2002). Bring-
ing words to life: Robust vocabulary instruction. New
York: Guilford Press.
Carrow-Woolfolk, E. (1999). Comprehensive assessment
of spoken language. Circle Pines, MN: American
Guidance Service.
Extended School Year (ESY) Services
Dunn, L. M., & Dunn, D. M. (2007). Peabody picture
vocabulary test (4th ed.). Bloomington, MN: NCS
Pearson.
Graham, T. (2010). Review of the expressive vocabulary
test, second edition. In R. A. Spies, J. F. Carlson, &
K. F. Geisinger (Eds.), The eighteenth mental mea-
surements yearbook (pp. 223–226). Lincoln, NE:
Buros Institute of Mental Measurements.
Paul, R., Chawarska, K., & Volkmar, F. (2008). Differen-
tiating ASD from DLD in toddlers. Perspectives on
Language Learning and Education, 15, 101–111.
Rathvon, N. (2010). Review of the expressive vocabulary
test, second edition. In R. A. Spies, J. F. Carlson, &
K. F. Geisinger (Eds.), The eighteenth mental mea-
surements yearbook (pp. 226–229). Lincoln, NE:
Buros Institute of Mental Measurements.
Semel, E., Wiig, E. H., & Secord, W. A. (2003). Clinical
evaluation of language fundamentals (4th ed.). San
Antonio, TX: Psychological Corporation.
Spaulding, T., Plante, E., & Farinella, K. (2006). Eligibil-
ity criteria for language impairment: Is the low end of
normal always appropriate? Language, Speech, and
Hearing Services in Schools, 37, 61–72.
Williams, K. T. (1997). Expressive vocabulary test. Circle
Pines, MN: American Guidance Service.
Williams, K. T. (2001). Group reading assessment and
diagnostic evaluation. Circle Pines, MN: American
Guidance Service.
Williams, K. T. (2007). Expressive vocabulary
test-second edition. Minneapolis, MN: NCS Pearson.
Extended School Year (ESY) Services
Brian Reichow1 and Fred R. Volkmar2
1
Child Study Center, Associate Research
Scientist, Yale University School of Medicine,
New Haven, CT, USA
2
Director – Child Study Center, Irving B. Harris
Professor of Child Psychiatry, Pediatrics and
Psychology, School of Medicine,
Yale University, New Haven, CT, USA
Synonyms
ESY
Definition
Some children with autism may lose skills that
they have learned (e.g., regress) if not provided
1189 E
with continuous programming (i.e., they regress
over the long traditional summer vacation from
school). Extended year services (often referred to
simply as ESY) can include both classroom-
based services and/or related services such as
occupational or speech therapy. These special
services are not simply the same as summer
school or summer enrichment programs and
indeed are not solely limited to summer, e.g.,
other periods might also be appropriate. Any
E
student receiving special education may be
eligible for such services although the need,
for a specific child, is determined by his or
her IEP team (which includes the parents). In
the USA, under the IDEA mandate, parents do
not pay for these services which must meet
acceptable state standards and be individual-
ized to meet each child’s specific needs. Many
of the mandates/guidelines in the area have
evolved based on legal decisions. Criteria fre-
quently used to determine need include, but
are not limited to, the child’s current rate of
progress, interfering behavioral concerns,
opportunities to master emerging skills, the
likelihood of regression, and the time that it
might take the child to regain skills that would
be lost.
See Also
▶ Education
▶ Individuals with Disabilities Education Act
(IDEA)
References and Readings
National Research Council. (2001). Educating young chil-
dren with autism. Washington, DC: National Academy
Press.
Volkmar, F., & Wiesner, L. (2009). A practical guide to
autism. Hoboken, NJ: Wiley.
Wrisht, P. W., & Wright, P. D. (2007). Wrightslaw:
Special education law (2nd ed.). Deltaville, VA:
Harbor House Law Press.
Yell, M. L. (2011). The law and special education
(3rd ed.). Boston: Pearson.
E 1190
External Validity
▶ Ecological Validity
Extinction Procedures
Mary Jane Weiss
Institute for Behavioral Studies,
Endicott College, Beverly, MA, USA
Definition
Extinction refers to the process of discontinuing
the reinforcer that historically follows a behavior
(Cooper, Heron, & Heward, 2007).
Historical Background
In operant psychology, behavior is influenced by
both the stimuli that occur prior to and following
it. The stimuli that follow behaviors are conse-
quences. Consequences influence behavior in
three ways – consequences can increase (strength
rate, frequency, etc.), decrease, or have no influ-
ence on strength. A reinforcing consequence
results in an increased strength (or frequency or
rate) of that behavior. Similar to the presentation
of a reinforcer strengthening a behavior, removal
of the reinforcer (or preventing it from occurring)
that follows a behavior will have a weakening
effect on that behavior; it will reduce in strength
(or frequency or rate).
Historically, the treatment of challenging
behaviors that interfere with developing inde-
pendence or adaptive skills has focused on the
application of punitive consequences that
reduce or eliminate the target behavior. It has
always been true that extinction is also relevant
in this context. Over the past 15 years, the use
of extinction has been explored as an alterna-
tive to aversive treatments and has been shown
to effectively reduce behavior under certain
conditions.
External Validity
Current Knowledge
Extinction is withholding of reinforcement that
typically follows a behavior and that served to
maintain the behavior. However, the actual form
that an extinction procedure will follow depends
upon the form of the reinforcement that will be
withheld. The reinforcers that maintain aberrant
behaviors are not uniform or singular; behaviors
serve different functions and are maintained by
multiple potential effects. Sometimes a behavior
will lead to the acquisition of desirable conse-
quences, such as access to attention, desired
objects, preferred activities, or internal, physio-
logical (e.g., sensory) stimulation. Consider
a child who acts out in class to obtain teacher
attention. The child engages in disruptive behav-
ior in order to garner teacher attention. (In fact,
teachers must often attend to such disruptions to
ensure minimal intrusion into the flow of instruc-
tion.) In this case, an extinction procedure would
involve the teacher ignoring the behavior or in
a similar case, consider a child who aggresses in
order to obtain a toy or other preferred object.
The child may aggress against a sibling and then
gain access to a preferred toy. In this case, extinc-
tion would consist of preventing the child from
obtaining that object contingent on aggression.
Another example would be a child who acts out
in order to get a preferred activity. For example,
consider a child who is on the playground and,
when told by the teacher that recess is ended and
the child must go back inside, tantrums and cries.
Historically, it could be the case that this behavior
leads to more time on the playground. For exam-
ple, the teacher might cajole the child, offer
5 more minutes, give several transition warnings,
etc. An extinction procedure would consist of the
teacher preventing the child from remaining on
the playground. Instead, the child would be made
to come inside.
Some behaviors exhibited by persons with
autism are labeled as “self-stimulatory,” due to
the belief that these behaviors are reinforced
immediately by specific sensory input. For exam-
ple, a child might wave her hand in front of her
face because the visual movement is highly
desired. These behaviors are also termed
Extinction Procedures
“automatically reinforcing” behaviors because of
their inherent sensory consequences that are pre-
sumably maintaining the behavior. Extinction in
this type of example would require that the sen-
sory input that the individual finds highly desir-
able is identified and prevented from happening.
For example, Rincover, Cook, Peoples, and
Packard (1979) used extinction to stop the self-
stimulatory behaviors of young children. One boy
engaged in spinning plates on a table and enjoyed
listening to the sound they made. The extinction
procedure consisted of carpeting the surface on
which he spun the plate. The carpet masked the
sound, and thus plate spinning stopped. Another
child engaged in flipping a light switch on and
off, presumably for the visual feedback of the
light. The extinction procedure for this behavior
consisted of disconnecting the switch from the
electrical source. From that point on, the behavior
of flipping the switch produced no visual conse-
quence, and the behavior eventually stopped. In
such sensory extinction procedures, the feedback
is either reduced or eliminated, and the behavior
diminishes.
With other situations, the reinforcement for
a behavior could be the escape or avoidance of
an aversive situation. Consider a child who tan-
trums when presented a difficult task. Historically,
the tantrum is reinforced by the removal of the
task. (A teacher may react to the tantrum by
removing the task, changing the task, providing
a break, etc.) Thus, in this particular example, the
extinction procedure would involve the prevention
of the termination of the task; that is, extinction in
this case would consist of the teacher continuing to
present the task, so that the child learns that tan-
trums will not be reinforced by task removal.
As noted above, if the behavior is followed by
the presentation of a reinforcer, such as attention,
preferred activities, or objects, then extinction is
implemented by preventing the delivery of those
reinforcing consequences or terminating them as
soon as possible. On the other hand, if the behav-
ior is reinforced by the cessation of something
unpleasant (consider a child asked to do
a difficult work task who has learned that
a tantrum will cease the work demand), then
extinction requires the continued presentation of
1191 E
the unpleasant stimulus. In the work demand
case, extinction would require that the teacher
continually present the work demand and make
sure that no escape or avoidance of the task is
possible. The teacher would be sensitive to even
small ways in which escape could be reinforced.
For example, a delay in the representation of the
instruction or a brief pause in instruction could
reinforce escape-motivated behavior.
Thus, it is important to understand that
E
extinction is a procedure that prevents the rein-
forcement – that has typically followed
a behavior – from occurring. However, since
there are different types of reinforcement for
behavior, the actual procedures for implementing
extinction may vary.
Research on extinction has identified several
effects of this process. One effect, which has been
shown to generalize across response classes and
settings, is a gradual decrease in rate, frequency,
or intensity of behavior. Although the behavior
that is extinguished will eventually return to
baseline (i.e., pretreatment) levels or be elimi-
nated altogether, the rate of decrease is slow. If
a behavior is extremely severe and immediate
cessation is imperative, extinction may not be
the best procedure to select.
Concomitant with this gradual decrease is
what is termed an “extinction burst,” a sudden
increase in strength (frequency, rate, and/or
intensity) of that behavior. Problem behaviors
could worsen before they reduce. For example,
with a young child who is crying at bedtime,
parents reentering the room to comfort the child
and then exiting often intensify the screaming. It
may lead to escalations of the behavior and new
forms of behavior during the burst that evening,
and future nights may be characterized by even
higher levels of the behavior. Essentially, the
parents going back into the bedroom to comfort
the child may reinforce screaming when being
put to bed at night. Once the parents stop
reentering the room, the crying may increase in
both frequency and intensity for a short while.
When the burst occurs, it is likely a confirmation
that the controlling reinforcer has in fact been
identified and successfully withheld following
the occurrence of the response. If the extinction
E 1192
plan stays in effect, the behavior will once again
reduce in strength, but some variations of an
extinction burst may occur for several sessions
once an extinction plan is put into place. In other
words, there could be several days with some
variability before the behavior is extinguished.
A phenomenon commonly associated with
extinction is that of “spontaneous recovery.” The
behavior is likely to recur the next day after the
first day of using extinction even though the rein-
forcement for that behavior is no longer occurring.
When this happens, the typical response is to
maintain the implementation of extinction. Each
day that goes by, the spontaneous recovery will be
a little less, and eventually the behavior will no
longer occur. This can also happen after a behavior
has been successfully extinguished, even in the
absence of new reinforcement for the behavior.
This can be very confusing for parents and
teachers. Generally, however, spontaneous recov-
ery is short-lived and consistent implementation of
extinction will successfully address the issue.
To implement extinction, the following con-
ditions must be met. First, the behavior must be
clearly defined so that all caregivers and inter-
ventionists know when it is occurring and
when it is not. Second, there should be some
preextinction data on the level of the behavior,
against which postextinction data can be com-
pared, to determine if the extinction program is
having the reductive effect that is intended.
Third, all reinforcers that maintain the behavior
must be clearly identified. This will likely require
conducting a functional assessment or preferably
a functional analysis (i.e., systematic manipula-
tion of potential consequences). Fourth, a plan for
either terminating the reinforcer when it occurs,
or preventing it from occurring in the first place,
must be developed. This is often the most difficult
part of implementing extinction. Often the rein-
forcer is identified but with little ability to prevent
it from occurring. For example, consider a child
who teases other peers in his classroom for atten-
tion. The teachers may correctly identify the rein-
forcer as attention of the other children, but there
may be a huge difficulty (and ethical consider-
ations) in preventing all of the children in the
classroom from attending to the misbehavior.
Extinction Procedures
If alternate sources of reinforcement remain
available for the target behavior, extinction is
not likely to be successful. Fifth, the people who
will implement the extinction plan must consider
whether they will be able to continue the extinc-
tion plan when the extinction burst occurs. Con-
sider the following scenario – a child with autism
has a history of tantrumming violently when
a difficult work task is presented. His teacher is
confident that the escape from the work demands
is reinforcing the tantrum. The teacher develops
a plan for continually presenting the work (i.e.,
making sure the work demands do not cease).
However, the teacher also considers how much
more violent the tantrums may become during the
extinction burst. For extinction to work effec-
tively, the plan must be put into place upon the
occurrence of the target behavior, regardless of
the severity of the extinction burst. The teacher
and other implementers must plan on how to react
to the possible increase in frequency and inten-
sity. If a child is likely to engage in topographies
of behavior that are unacceptable and not ignor-
able (e.g., throwing desks, self-injury), extinction
is not an appropriate choice.
Finally, the implementers must consistently
withhold the reinforcers each time the target
behavior occurs. This is one of the most difficult
parts of implementing extinction, and it is one of
the more critical aspects of the procedure. Failure
to implement extinction contingent upon each
occurrence will result of the target behavior
being reinforced occasionally, which is intermit-
tent reinforcement. Research has shown that
behaviors that are intermittently reinforced are
much more difficult to extinguish than behaviors
on a continuous schedule. So, when implementing
extinction, failure to withhold reinforcement for
each behavioral occurrence could likely result in
the behavior becoming even stronger in the per-
son’s repertoire. If some reinforcement is likely to
occasionally occur, extinction may not be the best
method to select.
Good practice suggests that extinction be
implemented in combination with other proce-
dures, such as differential reinforcement of
other behaviors or differential reinforcement of
alternative behaviors. Research suggests that
Extreme Male Brain (EMB) Theory
when used in combination, extinction becomes
more effective. Additionally, the use of reinforce-
ment procedures to strengthen appropriate behav-
iors is part of best clinical practice.
Future Directions
Extinction is considered a treatment for problem
behaviors that is not aversive and acceptable to
most staff. It is not as regulated as other more
intrusive procedures, such as time-out or
overcorrection. Although researchers have inves-
tigated the role of clinical treatment with and
without implementing extinction procedures, the
results remain ambiguous. Identification of
behavior classes and/or environmental conditions
under which extinction is necessary or optimal in
clinical application would be helpful. Clinically,
it is important to match the procedure of extinc-
tion to certain behavioral characteristics and
learners. Clinicians must be mindful of control-
ling all sources of reinforcement and of monitor-
ing behavioral escalations in bursts.
See Also
▶ Functional Analysis
▶ Functional Assessment
References and Readings
Cooper, J. O., Heron, T. E., & Heward, W. L. (2007).
Applied behavior analysis (2nd ed.). Upper Saddle
River, NJ: Pearson.
Rincover, A., Cook, R., Peoples, A., & Packard, D. (1979).
Sensory extinction and sensory reinforcement princi-
ples for programming multiple adaptive behavior
change. Journal of Applied Behavior Analysis, 12(2),
221–233.
Extraordinary
▶ Exceptionality
1193 E
Extreme Male Brain (EMB) Theory
Bonnie Auyeung1, Michael Lombardo1,
Rebecca Knickmeyer2 and Simon Baron-Cohen1
1
Autism Research Centre, University of
Cambridge, Cambridge, UK
2
Department of Psychiatry, University of North
Carolina, Chapel Hill, NC, USA
E
Definition
Autism spectrum conditions (ASC) have been
described as an extreme manifestation of certain
traits or as a consequence of an “extreme
male brain.”
Historical Background
The link between ASC and “maleness” was first
proposed by Hans Asperger in his 1944 clinical
account where he states, “The autistic personality
is an extreme variant of male intelligence. . . In the
autistic individual the male pattern is exaggerated to
the extreme.” More recent evidence has led to the
proposal that ASC may be an exaggeration of
certain male-typical characteristics (Baron-
Cohen, 2002; Baron-Cohen, Knickmeyer, &
Belmonte, 2005).
Current Knowledge
Autism spectrum conditions (ASC) are charac-
terized by impairments in social interaction and
communication, alongside unusually restricted,
repetitive, stereotyped patterns of behavior, inter-
ests, and activities. The American Psychiatric
Association uses the term ASD for autism spec-
trum disorders. The term ASC will be used as
those at the higher-functioning end of the autistic
spectrum do not necessarily see themselves as
having a “disorder,” and the profile of strengths
and difficulties in ASC can be conceptualized as
atypical but not necessarily disordered. ASC
remains a medical diagnosis, hence the use of
E 1194
the term “condition,” which signals that such
individuals need support. Use of the term ASC
recognizes that the profile in question does not fit
a simple “disease” model but includes areas of
strength (e.g., in attention to detail) as well as
areas of difficulty and does not identify the indi-
vidual purely in terms of the latter.
Approximately 1% of children have a diagnosis
of ASC. These conditions have a strong neurobio-
logical and genetic component. There is also
a clear male to female ratio in the incidence of
ASC, estimated at 4:1 for classic autism and over
10:1 in individuals with Asperger syndrome. The
cause of the male bias in ASC is not fully under-
stood. Many clinical conditions occur in males
more often than females, including autism,
dyslexia, specific language impairment, attention-
deficit/hyperactivity disorder (ADHD), and early-
onset persistent antisocial behavior. Depression,
anorexia, and the anxiety disorders show a female
bias in sex ratio, raising the question of whether
there are sex-linked or sex-limiting factors
involved in the etiology of conditions that exhibit
a male bias.
ASC in particular have been described as an
extreme manifestation of certain sexually dimor-
phic traits or as a consequence of an “extreme male
brain” (EMB) (Baron-Cohen, 2002; Baron-Cohen
et al., 2005). Individuals with ASC have been
shown to be impaired in empathy (the drive to
identify another person’s emotions and thoughts,
and to respond to these with an appropriate emo-
tion and an area where females show an advan-
tage), while being average or even superior in
systemizing (the drive to analyze, explore, and
construct a system and an area males show an
advantage).
Studies of Empathy and Systemizing
It is widely accepted that males and females show
significant differences in their neuroanatomy,
cognition, and behavior from an early age. Sex
differences in the precursors of empathy are seen
from birth, with female babies on average show-
ing a stronger preference for looking at social
Extreme Male Brain (EMB) Theory
stimuli (faces) from 24 h after birth (Connellan,
Baron-Cohen, Wheelwright, Batki, & Ahluwalia,
2000). Girls have also been found to make more
eye contact immediately after birth (Hittelman &
Dickes, 1979), at 12 months of age (Lutchmaya,
Baron-Cohen, & Raggatt, 2002a) and at 2 and
4 years of age (Podrouzek & Furrow, 1988).
Girls on average also exhibit more comforting,
sad expressions or more sympathetic vocaliza-
tions when witnessing another’s distress
(Hoffman, 1977). Girls on average also show
better quality of social relationships at 48 months,
as measured by a subscale of the Children’s Com-
munication Checklist. Similar patterns have been
observed in adults, with women on average being
more likely to report more intimate relationships,
having a confidant and receiving social support
and visits from friends and family (Baron-Cohen
& Wheelwright, 2003).
Using measures that directly assess aspects of
empathy, girls are on average better than boys at
evaluating the feelings and intentions of charac-
ters in a story (Bosacki & Astington, 1999) and
differentiating between the appearance and real-
ity of emotion (Banerjee, 1997). There is also
a female superiority on the “faux pas” test of
social sensitivity (Baron-Cohen, O’Riordan,
Stone, Jones, & Plaisted, 1999) which measures
the recognition of someone saying something that
might be hurtful. Sex differences in empathy
remain evident in adulthood: for example,
women on average score higher than men on the
“Reading the Mind in the Eyes” test, which
examines subtle mental state and emotion recog-
nition (Baron-Cohen, Wheelwright, & Hill,
2001).
In general, studies have shown that individuals
with ASC are also impaired on empathy-related
tasks that normally give rise to female superior-
ity, such as the “Social Stories Questionnaire”
(Lawson, Baron-Cohen, & Wheelwright, 2004),
the “Reading the Mind in the Eyes” task (Baron-
Cohen et al., 2001), and the recognition of “faux
pas” in short stories (Baron-Cohen et al., 1999).
Adults with ASC score lower on the Friendship
and Relationship Questionnaire, which assesses
empathic styles of relationships (Baron-Cohen &
Extreme Male Brain (EMB) Theory
Wheelwright, 2003). Children with autism per-
form less well than controls on the “Feshbach and
Powell Audiovisual Test for Empathy,”
a measure of empathy and emotional responsive-
ness (Yirmiya, Sigman, Kasari, & Mundy, 1992).
Children with ASC also show more difficulties
passing “theory of mind” tests compared to typ-
ically developing children (Happe, 1995).
Studies examining play preferences point
toward more interest in mechanical and construc-
tional play in boys, demonstrated by a preference
to play with toy vehicles or construction sets,
while girls are more likely to choose to play
with dolls or toy animals (Berenbaum & Hines,
1992). Males on average also score higher on
tasks that require systemizing such as using direc-
tional cues in map reading and map making
(Kimura, 1999), intuitive physics (Lawson
et al., 2004), and the SAT Math Test (Benbow
& Stanley, 1983). They are also more accurate on
measures of spatial ability such as mental rotation
and spatial visualization (Voyer, Voyer, &
Bryden, 1995). Finally, males on average score
higher on the Embedded Figures Test (EFT)
(Witkin, Dyk, Fattuson, Goodenough, & Karp,
1962), which measures attention to detail and
field independence – both prerequisites for sys-
temizing (Baron-Cohen, 2002).
Experimental evidence supporting the EMB
theory of autism includes findings that individ-
uals with ASC tend to show superior performance
compared to typical controls on tasks that involve
systemizing and on certain visuospatial tasks that
normally give rise to male superiority, such as
figure disembedding (Falter, Plaisted, & Davis,
2008; Jolliffe & Baron-Cohen, 1997; Ropar &
Mitchell, 2001; Shah & Frith, 1983), block
design (Ropar & Mitchell, 2001; Shah & Frith,
1993), and mental rotation (Brosnan, Daggar, &
Collomosse, 2009; Falter et al., 2008).
Brosnan et al. (2009) suggest that mental rota-
tion tasks can be separated into rotational and
non-rotational components and observed
a significant correlation between systemizing
and the non-rotational components of the mental
rotation task but not the rotational component of
the task (Brosnan et al., 2009). Individuals with
1195 E
high-functioning autism (and therefore intact IQ)
have also been observed to demonstrate superior
accuracy and shorter learning times in tasks that
involve maps (Caron, Mottron, Rainville, &
Chouinard, 2004).
A recent study by Pierce, Conant, Hazin,
Stoner and Desmond (2010) found that toddlers
with an ASD as young as 14 months spent signif-
icantly more time fixating on dynamic geometric
(“systemizable”) images, whereas typically
E
developing toddlers showed longer looking
times at social stimuli. Further, if a toddler spent
more than 69% of his or her time fixating on
geometric patterns, then the positive predictive
value for accurately classifying that toddler as
having an ASD was 100% (Pierce et al., 2010).
These findings suggest that these early looking
preferences can be found very early in life and
used to differentiate toddlers with ASC from typ-
ically developing toddlers.
However, the EMB theory has not been shown
to apply to all measures showing a male advan-
tage. For example, Falter et al. (2008) found that
children with autism do not show superior per-
formance on a measure of targeting ability com-
pared to typically developing boys. It is possible
that problems with motor coordination
(dyspraxia) in the ASC group may have affected
performance on this task. It is worth emphasizing
that the EMB theory predicts intact or superior
performance on measures of systemizing in ASC
and that the EMB theory does not focus on sys-
temizing alone, but on the discrepancy between
an individual’s empathy and systemizing
abilities.
The Empathy Quotient (EQ) and Systemizing
Quotient (SQ)
The Empathy Quotient (EQ) and Systemizing
Quotient (SQ) were developed in order to examine
trends in gender-typical behavior in adults. The EQ
and SQ are self-report questionnaires with a Likert
format and contain a list of statements about real-
life situations, experiences, and interests where
empathizing or systemizing skills are required.
Findings from the EQ in adults revealed
a significant sex difference, with women scoring
E 1196 Extreme Male Brain (EMB) Theory

significantly higher than men. Results from the SQ Extreme Male Brain (EMB) Theory, Table 1 A sum-
indicate that men score significantly higher than mary of the psychological evidence for the extreme male
brain (EMB) theory
women (Carroll & Chiew, 2006; Wheelwright
et al., 2006). A parent-report version of the EQ Autism > Female >
male > male >
and SQ for children between 4 and 11 years of Psychological measure female autism
age has also shown similar results with girls scor- Adult systemizing quotient ✓
ing significantly higher on the EQ and boys scoring (SQ)
significantly higher on the SQ (Auyeung, Baron- Child SQ ✓
Cohen, Wheelwright, Samarawickrema, & Embedded figures test ✓
Atkinson, 2009), suggesting that these patterns Intuitive physics test ✓
are present from an early age. Adult autism spectrum ✓
In adults, EQ and SQ scores have also been Quotient (AQ)
shown to be better predictors than sex for career Adolescent AQ ✓
Child AQ ✓
choice in science and engineering, or in degree
Childhood autism spectrum ✓
choice (e.g., science vs. humanities), suggesting Test (CAST)
that typical sex differences in interests or apti- Quantitative checklist for ✓
tudes may reflect the individual’s cognitive style, autism in toddlers
independent of their sex. (Q-CHAT)
In order to compare an individual’s empathiz- Reading the mind in the eyes ✓
ing and systemizing, Goldenfeld, Baron-Cohen adult empathy quotient (EQ) ✓
and Wheelwright (2005) examined standardized Child EQ ✓
(normalized) scores on the EQ and SQ. The dif- Faux pas test ✓
ferences between standardized scores demon-
strated strong sex differences and led to the
definition of empirical “brain types.” The five found to show the Type S or Extreme S “brain
“brain types” describe whether an individual is types” (Auyeung, Baron-Cohen, Wheelwright
“balanced” (Type B), better at empathizing (Type et al., 2009c; Goldenfeld et al., 2005;
E), or better at systemizing (Type S). “Extreme” Wheelwright et al., 2006). See Table 1 for
empathizing (Extreme E) or systemizing a summary of psychological evidence that –
(Extreme S) types were also assigned where an irrespective of the direction of sex difference –
individual showed a significant discrepancy in people with autism show an extreme of the male
different directions (Goldenfeld et al., 2005; profile Table 2.
Wheelwright et al., 2006). The assignment of In addition to the evidence at the behavioral
“brain types” based on relative EQ and SQ scores level, it has been suggested that characteristics of
in both children and adults appears to be a useful neurodevelopment in autism such as larger overall
method of describing differences in sex-typical brain volumes and greater growth of the amygdala
behavior, with the majority of females toward during childhood may also represent an exaggera-
Type E and the majority of males toward Type tion of typical sex differences in brain development
S (Auyeung, Baron-Cohen, Wheelwright et al., (Baron-Cohen et al., 2005). Studies using fMRI
2009c; Goldenfeld et al., 2005; Wheelwright indicate that typical females show increased activ-
et al., 2006). ity in the extrastriate cortex during the Embedded
Findings using the EQ and SQ questionnaires Figures Test and increased activity bilaterally in
also provide further evidence for the EMB theory the inferior frontal cortex during the “Reading the
of ASC. When the scores obtained from the EQ Mind in the Eyes” task. Parents of children with
and SQ are standardized using the method ASC also tend to show hyper-masculinization
suggested by Goldenfeld et al. (2005), the vast of brain activity, suggesting that hyper-
majority of children and adults with high- masculinization may be part of the broader autism
functioning autism or Asperger syndrome are phenotype.
Extreme Male Brain (EMB) Theory
Extreme Male Brain (EMB) Theory, Table 2 A
summary of the evidence consistent with the EMB theory
at the neural level
Autism > Female >
male > male >
Brain region female autism
Total brain volume ✓
Head circumference ✓ Development of Sex Differences
Grey and white matter ✓
Amgydala ✓ Though genetic sex is determined at conception,
Corpus callosum ✓ it is the gonadal hormones (i.e., androgens, estro-
Perisylvian language areas ✓ gens, and progestins) that are responsible for
(Heschl’s gyrus/planum
temporale)
L > R asymmetry in ✓
planum temporale
Lateral frontoparietal ✓
cortex
The Role of Social Factors in the
Development of Sex Differences
Social interactions undoubtedly play an impor-
tant role in the development of gender-typical
play and toy choices. Gender-based expectations
may cause parents, teachers or caregivers to elicit
and reinforce expected behavior from children
(Stern & Karraker, 1989), thus shaping the
child’s behavior. It has been shown that infant
gender labeling as male or female often elicits
sex-stereotypic responses from adults and chil-
dren (Stern & Karraker, 1989). It has also been
suggested that girls are encouraged to be more
sensitive and caring toward others than boys
(Gilligan, 1982). Findings from studies examin-
ing play preferences have indicated that boys are
encouraged by parents to play with masculine-
typical toys and discouraged from playing with
feminine-typical toys (Fagot & Hagan, 1991).
Girls, on the other hand, are also encouraged to
play with feminine-typical toys but not necessar-
ily discouraged from playing with masculine-
typical toys (Fagot & Hagan, 1991). While these
factors might influence the behavior exhibited by
typically developing children, studies examining
eye contact and preference for social stimuli in
newborn children provide convincing evidence
1197 E
for a biological basis for some sex differences.
It is also not clear how such social factors might
apply to the ASC group.
The Role of Prenatal Hormones in the
E
differentiation of the male and female pheno-
types in the developing human fetus. It is thought
that behaviors showing large sex differences are
the best candidates for studying effects of hor-
mones on later development (Hines, 2004). The
direct sampling of fetal serum or manipulation of
fetal hormone levels would be highly dangerous.
As a result, researchers have employed indirect
methods of measuring prenatal hormone expo-
sure to study effects on later development.
One such indirect measure is the ratio between
the length of the 2nd and 4th digit (2D:4D) of the
hand. This ratio has been found to be sexually
dimorphic, being lower in males than in females.
2D:4D ratio is thought to be fixed by week 14 of
fetal life and has been found to reflect fetal expo-
sure to prenatal sex hormones in early gestation
(Lutchmaya, Baron-Cohen, Raggatt, Knickmeyer,
& Manning, 2004; Manning, 2002). Results from
studies of 2D:4D ratios as proxies for fetal testos-
terone (fT) levels show that children with ASC
have more masculinized digit ratios compared to
typically developing boys. These patterns have
also been observed in the siblings and parents of
children with ASC, indicating the possibility
of a link between genetically based elevated fT
levels and the development of ASC (Manning,
Baron-Cohen, Wheelwright, & Sanders, 2001).
The medical condition of Congenital Adrenal
Hyperplasia (CAH) leads to abnormally high pre-
natal and neonatal androgen levels and has pro-
vided researchers with an indirect method of
examining the effects of elevated androgen expo-
sure. Girls with CAH have more autistic traits
(measured using the adult AQ) compared to
their unaffected sisters (Knickmeyer et al.,
2006a). Given that this condition is usually
E 1198
treated following birth, this suggests their higher
AQ scores reflect elevated prenatal androgen
levels. These findings should be interpreted with
caution, however, since CAH carries a number of
related problems (as well as extensive treatment)
which may affect the atypical cognitive profiles
found in this population.
Some studies have also compared measure-
ments of testosterone in umbilical cord blood
with postnatal development. A recent study
using umbilical cord blood testosterone measures
examined pragmatic language ability in girls
followed-up at 10 years of age. Results showed
that the higher a girl’s free testosterone level at
birth, the higher the scores on a pragmatic lan-
guage difficulties questionnaire (Whitehouse
et al., 2010). However, levels of fT are typically
at very low levels from about week 24 of gesta-
tion, umbilical cord samples can contain blood
from the mother as well as the fetus, and hormone
levels may vary due to labor itself, so umbilical
cord blood testosterone does not allow one to test
if outcomes reflect fT per se.
Currently the best method to examine the
effect of fT is to sample the amniotic fluid sur-
rounding the fetus via amniocentesis. An advan-
tage of amniotic fluid samples is that
amniocentesis is often performed for routine clin-
ical purposes within a relatively narrow time
period which coincides with the hypothesized
critical period for human sexual differentiation
between weeks 8 and 24 of gestation (Hines,
2004). This is also more direct than the 2D:4D
method as the hormones themselves can be
assayed, rather than relying on a proxy for these.
A number of studies have linked elevated
levels of fT in the amniotic fluid with the mascu-
linization of certain behaviors, beginning shortly
after birth. Elevated fT has been linked to reduced
eye contact in infants (Lutchmaya et al., 2002a),
smaller vocabulary in toddlers (Lutchmaya,
Baron-Cohen, & Raggatt, 2002b), narrower inter-
ests and poorer quality of social relationships at
4 years of age (Knickmeyer, Baron-Cohen,
Raggatt, & Taylor, 2005), less empathy at 4 and
8 years (Chapman et al., 2006; Knickmeyer,
Extreme Male Brain (EMB) Theory
Extreme Male Brain (EMB) Theory, Table 3 Evidence
from typically developing children for effects of fT
Evidence from typical
children Key references
Eye contact is inversely Lutchmaya et al. (2002b)
related to fT
Social skills are inversely Knickmeyer et al. (2005)
related to fT
Vocabulary size is inversely Lutchmaya et al. (2002c)
related to fT
Empathy is inversely related Chapman et al. (2006),
to fT Knickmeyer et al. (2005)
Autistic traits are positively Auyeung et al. (2009b,
associated with fT 2010)
Restricted interests are fT is Knickmeyer et al. (2005)
positively associated
Systemizing is positively Auyeung et al. (2006)
associated with fT
Rightward asymmetry in the Chura et al. (2010)
isthmus of the corpus
callosum is positively
associated with fT
Baron-Cohen, Raggatt, Taylor, & Hackett,
2006b), more male-typical play behavior
(Auyeung et al., 2009a), better performance on
the Children’s Embedded Figures Test (Auyeung
et al., in press), and increased systemizing at
8 years (Auyeung et al., 2006). In addition, fT
levels have been found to be positively correlated
with number of autistic traits (measured using the
Quantitative Checklist for Autism in Toddlers
(Allison et al., 2008)) in toddlers between 18
and 24 months of age (Auyeung, Taylor, Hackett,
& Baron-Cohen, 2010), as well as in older chil-
dren (ages 6–10 years old), using two indepen-
dent dimensional measures of autistic traits (the
child version of the AQ and the Childhood
Autism Spectrum Test (Auyeung et al., 2009b)).
Evidence from typically developing children for
effects of fT is summarized in Table 3.
The use of amniotic fluid to measure prenatal
hormonal exposure has several limitations. Ide-
ally, it would be best to make direct measure-
ments of testosterone at regular intervals
throughout gestation and into postnatal life.
However, it would be extremely hazardous to
Extreme Male Brain (EMB) Theory
Extreme Male Brain (EMB) Theory, Table 4 Evidence for testosterone effects in people with ASC
Evidence from people with ASC
10 sex steroid genes associated with AS or AQ or empathy
HSD11B1, LHCGR, CYP17A1, CYP19A1, SCP2,
CYP11B1*, ESR1, ESR2, HSD17B4, HSD17B2*
Timing of puberty Boys with ASC enter puberty earlier,
girls with ASC enter puberty later
Testosterone related medical conditions in women with
ASC and their mothers (e.g., PCOS, breast and ovarian
cancers, acne)
Testosterone related characteristics in women with ASC
and their mothers
Lower 2D:4D ratio in ASC, and parents
SRD5A1, and AR genes associated with ASC
attempt direct measurements from the fetus itself
for purely research purposes. It is not possible to
obtain repeated samples of fT because amniocen-
tesis itself carries a risk of causing miscarriage
(of about 1%). As a result, obtaining amniotic fT
measures are opportunistic, when the procedure
is being carried out for clinical reasons, with
never more than a single measurement of fT at
one time-point although it is known that hor-
mones fluctuate during the day and between
days, even in fetuses. The representativeness of
a single sample of fT thus remains unclear, but
would be difficult to explore in an ethical manner.
In addition, given the reported time course of
testosterone secretion, the most promising time to
measure fT is probably at prenatal weeks 8–24
(Smail, Reyes, Winter, & Faiman, 1981), but this
is still a relatively wide range. In addition, research
is nonhuman primates has shown that androgens
masculinize different behaviors at different times
during gestation, suggesting different behaviors
may also have different sensitive periods for devel-
opment. For all these reasons, the inferences that
can be drawn about a single measurement of fT are
therefore limited. However, where a significant
correlation between amniotic fT and a behavior is
observed, this should represent a very conservative
estimate of the correlation between overall fT
levels and that behavior.
1199 E
Key references
Chakrabarti et al. (2009)
Ingudomnukul, Baron-Cohen, Wheelwright, and
Knickmeyer (2007), Knickmeyer et al. (2006c), Tordjman,
Ferrari, Sulmont, Duyme, and Roubertoux (1997)
Ingudomnukul et al. (2007)
Ingudomnukul et al. (2007), Knickmeyer, Wheelwright,
E
and Baron-Cohen (2008)
Manning et al. (2001), Milne et al. (2006), Noipayak
(2009)
Henningsson et al. (2009), Hu et al. (2009)
Evidence Implicating Testosterone in
the Etiology of Autism
Genetic influences are undoubtedly involved
with other factors (such as prenatal hormone
levels) which lead to the development of ASC.
Evidence of a genetic link to ASC is provided by
a recent study which shows that genes regulating
sex steroids are associated with autistic traits, as
measured by scores on the Autism Spectrum
Quotient (AQ), in a typical adult sample
(Chakrabarti et al., 2009). A parallel study also
showed that genes regulating sex steroids are
associated with a diagnosis of Asperger syn-
drome in a case-control sample (Chakrabarti
et al., 2009).
Other lines of evidence implicating testoster-
one in the etiology of ASC are summarized in
Table 4:
Conclusions
There is a significant body of evidence
connecting the characteristic behaviors of ASC
to extremes of certain male-typical behaviors.
Evidence includes superior performance on
a range of tasks where males typically outperform
females but impairment compared to typical
E 1200
males on tasks showing a female advantage. This
observation has led to the development of the
“extreme male brain” theory of autism. Support
for this theory can also be found very early in life,
and also in some primate studies suggesting the
development of sex-typical behaviors is at least
partly biological.
Research using direct measures of potential
biological factors such as prenatal hormones as
well as multiple measures of empathizing and
systemizing, including both observational and
behavioral measures are needed to explore the
link between these factors in greater detail.
Although the findings presented in this chapter
lend support to the “extreme male brain” theory
of ASC and its link to fT, a thorough evaluation of
this theory will require testing not just for asso-
ciations between fT and autistic traits, but
between fT and clinically diagnosed ASC. This
remains an active area of research.
Future Directions
Future studies of empathizing and systemizing in
children could examine whether the relationships
between fT levels (and other biological factors)
remain consistent using multiple measures of
empathy and systemizing (e.g., observational,
experimental). In addition, the replication of the
findings related to fT levels in larger sample sizes
would assist in identifying any factors that are
linked with levels in the extreme ranges. Future
studies could assess whether relationships
between fT levels and the development of autistic
traits are consistent for individuals with a clinical
diagnosis of ASC since the current samples only
included typically developing children. Consid-
ering the current support for a role for fT in the
development of autistic traits, it would also be
beneficial for future studies to examine the rela-
tionships between fT levels, genetic variation,
and the development of autistic traits.
The EMB theory of autism has been devel-
oped from studies in typically developing and
high-functioning individuals with ASC. It would
be interesting to extend the scope of this theory
with an examination of individuals with more
Extreme Male Brain (EMB) Theory
severe forms of ASC. It is also important to assess
the validity of “empathizing” and “systemizing”
measures by correlating these with performance
and everyday measures of functioning, and future
studies could further explore how these domains
develop and also how they correlate with neural
structure and function.
See Also
▶ Broader Autism Phenotype
▶ Cognitive Skills
▶ Empathy
▶ Face Recognition
▶ Friendships
▶ Gender Differences
▶ Social Behaviors and Social Impairment
▶ Social Cognition
▶ Systemizing
▶ Theory of Mind
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Eye Gaze
Eye Contact
▶ Mutual Gaze
Eye Gaze
Atsushi Senju
Centre for Brain and Cognitive Development,
Birkbeck, University of London, London, UK
Definition
The term “eye gaze” may refer to either of the
two distinctive, but related, topics. Firstly,
it refers to the perception of other persons’ eye
gaze, which can be inferred from the relative
position of the iris within the eyelid, in conjunc-
tion with the orientation of the head and the body.
Secondly, it also refers to the production of eye
gaze by a patient or a participant, such as the
control of saccades and fixations. This entry
mainly covers the former topic. Perception of
others’ eye gaze is crucial for social interaction
and communication and its impairment in ASD
because eye gaze signals the direction of others’
attention and intention.
Current Knowledge
Fixations on Another Person’s Eyes
Atypical pattern of mutual gaze behavior, or eye
contact, is among the most distinguishable man-
ifestation of the qualitative impairment in social
interaction in ASD. Since Kanner’s first report
(Kanner, 1943), such atypical pattern of eye con-
tact has been reported and discussed in many
clinical and experimental settings, including
recent studies using eye-tracking methods
(Senju & Johnson, 2009a). Based on this clinical
significance, eye contact is currently included in
standardized diagnostic criteria such as DSM and
ICD. In DSM-IV-TR, it is defined as a “marked
impairment in the use of multiple nonverbal
1203 E
behaviors (e.g., eye-to-eye gaze) to regulate
social interaction and communication”
(American Psychiatric Association [APA],
2000, p. 70). Retrospective home video analyses
of infants who were later diagnosed with ASD
have revealed that atypical patterns of eye contact
can be observed within the first year of life, well
before the age of diagnosis (Maestro et al., 2005).
Some researchers and clinicians once proposed
that such atypical eye contact behavior results
E
from “gaze avoidance,” active avoidance of
others’ eye gaze due to negatively valenced
overarousal (e.g., Hutt & Ounsted, 1966).
However, follow-up studies reported mixed
results, suggesting that the gaze avoidance may
be present in some individuals with ASD, but
it may not be universal or predominant in this
population (Buitelaar, 1995).
Some of eye-tracking studies have revealed
that individuals with ASD fixate others’ eyes
less than typically developing individuals do,
but other studies failed to replicate or reported
mixed results (Senju & Johnson, 2009a). Such
inconsistencies may result from the differences
in task demands and/or the characteristics of
stimuli used. In general, reduced fixations on the
eyes are most prominent with complex and cog-
nitively demanding face stimuli and/or by using
dynamic videotape stimuli, including conversa-
tions. Moreover, individual differences in the
fixations on the eyes within ASD correlate with
the volume and the face sensitivity of amygdala
(e.g., Dalton et al., 2005), as well as the degree of
self-reported social anxiety (Corden, Chilvers, &
Skuse, 2008). However, it does not correlate with
autistic symptoms measured with ADOS or AQ
(Corden et al., 2008).
Perception of Direct Gaze
Direct gaze signals that the person is looking at
the perceiver. It also leads to the establishment of
mutual gaze or eye contact, which signals the
initiation of communication. In typically devel-
oped population, perceived direct gaze, or eye
contact, modulates concurrent and/or immedi-
ately following cognitive processing and/or
behavioral responses, a phenomenon called the
eye contact effect (Senju & Johnson, 2009b).
E 1204
For example, perceived eye contact facilitates
the performance of face-related tasks such as
gender discrimination, recognition of face iden-
tity, and detection of gaze direction. Results from
neuroimaging studies also indicate that perceived
eye contact modulates the activation of social
brain network (defined as the cortical and subcor-
tical structures specialized for the processing of
social information, such as fusiform gyrus, supe-
rior temporal sulcus, medial prefrontal and
orbitofrontal cortex, and amygdala). Sensitivity
to the direction of another person’s eye gaze
appears very early in typical development
(Johnson, Grossmann, & Kadosh, 2009). For
example, newborns preferentially look longer at
the faces with direct gaze than those with averted
gaze. Perceived eye contact also facilitates the
processing of face identity and communicative
facial expression during the first half year of life.
A series of studies have demonstrated atypical
processing of direct gaze in ASD (Senju &
Johnson, 2009a). For example, Senju, Yaguchi,
Tojo, and Hasegawa (2003) used an oddball pro-
cedure in which children were asked to detect
a rare stimulus presented occasionally within
the context of a frequently reoccurring stimulus.
The rare stimuli were either faces with direct gaze
or those with laterally averted eye gaze (i.e., faces
with eyes looking leftward or rightward).
The frequent stimuli were faces with eyes looking
downward. Thirteen children with autism (mean
age: 12 years) were compared with typically
developing children of the same range of the
age and nonverbal intelligence. Typically devel-
oping children showed the eye contact effect, that
they were better at detecting direct gaze than
averted gaze. By contrast, although children
with autism are equally good at detecting averted
gaze as typically developing children, they were
less skilled at detecting faces with direct gaze,
and they failed to show the eye contact effect or
the facilitation of performance caused by the
perceived direct gaze. Similarly, Pellicano and
Macrae (2009) assessed whether direct gaze
facilitates the person categorization in children
with autism (mean age: 10 years) and age- and
IQ-matched typically developing children.
Results revealed that typically developing
Eye Gaze
children were faster to categorize faces by sex
when they were with direct gaze than with
averted gaze. By contrast, although children
with autism were as fast as typically developing
children to categorize faces, their performance
were unaffected by the gaze direction of the
faces. These studies demonstrate that unlike typ-
ically developing individuals, individuals with
ASD do not show the eye contact effect or the
facilitation of face and gaze processing caused by
the perceived direct gaze.
Several studies have recorded field potentials
on the scalp with either EEG or MEG to assess
the cortical response to direct and averted gazes
in individuals with ASD, but results are mixed.
Two studies reported that 3- to 7-year-old chil-
dren (mean age: 5 years, Grice et al., 2005) as
well as 7- to 12-year-old children (mean age:
10 years old, Kylli€ainen, Braeutigam, Hietanen,
Swithenby, & Bailey, 2006) with ASD showed
larger event-related potential (ERP) or event-
related field (ERF) response to direct gaze than
averted gaze, but control children did not.
By contrast, Senju, Tojo, Yaguchi, and Hasegawa
(2005) reported that typically developing chil-
dren (9- to 14-year-olds, mean age: 12 years)
showed a larger ERP amplitude for direct than
for averted gaze, but ERPs of children with ASD
were not modulated by the presence of eye con-
tact. Moreover, Elsabbagh et al. (2009) recorded
EEG from high-risk infants (see also ▶ Early
Diagnosis) as well as from low-risk control
infants while they watched faces with either
direct or averted eye gaze and conducted ERP
and time-frequency analysis (TFA). Results
showed that a late ERP component (P400),
which is known to relate to face processing, has
a longer latency in response to direct gaze in
high-risk infants. Secondly, TFA analysis
revealed clearly distinguished and temporally
sustained high-frequency oscillatory activity in
the gamma-band frequency for direct gaze
compared to averted gaze in control infants.
In contrast, high-frequency oscillatory activity
in gamma band for direct gaze compared to
averted gaze in high-risk infants was delayed
and less persistent. These results suggest that
atypical eye contact processing in high-risk
Eye Gaze
infants relates to the top-down modulation
(as indicated by the slower P400 latency)
and task-relevant synchronization of brain acti-
vations (as indicated by the lack of differential
gamma-band activation in response to eye
contact).
Two studies have assessed skin conductance
response (SCR), an index of physiological
arousal, while individuals with ASD observe
faces with either direct or averted eye gaze. How-
ever, the results are again mixed – one study
found larger SCR in response to direct gaze in
10-year-old children with ASD (Kylli€ainen &
Hietanen, 2006), but the other study did not
replicate this findings in 12-year-old children
(Joseph, Ehrman, McNally, & Keehn, 2008).
Such inconsistency between physiological stud-
ies may result from the different age ranges of the
participants and/or the different experimental
tasks used for EEG/MEG/SCR recordings.
To summarize, behavioral studies have con-
sistently found that direct gaze facilitates cogni-
tive processing of faces in typically developing
children, but the face and gaze processing of
individuals with ASD are unaffected by the
presence of direct gaze (Senju & Johnson,
2009a). Inconsistencies in the physiological
studies make it difficult to understand the neural
basis of such atypical processing of direct gaze in
individuals with ASD.
Perception of Averted Gaze
Averted gaze, by contrast, signals that the person
is looking at something in the environment. Thus,
following another person’s gaze helps enable the
perceiver to infer his or her attention, goal, and/or
intention (see also ▶ Gaze). In typical develop-
ment, perceived averted gaze reflexively shifts
the attention of the perceiver to the corresponding
direction, which is often called gaze cueing effect
(Frischen, Bayliss, & Tipper, 2007). The gaze
cueing effect can be observed from 3 months of
age, which corresponds to the age range when
a rudimentary form of gaze following starts to
appear.
Individuals with ASD do not have an overall
impairment in detecting the direction of others’
eye gaze. For example, Leekam, Baron-Cohen,
1205 E
Perrett, Milders, and Brown (1997) demonstrated
that children with autism are as good as typically
developing children at discerning the subtle dif-
ferences in gaze direction. Moreover, majority of
studies demonstrated that individuals with autism
across the wide age range, from 2-year-old tod-
dlers to adults, show apparently typical gaze cue-
ing effect (Nation & Penny, 2008). In these
studies, participants are presented with a picture
of a face with gaze averted to the left or right
E
followed by a target stimuli presented either to
the left or right of the face. Individuals with ASD,
as well as typically developing individuals, are
faster to detect the target when the face was
looking at the location than when the face was
looking at the opposite direction. These studies
contrast with the impairment in gaze following
behavior in individuals with ASD (see also
▶ Gaze).
However, several studies also suggest the
qualitative differences in the gaze cueing effect
between individuals with ASD and typically
developing individuals. For example, Senju,
Tojo, Dairoku, and Hasegawa (2004) compared
the cueing effect of eye gaze and an arrowhead
and found that children with autism do not show
preferential sensitivity to eye gaze unlike typi-
cally developing children. Other studies (e.g.,
Ristic et al., 2005) used a schematic face, instead
of a photographic image of a face, and found that
only typically developing individuals show the
gaze cueing effect in response to the schematic
eyes. By contrast, individuals with ASD do not
show gaze cueing effect in response to these
stimuli. These studies suggest that the gaze cue-
ing effect in individuals with ASD is not as robust
as in typically developing individuals and per-
haps is not processed in a functionally specialized
cognitive mechanism.
Individuals with ASD also show difficulties in
inferring mentalistic and communicative signifi-
cance of the eyes. For example, Baron-Cohen,
Baldwin, and Crowson (1997) presented two
novel objects to 7- to 12-year-old children with
ASD as well as typically developing children
matched by the mental age and verbally labelled
one of these objects. Typically developing chil-
dren correctly associated the label with the object
E 1206
being looked at by the experimenter, even when
the child was looking at the other object when the
experimenter uttered the label. By contrast,
children with autism tended to apply the label to
objects in their own focus rather than the one the
experimenter was looking at. An adult neuroim-
aging study also demonstrated that individuals
with ASD, unlike typically developing individ-
uals, do not show differential cortical activation
in response to the referential gaze (Pelphrey,
Morris, & McCarthy, 2005).
To summarize, individuals with ASD have
relatively good capacity to encode the direction
of others’ eye gaze and reflexively shift their
attention to the corresponding direction. How-
ever, the gaze processing in individuals with
ASD may not be as robust or specialized as
those of typically developing individuals, which
may be related to the difficulty in using others’
eye gaze in the context of social learning.
Future Directions
Further studies will be required to clarify the
neurodevelopmental basis of eye gaze processing
in ASD and its relationship with other clinical
symptoms. Firstly, it is not clear why there are
such inconsistencies between different neuro-
physiological studies contrasting direct and
averted gaze processing in ASD, as well as the
different eye-tracking studies investigating the
pattern of face scanning in ASD (Senju &
Johnson, 2009a). Thus, further studies will be
required to systematically control the background
of participants (e.g., age, gender, and/or comor-
bidity) as well as the properties of the stimuli
and the tasks used (e.g., dynamic vs. static, active
task vs. passive viewing, size and/or facial
expression) to reveal the neurophysiological
basis of direct gaze processing in ASD.
Secondly, it will be important to investigate the
relationship between atypical cortical response to
eye gaze in early infancy (e.g., Elsabbagh et al.,
2009) and the later manifestation of clinical
symptoms.
Eye Gaze
References and Readings
American Psychiatric Association. (2000). Diagnostic
and statistical manual of mental disorders (4th ed.,
Text Rev.), DSM-IV-TR. Washington, DC: Author.
Baron-Cohen, S., Baldwin, D. A., & Crowson, M. (1997).
Do children with autism use the speaker’s direction of
gaze strategy to crack the code of language? Child
Development, 68(1), 48–57.
Buitelaar, J. K. (1995). Attachment and social withdrawal
in autism – hypotheses and findings. Behaviour, 132,
319–350.
Corden, B., Chilvers, R., & Skuse, D. (2008). Avoidance
of emotionally arousing stimuli predicts social-
perceptual impairment in Asperger’s syndrome.
Neuropsychologia, 46(1), 137–147.
Dalton, K. M., Nacewicz, B. M., Johnstone, T.,
Schaefer, H. S., Gernsbacher, M. A., Goldsmith, H. H.,
et al. (2005). Gaze fixation and the neural circuitry of
face processing in autism. Nature Neuroscience, 8(4),
519–526.
Elsabbagh, M., Volein, A., Csibra, G., Holmboe, K.,
Garwood, H., Tucker, L., et al. (2009). Neural corre-
lates of eye gaze processing in the infant broader
autism phenotype. Biological Psychiatry, 65(1),
31–38.
Frischen, A., Bayliss, A. P., & Tipper, S. P. (2007). Gaze
cueing of attention: Visual attention, social cognition,
and individual differences. Psychological Bulletin,
133(4), 694–724.
Grice, S. J., Halit, H., Farroni, T., Baron-Cohen, S.,
Bolton, P., & Johnson, M. H. (2005). Neural correlates
of eye-gaze detection in young children with autism.
Cortex, 41(3), 342–353.
Hutt, C., & Ounsted, C. (1966). The biological signifi-
cance of gaze aversion with particular reference to
the syndrome of infantile autism. Behavioral Science,
11(5), 346–356.
Johnson, M. H., Grossmann, T., & Kadosh, K. C. (2009).
Mapping functional brain development: Building
a social brain through interactive specialization.
Developmental Psychology, 45(1), 151–159.
Joseph, R. M., Ehrman, K., McNally, R., & Keehn, B.
(2008). Affective response to eye contact and face
recognition ability in children with ASD. Journal of
International Neuropsychological Society, 14(6),
947–955.
Kanner, L. (1943). Autistic disturbances of affective
contact. The Nervous Child, 2, 217–250.
Kylli€ainen, A., Braeutigam, S., Hietanen, J. K.,
Swithenby, S. J., & Bailey, A. J. (2006). Face and
gaze processing in normally developing children:
A magnetoencephalographic study. European Journal
of Neuroscience, 23(3), 801–810.
Kylli€ainen, A., & Hietanen, J. K. (2006). Skin conduc-
tance responses to another person’s gaze in children
with autism. Journal of Autism and Developmental
Disorders, 36(4), 517–525.
Eye-to-Eye Gaze
Leekam, S., Baron-Cohen, S., Perrett, D., Milders, M., &
Brown, S. D. (1997). Eye-direction detection:
A dissociation between geometric and joint attention
skills in autism. British Journal of Developmental
Psychology, 15(1), 77–95.
Maestro, S., Muratori, F., Cavallaro, M. C., Pecini, C.,
Cesari, A., Paziente, A., et al. (2005). How young
children treat objects and people: An empirical study
of the first year of life in autism. Child Psychiatry and
Human Development, 35, 383–396.
Nation, K., & Penny, S. (2008). Sensitivity to eye gaze in
autism: Is it normal? Is it automatic? Is it social?
Development and Psychopathology, 20(01), 79–97.
Pellicano, E., & Macrae, C. N. (2009). Mutual eye gaze
facilitates person categorization for typically develop-
ing children, but not for children with autism.
Psychonomic Bulletin and Review, 16(6), 1094–1099.
Pelphrey, K. A., Morris, J. P., & McCarthy, G. (2005).
Neural basis of eye gaze processing deficits in autism.
Brain, 128(Pt 5), 1038–1048.
Ristic, J., Mottron, L., Friesen, C. K., Iarocci, G.,
Burack, J. A., & Kingstone, A. (2005). Eyes are special
but not for everyone: The case of autism. Cognitive
Brain Research, 24(3), 715–718.
Senju, A., & Johnson, M. H. (2009a). Atypical eye contact
in autism: Models, mechanisms and development.
Neuroscience and Biobehavioral Reviews, 33(8),
1204–1214.
Senju, A., & Johnson, M. H. (2009b). The eye contact
effect: Mechanisms and development. Trends in
Cognitive Sciences, 13(3), 127–134.
Senju, A., Tojo, Y., Dairoku, H., & Hasegawa, T. (2004).
Reflexive orienting in response to eye gaze and an
arrow in children with and without autism. Journal of
Child Psychology and Psychiatry, 45(3), 445–458.
Senju, A., Tojo, Y., Yaguchi, K., & Hasegawa, T. (2005).
Deviant gaze processing in children with autism:
An ERP study. Neuropsychologia, 43(9), 1297–1306.
Senju, A., Yaguchi, K., Tojo, Y., & Hasegawa, T. (2003).
Eye contact does not facilitate detection in children
with autism. Cognition, 89(1), B43–B51.
Eyeblink Reflexes
Lindsey Sterling
Department of Psychiatry, Jane & Terry Semel
Institute for Neuroscience & Human Behavior
UCLA, Los Angeles, CA, USA
Synonyms
Corneal reflex; Startle response
1207 E
Definition
The first and most reliable component of the
startle reflex in humans. The blink reflex is an
involuntary blinking of the eyelids elicited when
the cornea is stimulated by touch, bright light,
loud sounds, or other peripheral stimuli. The
evolutionary purpose of this involuntary response
is believed to be a survival-related function, to
protect the eyes from potentially harmful stimuli
E
(i.e., threat). When a stimulus is presented to the
cornea of the eye, sensory information is carried
to the trigeminal nucleus and relayed to the
accessory abducens and abducens motor nuclei,
initiating a motor response. The eyeblink consists
of a rapid contraction of the orbicularis oculi
muscle surrounding the eye; this is the most
sensitive component of the blink. Strength of
the response can be measured by electromyo-
graphic activity (EMG) of the orbicularis muscle
during the eyeblink, or blink magnitude. Because
EMG is quantifiable, it is the behavioral variable
often used in startle response experiments
designed to investigate neurological indices of
fear and anxiety (i.e., amygdala activation).
See Also
▶ Startle Reflex
References and Readings
Blumenthal, T. D., Cuthbert, B. N., Filion, D. L., Hackley, S.,
Lipp, O. V., & van Boxtel, A. (2005). Committee report:
Guidelines for human startle eyeblink electromyographic
studies. Psychophysiology, 42, 1–15.
Dichter, G. S., Benning, S. D., Holtzclaw, T. N., &
Bodfish, J. W. (2010). Affective modulation of the
startle eyeblink and postauricular reflexes in autism
spectrum disorder. Journal of Autism and
Developmental Disorders, 40, 858–869.
Eye-to-Eye Gaze
▶ Mutual Gaze
E 1208
Eye-Tracking
Frederick Shic
School of Medicine, Yale Child Study Center,
Yale University School of Medicine,
New Haven, CT, USA
Definition
Eye-tracking is a technique in which one or more
of a subject’s eyes are tracked with the intent of
inferring, in a moment-by-moment fashion, what
the individual is attending to in his or her visual
world.
Historical Background
Eye-tracking has had a long history in psycholog-
ical research and vision science. Some of the
earliest reported work using eye-tracking
appeared in the late 1800s and early 1900s, focus-
ing primarily on understanding and optimizing
visual processes during reading (e.g., the work
of Huey, 1898, 1910). Later work, by Guy
Buswell (1935), Alfred Yarbus (1967), and
others, would use eye-tracking to study more
natural visual scanning processes during the
viewing of complex scenes such as those found
in paintings or photographs. From these early
experiments, it was noted that typical individuals,
both young and old, when presented visually with
scenes with people, and unless given instructions
to the contrary, would spend much of their time
looking at the people portrayed. Furthermore, it
was noted that given a face to view, subjects
would largely attend to the eyes and mouth of
the face, despite the fact that these static stimuli
never changed. Yarbus noted, in his treatise on
eye movements: “The observer’s attention is fre-
quently drawn to elements which do not give
important information but which, in his opinion,
may do so.” This early work, which advanced the
primary of social information processing in nat-
ural viewing for typically developing individuals,
Eye-Tracking
set the stage for modern investigations of the
visual strategies employed by individuals with
autism spectrum disorders (ASD).
Current Knowledge
The use of eye-tracking for understanding neuro-
psychiatric conditions and special populations in
general is attractive for a number of reasons.
First, at its essence, eye-tracking is a method for
seeing how others see, providing a robust, quan-
titative measure of where someone is looking.
Since where someone is looking is highly corre-
lated to where that person’s attention is deployed,
eye-tracking can be used to understand tempo-
rally changing cognitive processes as they unfold
(with caveats; see section “Limitations of Eye-
Tracking”). Second, eye-tracking is today
a relatively noninvasive and easily tolerated
experimental technology. As compared to the
original systems of the early nineteenth century,
which were often so uncomfortable that the eye
had to be anesthetized with cocaine, modern
desktop-mounted video oculography eye-
tracking systems (see section “Types of Eye-
Trackers”) can obtain precise measurements of
the eye without ever touching any part of the
participant. Third, the oculomotor system is
early maturing and highly preserved neurophysi-
ological control system. This means that eye-
tracking can be an applicable and appropriate
technique across the vast cognitive, behavioral,
and physiological heterogeneity found in many
neuropsychiatric conditions.
The earliest published work using eye-
tracking to study individuals with ASD appeared
in 2002 (Klin, Jones, Schultz, Volkmar, & Cohen,
2002; Pelphrey et al., 2002; van der Geest,
Kemner, Camfferman, Verbaten, & Van
Engeland, 2002; van der Geest, Kemner,
Verbaten, & van Engeland, 2002). The general
pattern of this work suggested that in many cases,
the visual scanning strategies of individuals with
ASD are significantly different than that of con-
trols. These initial reports found, for example,
that older adolescents and adults with ASD
tended to look more at the mouth and less at the
Eye-Tracking
eyes in comparison to control individuals. They
also highlighted relationships between communi-
cative ability and scanning patterns, with the
somewhat surprising finding that individuals
with ASD who looked more at the mouth were
actually more communicatively capable than
those who looked less. Additional studies have
largely confirmed the atypical nature of visual
scanning strategies in individuals with ASD,
especially under conditions where choices in
attentional selection must be made between
social and nonsocial stimuli. Results of several
studies show, for instance, decreased attention
toward social actors, people in general, and
faces, and increased attention toward nonsocial
background elements of scenes (e.g., Jones, Carr,
& Klin, 2008; Klin et al., 2002; Pierce, Conant,
Hazin, Stoner, & Desmond, 2011; Riby &
Hancock, 2009; Shic, Bradshaw, Klin,
Scassellati, & Chawarska, 2011). Other studies
also highlight decreased sensitivity in individuals
with ASD to communicative and social aspects
of interactions, such as gaze cues and shared
activities (Freeth, Chapman, Ropar, & Mitchell,
2009; Riby & Doherty, 2011; Shic et al., 2011).
Finally, eye-tracking studies have related ineffi-
cient social information–gathering strategies to
poor performance in face recognition tasks in
both adults (Spezio, Adolphs, Hurley, & Piven,
2007) and toddlers and children with ASD
(Chawarska & Shic, 2009). Taken together,
these studies provide evidence for atypical visual
exploratory behaviors in individuals with ASD
and promote the use of eye-tracking technology
in efforts toward understanding the mechanisms
underlying atypically developing social skills in
individuals with ASD.
However, it is important to note that the use of
eye-tracking in studying ASDs is a developing
and emerging field. While originally there was
a great deal of enthusiasm regarding atypical
distributions of attention toward specific ele-
ments of the face (e.g., proportions of mouth
and eye scanning), recent reports have
highlighted the complex interrelationships
between cognitive, social, and behavioral pheno-
types and visual exploratory behavior
(Chawarska & Shic, 2009; Norbury et al.,
1209 E
2009). Indeed, several studies did not replicate
atypical patterns of looking at faces or social
scenes, even as early as 2002 (van der Geest,
Kemner, Camfferman, et al., 2002; van der
Geest, Kemner, Verbaten, et al., 2002). The rea-
sons for these disagreements are currently active
areas of exploration. However, there are likely
several factors involved, such as heterogeneity of
sample populations, variety of experimental par-
adigms and contexts, and inconsistencies across
E
research sites in use of preprocessing methodol-
ogy and analytical techniques. Nevertheless, eye-
tracking has been and continues to be a powerful
methodology for understanding the nature of
ASD; as more research using eye-tracking
is conducted, its application will likely extend
further toward questions regarding the heteroge-
neity of behavioral and visual exploratory
activities in ASD.
Types of Eye-Trackers
There are several types of eye-tracking technolo-
gies still in widespread use (Duchowski, 2007).
However, recently, psychological and behavioral
studies of individuals with ASD and other neuro-
psychiatric conditions have largely begun to rely
exclusively on the use of remote video
oculography (VOG) methods. In modern video
oculography, a video camera or multiple video
cameras are positioned so as to be able to obtain
a clear image of the participant’s eye. These
cameras, typically linked up to either specialized
hardware or a computer, employ sophisticated
computational algorithms in order to extract
from the video the position of the participant’s
pupil(s). In the most common methodology,
infrared filters are used to remove contaminating
light sources which otherwise complicate signal
analysis extraction of the pupil location. In these
infrared systems, additional infrared light
sources, which are largely invisible to the
human eye, are used in order to generate “glints”
or corneal reflections which serve as a reference
coordinate system for the pupil that is more
invariant to participant motion. Additionally,
the eye and face of the participants can be lit by
on-camera-axis lighting or off-camera-axis light-
ing. On-camera-axis lighting generates a form of
E 1210
infrared video oculography called “bright-pupil”
eye-tracking. In bright-pupil eye-tracking, illu-
mination of the eye causes a “red-eye effect”
(similar to what occurs when a flash is reflected
off someone’s eye in a camera photograph). This
makes the pupil appear bright. In off-camera-axis
lighting, the pupil remains dark because infrared
light is not reflected, resulting in a “dark pupil.”
Though some manufacturers suggest one form of
lighting is superior for certain individuals (e.g.,
for those with light blue eyes as compared to
those with dark brown eyes), there have been no
independent scientific studies showing one
method is actually superior in practical applica-
tions and modern use.
Another form of eye-tracking which has been
in many ways superseded by video oculography
methods, at least in behavioral studies of individ-
uals with neuropsychiatric disorders, is electro-
oculography (EOG). Electrooculography uses
conductive electrodes placed nasally and tempo-
rally to the eye, together with a reference elec-
trode, in order to measure the potential difference
between the front of the eye and the back of the
eye (the corneofundal potential; see Brown et al.,
2006; Marmor & Zrenner, 1993). This method of
eye-tracking typically is noisier than commercial
video oculography systems, and the head must
remain relatively immobilized, as compared to
video oculography techniques which can accom-
modate relatively larger amounts of head move-
ments. However, EOG systems are relatively
inexpensive compared to VOG eye-tracking sys-
tems, making their use a viable alternative in
situations where precision is not at a premium
and participants are very compliant to instruc-
tions and immobilization.
Finally, a form of eye-tracking used primarily
in primate and animal research employs scleral
coils. With scleral coils, a conducting ring is
placed directly on the sclera of the eye and an
enclosing alternating magnetic field induced
around the head of the participant. As the eye
changes position, voltages generated within the
coil give the position of the eye, giving extremely
precise recordings of eye position. The main
drawback of this technique is the physical dis-
comfort associated with inserting the coil directly
Eye-Tracking
into the eye and the risk of corneal abrasion. Still,
recent work has identified the lead from the coil
to the measuring device as a major source of
discomfort for scleral coils, and strides have
been made using wireless scleral coils which
may make the technology more usable for fine-
grained detection of eye movements in the future
(Roberts, Shelhamer, & Wong, 2008).
Mechanics of Eye Movements and Common
Eye-Tracking Outcome Variables
Primary classifications of eye movements include
saccades, fixations, and smooth pursuit. Sac-
cades, a term coined by French psychologist
Louis Javal in 1879, are rapid, ballistic move-
ments of the eye. Research has shown that aware-
ness of the visual world is suppressed during
saccades, an effect neatly summarized by Dodge
(1900). Dodge’s observation was that when an
individual stands in front of a mirror, looking at
different positions on his or her own eyes, that
individual does not detect any movement of the
eyes. However, an observer standing immedi-
ately to the side of the person in the mirror will
see the eyes moving rapidly. This effect, known
as saccadic suppression, is associated with
decreased conscious awareness of the visual
world during saccades. Fixations are the comple-
ment of saccades and represent periods in which
the pupil is focused relatively stably and steadily
on a particular location. By contrast, smooth pur-
suits are indicated by slower, sweeping motions
of the eye and are found when the eye is used
employed to visually track a moving target. Inter-
estingly, smooth pursuits cannot be elicited vol-
untarily in the absence of a target and require
a slow-moving target to manifest.
Fixation/saccade identification algorithms
have been advanced in order to segregate sac-
cades from fixations in eye-tracking data. How-
ever, it is unclear if these algorithms are effective
in drawing clear distinctions between saccades
and fixations at modern eye-tracking speeds (60
Hz) and resolutions (Shic, Chawarska, &
Scassellati, 2008a, 2008b). Nevertheless, these
fixation identification algorithms are in wide-
spread use and are supported by most eye-
tracking manufacturers. By comparison, smooth
Eye-Tracking
pursuit recognition, which would affect the inter-
pretation of studies employing dynamic stimuli,
is currently not a standard analytical technique.
Perhaps the most common technique used in
analysis of eye-tracking data is region-of-interest
(ROI) analysis. In ROI analysis, the scene
presented to the participant is divided into
a series of not necessarily (but usually)
nonoverlapping regions, and the amount of time
spent by the participant looking at each of these
regions is calculated. As studies of natural activ-
ities have shown that people tend to be looking
for information they need, it is inferred that more
examined areas correspond to areas found by
observers to be more important. Typically, for
comparability purposes, looking times are
expressed as a proportion of the trial time. Some
researchers choose to exclude from analyses eye-
tracking data acquired during saccades due to
diminished awareness of the scene by the partic-
ipant, but others choose to incorporate all data
into proportion data and/or looking time reports.
Additional measures employed in eye-
tracking research are extensive (Jacob & Karn,
2003), and there exists a large body of research on
sophisticated techniques for processing eye-
tracking data (see Duchowski, 2007; see
Holmqvist, Nystrm, Andersson, Jarodzka, & van
de Weijer, 2011 for reference). While many of
these techniques are theoretically and conceptu-
ally interesting, it is also important to note that, in
many cases, the relationships between derived
eye-tracking variables and physiological or
behavioral constructs is unclear. A notable
exception is the detection of blinks. The inhibi-
tion of blinks has recently been shown to corre-
spond to decreased attribution of salience to
social scenes in toddlers with ASD (Shultz,
Klin, & Jones, 2011). Concerted and rigorous
explorations of the space of possible eye-tracking
measures may thus more firmly ground our
understanding of outcome eye-tracking mea-
sures, from psychological, neurophysiological,
and behavioral perspectives, in the years to come.
Limitations of Eye-Tracking
Interpretations of the results of eye-tracking
experiments often involve assumptions regarding
1211 E
the concurrent relationship between the position
of eye and the allocation of attention. However,
attention and eye movements are not always
coupled; indeed, research suggests that the move-
ment of attention toward a particular point in the
world precedes an eye movement toward that
location by 100–120 ms. In addition, attention
can be moved covertly, i.e., without an explicit,
overt eye movement. Research has shown, how-
ever, that when a movement of the eye is made, it
E
must be preceded by focal attention to that loca-
tion. Thus, the occurrence of an eye movement
suggests that attention has already been deployed
to the target of that eye movement; on the other
hand, when the eye is relatively still, standard
interpretations of eye-tracking data rely on an
assumption that the point of fixation is the same
as the point of attention. For practical purposes,
this is often the case (Duchowski, 2003;
Holmqvist et al., 2011; Kowler, 1990).
Future Directions
Keith Rayner, one of the pioneers of eye-tracking
research, especially in studies of reading, notes
that there have been four main eras of eye-
tracking research (Rayner, 2009). In the first
era (early 1900s), many of the basic properties
about eye movements were discovered. In the
second era (1930s to 1950s), experimental
work in eye-tracking research took a behavior-
ist position, classifying and quantifying, in
context, the myriad behaviors comprising eye
movements. In the third era (1970s to 1990s),
the cognitivist revolution brought new perspec-
tives for delving deeper into the mechanisms
and cognitive processes underlying eye move-
ments. Rayner notes that we are now in the
fourth era of eye-tracking research, one where
quantifiable and predictive models of eye
movements, indexing underlying cognitive
substrates, can be developed.
While Rayner’s summary mainly refers to
studies of reading, the same classification of
eras can be applied to eye-tracking research in
social visual information processing, with the
understanding that this field lags research in
E 1212
reading by about a decade. Currently, there is
a great deal of interest in using eye-tracking
technology for understanding autism, and much
of this effort is aimed at understanding the
specific individual behavioral and cognitive
characteristics that affect visual scanning of
social information in autism. Once this heteroge-
neity of behavior can be decoded, it is hoped that
eye-tracking research in autism will also enter
into its fourth era, where the accurate models
of eye movements can help us both understand
individual variability as well as predict those
forms of intervention that will be most
efficacious.
The fourth era of eye-tracking research also
corresponds with the proliferation and techno-
logical development of eye-tracking technol-
ogy as a whole. In many ways, eye-tracking is
now appearing as an almost requisite adjunct
methodology for social information processing
paradigms that directly target underlying neu-
ral substrates, such as functional magnetic
resonance imaging and electroencephalogra-
phy. Combining these multiple sources of
information will provide a more complete pic-
ture of the multifaceted complexities in ASDs.
Given the wealth of information, an increased
focus on computational and statistical
approaches toward integrating and unifying
eye-tracking data with other sources of infor-
mation will be critical to future research.
Finally, while atypical scanning of social
scenes in individuals with ASD has been
found by several research groups employing
eye-tracking, there is still much work left to
do in terms of pinpointing specific behavioral
markers of ASD. It is yet unknown whether
atypical gaze patterns in ASD are a secondary
manifestation of social perceptual disadvan-
tages and to what extent the compounding
effects of the atypical experience reflected by
these gaze patterns diminish prototypical social
development. Current and future work with
eye-tracking will thus continue to isolate
autism-specific developmental processes and
deepen our appreciation of the roles of typical
and atypical gaze patterns in shaping the
behavioral phenotype of individuals with ASD.
Eye-Tracking
See Also
▶ Eye Gaze
▶ Visual Processing
References and Readings
Brown, M., Marmor, M., Vaegan, Zrenner, E., Brigell, M.,
& Bach, M. (2006). ISCEV standard for clinical
electro-oculography (EOG) 2006. Documenta
Ophthalmologica, 113(3), 205–212. doi:10.1007/
s10633-006-9030-0.
Buswell, G. T. (1935). How people look at pictures:
A study of the psychology of perception in art. Chi-
cago: The University of Chicago Press.
Chawarska, K., & Shic, F. (2009). Looking but not seeing:
Atypical visual scanning and recognition of faces in 2
and 4-year-old children with autism spectrum disorder.
Journal of Autism and Developmental Disorders,
39(12), 1663–1672. doi:10.1007/s10803-009-0803-7.
Dodge, R. (1900). Visual perception during eye move-
ment. Psychological Review, 7(5), 454–465.
doi:10.1037/h0067215.
Duchowski, A. T. (2003). Eye tracking methodology:
Theory and practice (1st ed.). New York: Springer.
Duchowski, A. T. (2007). Eye tracking methodology:
Theory and practice. New York: Springer.
Freeth, M., Chapman, P., Ropar, D., & Mitchell, P. (2009).
Do gaze cues in complex scenes capture and direct the
attention of high functioning adolescents with ASD?
Evidence from eye-tracking. Journal of Autism and
Developmental Disorders, 40(5), 534–547.
Holmqvist, K., Nystrm, M., Andersson, R., Jarodzka, H.,
& van de Weijer, J. (2011). Eye-tracking data and
dependent variables. Oxford: Oxford University Press.
Holmqvist, K., Nyström, M., Andersson, R., Dewhurst, R.,
Jarodzka, H., & Van de Weijer, J. (2011). Eye track-
ing: A comprehensive guide to methods and measures.
New York: Oxford University Press Inc.
Huey, E. B. (1898). Preliminary experiments in the physi-
ology and psychology of reading. The American Journal
of Psychology, 9(4), 575–586 Retrieved July 21, 2008.
Huey, E. B. (1910). The psychology and pedagogy of read-
ing: With a review of the history of reading and writing
and methods, texts, and hygiene in reading. New York:
Macmillan.
Jacob, R. J. K., & Karn, K. S. (2003). Eye tracking in
human-computer interaction and usability research:
Ready to deliver the promises (section commentary).
In J. Hyona, R. Radach, & H. Deubel (Eds.), The
mind’s eye: Cognitive and applied aspects of eye
movement research (pp. 573–605). Oxford, England:
Elsevier Science.
Jones, W., Carr, K., & Klin, A. (2008). Absence of pref-
erential looking to the eyes of approaching adults pre-
dicts level of social disability in 2-year-old toddlers
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