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Journal of Applied Research in Intellectual Disabilities 2013, 26, 81–107
Autism Research and Services for Young
Children: History, Progress and Challenges
Travis Thompson
Special Education Program, Department of Educational Psychology, University of Minnesota, Minneapolis, MN, USA
Accepted for publication 8 January 2013
For three decades after Leo Kanner’s first clinical
description, research progress in understanding and
treating autism was minimal but since the late
1960s the growth of autism discoveries has been
exponential, with a remarkable number of new findings
published over the past two decades, in particular. These
advances were made possible first by the discovery
and dissemination of early intensive behavioural
intervention (EIBI) for young children with autism that
created the impetus for earlier accurate diagnosis. Other
factors influencing the rapid growth in autism research
were the first accepted diagnostic test for autism, the
Autism Diagnostic Interview and Observation Schedule
(ADI and ADOS). Developments in brain imaging
and genetic technology combined to create a fuller
understanding of the heterogeneity of autism, its multiple
aetiologies, very early onset and course, and strategies for
treatment. For a significant proportion of children with
autism, it appears EIBI may be capable of promoting
brain connectivity in specific cerebral areas, which is one
Introduction
Using modern clinical methods in the early 1940s, Leo
Kanner systematically observed a small group of
children with a condition he called Infantile Autism,
launching the scientific study of autism. When he
published his findings, human kind began to realize
there was order to be found in this very puzzling
condition. Autism research and practice languished for
many years subsequent to Kanner’s first clinical
characterization of the syndrome (Kanner 1943), but
beginning in the 1960s, that trend began to change. For
nearly three decades ensuing Kanner’s classic article,
most of the autism literature consisted of misguided
theories (Spitz 1945; Bettleheim 1967), diagnostic
© 2013 Blackwell Publishing Ltd
Published for the British Institute of Learning Disabilities
of autism’s underlying challenges. Disagreements about
the most appropriate early intervention approach
between developmental and behavioural psychologists
have been unproductive and not contributed to
advancing the field. Naturalistic behavioural and
structured discrete trial methods are being integrated
with developmental strategies with promising outcomes.
Over these past 30 years, young people with autism have
gone from receiving essentially no proactive treatment,
resulting in lives languishing in institutions, to today,
when half of children receiving EIBI treatment sub-
sequently participate in regular classrooms alongside
their peers. The future has entirely changed for young
people with autism. Autism has become an eminently
treatable condition. The time is overdue to set aside
philosophical quarrels regarding theories of child
development and apply what we know for the benefit of
children with autism and their families.
Keywords: autism, research progress, theoretical approaches
misadventures (Bender 1947; Silver 1954) and mistaken
approaches to intervention (Bender et al. 1962). It was
recognized by some professionals that autism very
likely had a biological foundation (e.g. Rimland 1964;
Rutter 1971) and was believed to be ‘incurable’, despite
it is being widely viewed as a largely psychogenic
disorder (Bettleheim 1967). In the 1960s and early 70s,
some clinicians continued to follow Bettleheim’s
mistaken advice and attempted to treat children with
autism using psychoanalytic therapy, which was of very
little value. A 1973 article in California Medicine
(Langdell 1973) presented outcomes of seven autism
psychotherapy studies (mostly psychoanalytic)
contending ‘best outcomes’ were obtained in 5–42% of
cases, with the mean of 14.8%. No actual direct evidence
10.1111/jar.12021
82 Journal of Applied Research in Intellectual Disabilities
from studies was presented. The criteria for claiming a
best outcome had been obtained, was not provided.
It was widely incorrectly thought by practitioners and
educators at that time, despite these psychoanalytic
claims, that little could be done to improve functioning
or enable affected individuals to lead better lives. In a
longitudinal follow-up article, DeMyer et al. (1973) found
that ‘Most autistic children remained educationally
retarded and 42% were institutionalized…. (their
findings) indicated the following prognosis in autism: 1–
2% recovery to normal, 5–15% borderline, 16–25% fair,
and 60–75% poor’. Other than being higher functioning
at intake, nothing else predicted a better outcome.
Through the 1970s and early 1980s, most identified
autism cases participated in classrooms for students with
severe intellectual disabilities or emotional disturbance
and resided in public institutions beyond childhood,
with only a negligible number of members of affluent
families cared for in private retreats where at that time,
they received largely palliative care. Professional
perceptions of autism were based largely on the selective
sample of people studied by child psychiatrists who
worked with institutional populations, largely people
with severe intellectual disability, without language,
who exhibited non-functional repetitive behaviour, often
displaying aggression and self-injury (Bender 1959;
Despert 1971).
Growth in Published Research
There were few noteworthy autism publications between
Itard’s (1802), An historical account of the discovery and
education of a savage man, and Leo Kanner’s (1943), Autistic
disturbances of affective contact, 141 years hence. The pace of
scientific productivity was very modest through the early
1960s, but behavioural research began demonstrating that
children with autism were capable of learning, if taught
systematically and intensively using operant learning
methods. Each subsequent finding created the scaffolding
for the next in a gradually accelerating fashion (Wolf,
Risley and Mees, 1964, Løvaas, 1967).
The author has selected 75 especially noteworthy
articles or books that have had a significant impact on
our understanding of autism and played a role in
shaping the direction of autism research (see Table 1 for
the list). These publications emerge from three
theoretical traditions, clinical nosology and epidemiology
(Figure 1), developmental theory (Figure 2) and
behaviour analytic theory (Figure 3). These figures are
intended to illustrate major ordinal pathways of
empirical and theoretical influence leading to the current
status of the field of behavioural autism research and
practice. There is likely to be agreement regarding the
importance of most of the early contributions in the
development of the field listed, but greater differences of
opinion may exist regarding some publications of special
of note in recent years. Despite this caveat, it is unlikely
that the overall trajectory of the autism research curve
would be substantially different should some different or
additional recent publications be added making up the
graph. The publication rate shows an exponential growth
with time. The growth rate, averaged over the past
70 years, is about 6% per year.
Autism-related publications have grown from a trickle
to an avalanche over the past two decades. The US
PubMed database is a major repository of biomedical
and behavioural science research, which included 2207
entries during 2011 under the combined search terms
‘autism’ and ‘research’. Figure 4 shows the number of
PubMed autism research publications from 1998 to 2008,
yielding an exponential growth, with a dramatic
increase after 2004, at which point the slope of
publications by years is 3.459, a remarkable rate of
published research, indeed.
While these quantitative findings are heartening,
scientific progress is measured more importantly in
specific discoveries and patterns of outcomes than in
numbers of published articles or books alone. The
remainder of this review discusses those substantive
advances. That a great deal remains to be discovered
regarding the causes and nature of autism subtypes,
autism prevention and the most effective interventions
for various autism subtypes, is a given. This does not
detract in the least from what has already been
accomplished. The present discussion focuses on
advances in behavioural, cognitive, and affective autism
research, and touches on brain and genetic findings
insofar as they are directly related to the former. It is not
the purpose of this discussion to review important
genetic and brain science autism research that are
beyond the scope of this review.
Main Factors Contributing to Scientific
Advances in Autism Research
Three main factors have contributed to the proliferation
of autism research. Subsequent to the demonstration
that many children with autism could be effectively
treated using early intensive behavioural intervention
(EIBI) methods (Løvaas 1987), the idea that autism was
an immutable condition largely vanished. Autism has
become an imminently treatable condition, given
© 2013 Blackwell Publishing Ltd, 26, 81–107
 Journal of Applied Research in Intellectual Disabilities 83

Table 1 Influential autism-related* publications 1800–2010

1. Itard, J-MG (1801) M
emoire et Rapport sur Victor de l’Aveyron [The first detailed account of a youth with autism]
2. Skinner, BF (1938) Behavior of Organisms. New York: Appleton & Co. [The first book spelling out the principles of behaviour
analysis that was the basis for Løvaas’s later application of the method]
3. Leo Kanner (1943) Autistic Disturbances of Affective Contact. Nervous Child 2:217–50, 1943 [The first clinical description of
autism]
4. Hans Asperger (1944) Die “Autistischen Psychopathen” in kindersalter. Archiv fur Psychiatrie und Nervenkrankheiten. 117: 76–136
[The first clinical description of Asperger disorder]
5. Bijou, S. (1955) A systematic approach to an experimental analysis of young children. Child Development 26, 161–8 [First
published study of applicability of operant learning principles to young children]
6. Lindsley, OR (1956) Operant conditioning method applied to research in chronic schizophrenia. Psychiatric Research Reports. 5:
118–39 [First published study of applicability of operant learning principles to human adults]
7. Skinner, BF (1957) Verbal Behavior. New York: Appleton Century Crofts, Inc. [Skinner’s classic theoretical analysis of verbal
behaviour and language]
8. Gewirtrz, JL and Baer, DM (1958) Deprivation and satiation of social reinforcers as drive conditions. Journal of Abnormal and
Social Psychology. 56: 165–71 [First study demonstrating applicability of operant learning principles to infants]
9. Orlando, R and Bijou, SW (1960) Single and multiple schedules of reinforcement in developmentally retarded children. Journal
of the Experimental Analysis of Behavior. 3, 339–348 [One of the earliest demonstration of applicability of operant principles to the
behavior of children with developmental disabilities]
10. Ferster, CB (1961) Positive reinforcement and behavioral deficits in autistic children. Child Development. 32: 437–456 [The first
study demonstrating learning in children with autism using operant procedures]
11. Creak EM (1963) Childhood psychosis: a review of 100 cases. British Journal of Psychiatry, 109: 84–89 [First attempt to develop
diagnostic criteria for autism]
12. Rimland B (1964) The etiology of infantile autism: the problem of biological versus psychological causation. In B. Rimland
Infantile autism. New York: Appleton Century Crofts, pp. 39–66 [First systematic science-based book attempting to make sense of
autism by the parent of a child with autism]
13. Wolf, MM, Risley, T and Mees, H (1964) Application of Operant Conditioning Procedures to the Behavior Problems of an
Autistic Child. Behaviour Research & Therapy, 1964, 1:305–312 [The first demonstration of the use of operant learning procedures in
an applied clinical setting]
14. Lotter V (1966) Epidemiology of autistic conditions in young children. Social Psychiatry and Psychiatric Epidemiology 1:124–135
[First estimate of autism prevalence]
15. Løvaas OI (1967) A behavior therapy approach to the treatment of childhood schizophrenia. Minnesota Symposia on Child
Psychology, 1967, 1, 108–159 [First exposition by Løvaas of his method for early autism intervention]
16. Sidman, M and Stoddard, LT (1967) The effectiveness of fading in programming a simultaneous form discrimination for
retarded children. Journal of the experimental analysis of behavior. 10 (1):3–15 [The first demonstration of an errorless learning
method among children with developmental disabilities]
17. Baer, D. Wolf, M. and Risley, T (1968) Some dimensions of applied behavior analysis. Journal of Applied Behavior Analysis. 1,
91–7 [The definition of applied behaviour analysis]
18. Girardeau, FL and Spradlin, JE (1970) A functional analysis approach to speech and language. Monograph 14. American Speech and
Hearing Association [one of the first attempts to analyze and conduct communication to individuals with developmental
disabilities using a behaviour analytic approach]
19. Løvaas, OI & Schreibman, L (1971) Stimulus overselectivity of autistic children in a two stimulus situation. Behaviour Research
and Therapy, 1971, 9, 305–310 [The first laboratory description of stimulus overselectivity in autism]
20. DeMyer, MK, Barton, S, DeMyer, WE, Norton, JA, Allen J and Steele R (1973) Prognosis in autism: A follow-up study. Journal
of Autism Child Schizophrenia. 1973;3:199–246 [First longitudinal follow up study of outcomes of children diagnosed with autism
without treatment]
21. American Psychiatric Association (1974) Diagnostic and Statistical Manual of Mental Disorders (DSM III). Arlington, VA [First
DSM that included autism]
22. Rutter, M (1974) The development of infantile autism. Psychological Medicine. 4:147–63 [The first theoretical discussion of
modern thinking regarding the development of autism]
23. Hart, B and Risley, TR (1975) Incidental teaching of language in preschool. Journal of applied behavior analysis. 8: 411–20 [Earliest
behavior analytic demonstration of naturalistic teaching of language to preschool children]
24. World Health Organization (1975). ICD 9. Geneva: WHO [first official international diagnostic manual including autism]

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84 Journal of Applied Research in Intellectual Disabilities

Table 1 (continued)

25. Spradlin, JE and Dixon, MH (1976) Establishing conditional discriminations without direct training: Stimulus classes and
labels. American Journal on Mental Deficiency. 80: 555–61 [Earliest demonstration of generative teaching of stimulus classes among
individuals with developmental disabilities]
26. Carr, EG (1977) The motivation for self-injurious behaviour: A Review of some hypothesis. Psychological Review. 84: 800–16
[Origin of the notion of functional communication alternative to punishment for self-injury]
27. Rutter, M (1978) Diagnosis and definition of childhood autism. Journal of Autism and Developmental Disorders 8: 2139–61 [One of
the earliest science based discussions of autism diagnosis]
28. Wing, L & Gould, J (1979), “Severe Impairments of Social Interaction and Associated Abnormalities in Children: Epidemiology
and Classification”, Journal of Autism and Developmental Disorders, 9, pp. 11–29 [Early prevalence and nosology study of autism
prevalence]
29. American Psychiatric Association (1980) Diagnostic and Statistical Manual of Mental Disorders, III. Arlington, VA: American
Psychiatric Publishing, Inc [First American medical diagnostic manual including autism]
30. Wing L (1981). Asperger’s syndrome: a clinical account. Psychological Medicine 11 (1): 115–29 [First English language article on
Asperger disorder]
31. Wetherby, B, Karlan, GR, & Spradlin, JE (1983). The development of derived stimulus relations through training in arbitrary-
matching sequences. Journal of the Experimental Analysis of Behavior, 40, 69–78 [Early study showing establishment of semantic
stimulus classes among individuals with developmental delays]
32. McGee, GG, Krantz, PJ, Mason, D, & McClannahan, LE (1983). A modified incidental-teaching procedure for autistic youth:
Acquisition and generalization of receptive object labels. Journal of Applied Behavior Analysis, 16, 329–338 [One of the first
demonstrations of incidental teaching in autism]
33. Murphy, G and Wilson, BA (1985) Self-injurious behaviour: a collection of published papers on prevalence, causes, and treatment in
people who are mentally handicapped or autistic. British Institute of Mental Handicap [First systematic discussion of self-injury in
autism]
34. Baron Cohen, S, Leslie, AM and Frith, U (1985) Does the autistic child have a “theory of mind”? Cognition, 21 (1985) 37–46
[First discussion of “Theory of Mind” in as it was thought to apply to autism]
35. Schopler, E., Reichler, RJ & Renner, BR (1986) The childhood autism rating scale (CARS) for diagnostic screening and
classification of autism (New York: Irvington) [Introduction of the Childhood Autism Rating Scale for autism screening]
36. Felce, D, de Kock U & Repp, A (1986) An eco-behavioral analysis of small community-based houses and traditional large
hospitals for severely and profoundly mentally handicapped adults. Applied Research in Mental Retardation 7:393–408
37. Løvaas OI (1987). Behavioral treatment and normal educational functioning in young autistic children. Journal of Consulting and
Clinical Psychology 55 (1): 3–9 [Landmark article demonstrating nearly half of children receiving EIBI treatment function similar to
same age peers]
38. Dube, WV, McIlvane, WJ, Mackay, HA, & Stoddard, LT (1987). Stimulus class membership established via stimulus-reinforcer
relations. Journal of the Experimental Analysis of Behavior, 47, 159–175 [Early study showing establishment of classes of semantically
equivalent stimuli among individuals with developmental delays]
39. Ritvo ER, Freeman BJ, Pingree C, Mason-Brothers A, Jorde L, Jenson WR, McMahon WM, Petersen PB, Mo A, and Ritvo A.
(1970) The UCLA-University of Utah epidemiologic survey of autism: prevalence. American Journal of Psychiatry. 1146:194–9 [An
early attempt to evaluate autism prevalence]
40. Warren SF and Bamb, LM (1989) An Experimental Analysis of Milieu Language Intervention. Journal of Speech and Hearing
Disorders. 54: 448–461 [One of the first articles experimentally analyzing incidental language teaching strategy for children with
developmental disabilities]
41. Lord C, Rutter, M, Goode S et al. (1989). “Autism diagnostic observation schedule: a standardized observation of
communicative and social behavior”. J Autism Dev Disord 19 (2): 185–212 [First validated and widely accepted test instrument for
differential diagnosis of autism]
42. O’Neill, RE, Horner, RH, Albin, RW, Storey, K, & Sprague, JR (1990). Functional analysis of problem behavior: A practical
assessment guide. Pacific Grove, CA: Brooks/Cole Publishing [One of the earliest presentations of methods for evaluating social
functions of challenging behavior]
43. Sundberg, ML (1990). Teaching verbal behavior to the developmentally disabled.
Danville, CA: Behavior Analysts, Inc [Systematic presentation of applicability of Skinner’s Verbal Behavior to teaching
communication in developmental disabilities, including autism]

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 Journal of Applied Research in Intellectual Disabilities 85

Table 1 (continued)

44. Baron-Cohen, S, Allen, J, & Gillberg, C (1992) Can autism be detected at 18 months? The needle, the haystack, and the CHAT.
British Journal of Psychiatry, 161, 839–843 [First demonstration that it may be possible to screen for autism to 18 months of age]
45. Iwata, B, Pace, GM, Dorsey, MF, Zarcone, JR, Vollmer, TR, et al. (1994) The functions of self-injurious behavior: An
experimental-epidemiological analysis. Journal of Applied Behavior Analysis. 27(2): 215–240 [First clinical setting approach for
functional analysis of behavior challenges]
46. Bondy A, Frost L (1994). The Picture Exchange Communication System. Focus on Autisim. 9(3), 1–19 [First description of the
PECs augemtative communication strategy in autism]
47. Harris, SL, Handleman, JS, Gordon, R, Kristoff, B, & Fuentes, F (1991). Changes in cognitive and language functioning of
preschool children with autism. Journal of Autism and Developmental Disorders, 21, 281–286 [One of the first studies subsequent to
Løvaas 1987 to show intellectual and language changes resulting from EIBI]
48. Koegel, RL, & Frea, WD (1993). Treatment of social behavior in autism through the modification of pivotal social skills. Journal
of Applied Behavior Analysis, 26, 369–377 [First use of the term Pivotal Response Training]
49. Krantz PJ, MacDuff MT, McClannahan LE (1993) Programming participation in family activities for children with autism:
parents’ use of photographic activity schedules. Journal of the Applied Behaviour Analysis 26 (1):137–138 [First discussion of the use
of photographic activity schedules and augmentative communication method]
50. Michael, J (1993) Establishing operations. Journal of Applied Behavior Analysis. 16: 191–206 [First theoretical discussion of
establishing operations, not specific to autism]
51. Carr, EG (1994). Emerging themes in the functional analysis of problem behavior. Journal of Applied Behavior Analysis, 27, 393–
399 [First discussion of functional assessment of behavior challenges in autism and teaching of functionally equivalent responses]
52. Happe ́, FGE (1996). Studying weak central coherence at low levels: Children with autism do not succumb to visual illusions,
a research note. Journal of Child Psychology and Psychiatry, 37, 873–877 [Introduction of the weak central coherence theory of
autism]
53. Gena, A, Krantz, PJ, McClannahan, LE, & Poulson, CL (1996). Training and generalization of affective behavior displayed by
youth with autism. Journal of Applied Behavior Analysis, 29, 291–304 [One of first demonstration of teaching expression of
emotional skills in autism using behavioral methods]
54. Schreibman, Laura; Koegel, Robert L (1996) Fostering self-management: Parent-delivered pivotal response training for children
with autistic disorder. In Hibbs, Euthymia D. (Ed); Jensen, Peter S. (Ed) Psychosocial treatments for child and adolescent disorders:
Empirically based strategies for clinical practice. (pp. 525–552). Washington, DC, US: American Psychological Association [Early
description of Pivotal Response Training]
55. Krantz, PJ and McClannahan, LE (1998) Social interaction skills for children with autism: a script-fading procedure for
beginning readers. Journal of Applied Behaviour Analysis. 31(2): 191–202 [First description of use of scripts in teaching
communication in autism]
56. Emerson E, Hatton C, Bromley J & Caine A (Eds) (1998) Clinical. Psychology and People with Intellectual Disabilities. Chichester:
John Wiley & Sons [Clinical review of policy implications of behavioral analyses of individuals with severe disabilities, including
autism]
57. Gillberg, C and Wing, L (1999) Autism: Not an extremely rare disorder. Acta Psychiatrica Scandinavica. 99: 399–406 [Early article
suggesting Asperger disorder is much more common than previously thought]
58. Baron-Cohen S, Ring HA, Wheelwright S, Bullmore ET, Brammer MJ, Simmons A, Williams SC. (1999) Social intelligence in
the normal and autistic brain: an fMRI study. European Journal of Neuroscience 11(6):1891–8 [First fMRI evidence of differential
functioning of specific brain areas among individuals with autism spectrum disorders]
59. New York State Department of Health Early Intervention Program. (1999). Clinical Practice Guideline Report of the
Recommendations for Autism/Pervasive Developmental Disorders. New York State Department of Health, Albany, NY [First review of
evidence supporting efficacy of early intensive behavioral intervention in autism]
60. Rogers, SJ, Hall, T, Osaki, D, Reaven, J and Herbison J (2000) A comprehensive, integrated, educational approach to young
children with autism and their families. In S. L. Harris and J.S. Handleman (Eds) Preschool education programs for children with
autism (2nd Ed). Austin TX: Pro-Ed [First comprehensive discussion of the Denver Early Start model]
61. American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders Text Revision (DSMIV-TRa0.
Arlington, VA

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86 Journal of Applied Research in Intellectual Disabilities

Table 1 (continued)

62. Lord, C and McGee, JP (Eds) (2001) Educating children with autism. Committee on Educational Interventions for Children with
Autism. Division of Behavioral and Social Sciences and Education, National Research Council Washington, DC: National
Academies Press, Inc. [First unbiased review of autism early intervention research literature concluding applied behavioral
analysis interventions were effective for many children with autism]
63. Wing, L and Potter, D (2002) The epidemiology of autistic spectrum disorders: is the prevalence rising? Mental Retardation and
Developmental Disabilities Research Reviews. 8: 151–161 [Early discussion of prevalence with reference to contribution of Asperger
disorder]
64. Gutstein, S & Sheely, R (2002): Relationship Development Intervention with Young Children: Social and Emotional Development
Activities for Asperger’s, Autism, PDD and NLD. Jessica Kingsley Publications: London [First comprehensive presentation of the
Relationship Development Intervention approach]
65. Yeargin-Allsopp, M, Rice, C, Karapurkar, T, Doernberg, N, Boyle, C and Murphy, C (2003) Prevalence of Autism in a US
Metropolitan Area. Journal of the American Medical Association .289(1):49–55 [First US governmental publication suggesting a
markedly greater prevalence of autism than had been previously believed to be the case]
66. Prizant, BM, Wetherby, A, Rubin, E, Rydell, P, and Laurent, A (2003). THE SCERTS Model: A family-centered, transactional
approach to enhancing communication and socioemotional abilities of young children with ASD. Infants and young children, 16,
296–316 [An early presentation of the rational for the SCERTS intervention approach]
67. Gary B, Mesibov, Victoria Shea & Eric Schopler. The TEACCH Approach to Autism Spectrum Disorders (Plenum US, 2004) [First
comprehensive presentation of the TEACCH approach to teaching children with autism]
68. Rutter, M (2005) Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatrica 94:2–15 [One
of the first rational interpretations of increased autism prevalence data]
69. Klin, A, Pauls, D, Schultz, R, & Volkmar, F (2005). Three diagnostic approaches to asperger syndrome: Implications for
research. Journal of Autism and Developmental Disorders, 35(2), 221–234 [Argument for evaluating Asperger disorder as a
distinctive condition
70. Carbone, VJ, Lewis, L, Sweeney-Kerwin, E, Dixon, J, Louden, R and Quinn, S (2006) A comparison of two approaches to
teaching VB functions: Total communication vs. vocal Alone. SLP-ABA. 1: 181–91 [One of the only articles demonstrating
usefulness of Carbone’s Verbal Behaviour intervention approach]
71. Wetherby, A & Woods, J (2006). Effectiveness of early intervention for children with autism spectrum disorders beginning in
the second year of life. Topics in Early Childhood Special Education, 26, 67–82 [First empirical report showing effectiveness of the
comprehensive application of the SCERTS early intervention model]
72. Newschaffer CJ, Croen LA, Daniels, Giarelli E, Grether JK, Levy SE, Mandell DS, Miller LA, Pinto-Martin J, Reaven J,
Reynolds AM, Rice CE, Schendel D and Windham GC. (2007) The epidemiology of autism spectrum disorders Annual Review of
Public Health. 28:235–58 [Recent review article evaluating evidence of greater autism prevalence]
73. Remington, B, Hastings, RP, Kovshoff, H, Degli Espinosa, F, Jahr, E et al. (2007) Early intensive behavioral intervention:
outcomes for children with autism and their parents after two years. American journal of mental retardation: American Journal of
Developmental and Intellectual Disability 112(6):418–38 [One of the first detailed replication of the Løvaas 1987 early intervention
study outside the US]
74. Dawson G, Rogers S, Munson J, Smith M, Winter J, Greenson J, Donaldson A, Varley J. (2010) Randomized, controlled trial of
an intervention for toddlers with autism: the Early Start Denver Model. Pediatrics. 125(1):e17–23 [First empirical study
demonstrating effectiveness of the Denver Early Start early intervention model]
75. Thompson, T and collaborators (2011) Individualized intervention for young children with autism: Blending Discrete Trial and
naturalistic approaches. Baltimore MD: Paul H. Brookes, Inc. [One of the first comprehensive approaches to combining discrete
trial and naturalistic incidental behavioural approaches to autism early intervention]

Publications selected by the author as having made a significant contribution to the course of research, theory and practice. Some of
the publications on this list have influenced later work, but not led to evidence-based practical outcomes; however, most have done
so.
*Figures 1–3 and Table 1 illustrate approximately ordinal sources of influence on our theoretical formulations, research and practice
in the scientific behavioural understanding of, and intervention for symptoms of autism. All citations do not necessarily represent
significant scientific contributions. Some cited references influenced later work that has not been replicated. One measure of the
effects of contributions can be seen in evidencebased outcomes. Diamond shaped outcomes have empirical support in well
controlled or quasicontrolled studies, while those in octagons do not yet have such support.

© 2013 Blackwell Publishing Ltd, 26, 81–107

 Journal of Applied Research in Intellectual Disabilities 87

Wing & Rutter Creak

Gould 1974 & 1963
1979 1978

Rimland
Klin 1964
et.al
2005

Features
Gilberg
Wing Wing 1981
1999
Asperger
Translation

Frith
1991

Schopler
Baron- et.al 1986
Cohen CARS
CHAT
1992
ICD9
Autism Kanner
ICD 10 1975 1943
2004 Diagnostic
Assessments Clinical Nosology Tradition:
Itard
1801 Kraeplin, Tourette, Esquirol,
Lord, Meyer
Rutter
etal ADOS
DSMIII Asperger
Autism 1944
1980

DSMIV Prevalence
1994,
2000
Lotter
1966
Wing Potter Ritvo,
2002 Freeman
et.al. 1989
Gilberg
Wing
1999
Rutter
2005
Newschaffer
et.al. 2007

Yeargin-
Allsop 2003

Figure 1 Theoretical origins and empirical influences on autism diagnostic nosology and prevalence.
* Figures 1–3 and Table 1 illustrate approximately ordinal sources of influence on our theoretical formulations, research and practice
in the scientific behavioural understanding of, and intervention for symptoms of autism. All citations do not necessarily represent
significant scientific contributions. Some cited references influenced later work that has not been replicated. One measure of the
effects of contributions can be seen in evidencebased outcomes. Diamond shaped outcomes have empirical support in well
controlled or quasicontrolled studies, while those in octagons do not yet have such support.

effective methods are used with sufficient intensity. have occurred, and the lives of people with autism
Persistent barriers to treatment are continued theoretical spectrum disorders would be more limited as a
quibbling, insufficient personnel training and limited consequence.
political willingness to invest in treatment, although in
some countries antiquated theoretical ideas persist
Summary of Technological Advances
(Feinstein, 2011; Haag et al. 2005). Second, it is widely
recognized that autism has its basis in cerebral
Identification
dysfunction, and some of the brain are as known to be
involved in autism symptoms are established. Different Introduction for the first time, of a widely accepted
types of events can lead to brain malfunctioning to and validated diagnostic instrument, the Autism
varying degrees with corresponding variations in Diagnostic Observation Schedule (ADOS) and its sister
symptoms (e.g. genetic conditions, syndromal research instrument, the Autism Diagnostic Interview
developmental conditions, toxin exposures). Autism is a Revised (ADIR-R), made it possible to reliably
family of overlapping conditions; there is no single distinguish individuals with autism spectrum disorders
homogeneous autism disorder. Third, several from those with other mental health conditions or
technological advances greatly contributed to a rapid developmental disorders by 2 years of age (Lord et al.
increase in autism research and changes in practice 1989). The introduction of the ADOS and training of a
beginning in the mid-1960s and abruptly increasing in substantial cohort of test examiners revealed that a
the early 1990s. Without those technological advances, great many more children met the criteria for autism
only a limited number of these discoveries would likely than had previously been recognized. It became

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88 Journal of Applied Research in Intellectual Disabilities

Floortime,
Greenspan Floortime
Weider 2008

Relationship
Development
Intervention, RDI
Psychoanalytic Gutstein
Theory Tradition Sheely 2002

Bowlby
Mesibov,
Shea & TEACCH
Schoppler
, TEACCH
Developmental 2004
Psychology
Dawson,
Rogers Rogers et.al. EDSM
Piaget &
et.al. Early Start
Vygotsky
2000 Random Trial

Philosophy Tradition:
Epistemology
Prizant
Wetherby SCERTS
Wetherby
et.al. 2003 Woods
SCERTS 2006

Happe 1996
Baron Weak Cent
Cohen, Coherence
Leslie &
Frith Magiati, ‘Mind
(1985) Charman Reading’
TOM & Howlin
2007

Figure 2 Theoretical origins and empirical influences on developmental psychology approaches to understanding and intervention
in autism. Presence of an article or book is not intended to imply empirically based contributions. The two intervention approaches
indicated by diamond shapes have been demonstrated empirically to be effective.
* Figures 1–3 and Table 1 illustrate approximately ordinal sources of influence on our theoretical formulations, research and practice
in the scientific behavioural understanding of, and intervention for symptoms of autism. All citations do not necessarily represent
significant scientific contributions. Some cited references influenced later work that has not been replicated. One measure of the
effects of contributions can be seen in evidencebased outcomes. Diamond shaped outcomes have empirical support in well
controlled or quasicontrolled studies, while those in octagons do not yet have such support.

apparent that the earlier notion of autism from the
1960s was very misguided, and that many people
with autism have some spoken intentional commu-
nication, exhibit social interest and display little
aggression or self-injury, unlike what had previously
been believed. Most of those people had gone
undiagnosed prior to 1990, or if they were diagnosed,
it was with learning disability or another mental health
label (Rutter 2005a,b).
Measuring bain dysfunction
Although most early brain morphological or histological
brain research before 1990 revealed limited differences
among individuals with autism (Prior et al. 1984;
Harcherik et al. 1985), the emergence of brain imaging
technologies, especially functional magnetic resonance
imaging (fMRI), has made it possible to identify specific
brain regions that are active during specific cognitive
and affective tasks related to core autism symptoms that
differentiate autism brain function from that of other
conditions (Baron-Cohen et al. 1999; Schultz 2005). While
there has been variability in these findings, several
common dysfunctional characteristics have emerged
across numerous publications (Schultz et al. 2003;
Sugranyes et al. 2011). Variability in brain processing
should be expected because such dysfunctions are
brought about by different mechanisms in varying
degrees.
Genetic causes
Emergence of advanced genetic methods, including
polymerase chain reaction (PCR) (Mullis 1985),
recombinant DNA technology (Jackson et al. 1972) and
microarray technology (Brown 1990) made it possible

© 2013 Blackwell Publishing Ltd, 26, 81–107

 Journal of Applied Research in Intellectual Disabilities 89

Autism Intervention
Approach Ordinal Outcomes
Domain Influences

Hart & Warren & Bondy &

Risley 1975 Lamb Frost Behavioral
Communication Milieu PECS Communicaiton
Milieu
Language Teaching Strategies
Krantz
McClannahand
1998 Scripts
PRT Pierce
Schreibman
Wolfe, 1995
Risley & Krantz
Social Meese McClannahan
1964 1993 Activity
Schedules Pivotal
Koegel Response
Frea 1993 Training
McGee PRT
Applied
et.al. Inc.
Teaching
1983
Comprehensive Løvaas Gena, Blended
1967 Krantz et.al. Intervetnion,
1996 Thompson
Løvaas 87 affective et.al 2011
Long. generaliz.
Skinner Study
VB 1957

Repetitive &
Challenging Replication
Behaviour Studies
Baer, Wolf, Early Intensive
Risley 1968 Behavioral
Intervention

Verbal Behavior,
Sundberg and
Partington 1998

Experimental Analysis Carr 1977 Verbal

Beahvior
Tradition: Intervention
Sherrington's Reflex, Skinner Verbal
Pavlov's Cond. Reflex, 1938 Behavior,
Carbone 2006
General Physiology,
Watson

NY Iwata FBA Clinics,

Review Practice Func.Anal. Schools,
Articles Param. 1994 Residences
1999

Felce et.al.
Eco-
Behavioral
Analysis Carr 1994
Functional
NAS- Assessment
NRC Murphy &
2001 Wilson
Review 1985

Postive
Horner 1994 Bhavior
Support

Ferster
1961

Experimental Emerson,
Autism Hatton
et.al. 1998

Løvaas UK quality of
Schreibman care
1971 Stim standards
Overselectivity

Human Gewirz Orlando

Non- & Baer Bijou
Autism 1958 1960
Studies

Reinforcement Bijou
1955
Lindsley
Stimulus 1954
Control

Spradlin Stim
Stimulus Equivalence
Control

Motivation

Sidman
Errorless
Learning;
Stimulus
Equivalence

Michael,
EO's 1993

Figure 3 Theoretical origins and empirical influences of behaviour analytic approaches to understanding and intervention in autism.
Labels across the top indicate the domain of autism under question, the experimental versus applied approach and the
approximately ordinal sequence in which contributions were made. The final column indicates evidence-based contributions.
* Figures 1–3 and Table 1 illustrate approximately ordinal sources of influence on our theoretical formulations, research and practice
in the scientific behavioural understanding of, and intervention for symptoms of autism. All citations do not necessarily represent
significant scientific contributions. Some cited references influenced later work that has not been replicated. One measure of the
effects of contributions can be seen in evidencebased outcomes. Diamond shaped outcomes have empirical support in well
controlled or quasicontrolled studies, while those in octagons do not yet have such support.

© 2013 Blackwell Publishing Ltd, 26, 81–107

90 Journal of Applied Research in Intellectual Disabilities
for the first time to scour the entire human genome
for small DNA differences distinguishing individuals
with autism spectrum disorders from those without
autism and to identify subtypes with the potential
for developing differential prognostic profiles (Miles
et al. 2005).
Increasing neurogenetic evidence suggests some forms
of autism arise from genetic errors related to brain
synapse formation in specific structures related to
autism symptoms (the amygdala, cingulate cortex and
orbitofrontal cortex) with some evidence implicating the
mirror neuron system (Oberman et al. 2005).
There is extensive laboratory evidence that activity-
dependent synaptogenesis occurs in brain areas which
are involved in executing specific reinforced responses
(Nudo et al. 1996; Kleim et al. 1998, 2002). These
associations between synaptogenesis failures in specific
symptom-related structures, disuse-produced apoptosis
and neuronal loss, it appears can be at least partially
overcome by intensive early behavioural intervention,
and this has opened a window to a better under-
standing of autism and may explain why some
treatments appear to be effective for some people with
autism (Thompson 2005).
Effective intervention
The most compelling factor driving identification of
individuals on the autism spectrum as early as possible
was the creation of a highly effective intervention
strategy based on principles of applied behaviour
analysis (Baer et al. 1968) that made it possible to
significantly improve life outcomes for most young
children with autism spectrum disorders. Early
behavioural research with children on the autism
spectrum by Ferster (1961), Wolf, Risley and Mees,
(1964) and Løvaas, (1967), although modest in their
scope and extent of improvements, laid the foundation
for a landmark treatment longitudinal follow-up study
by Løvaas published in 1987. This latter finding has
been widely replicated with similar outcomes across
most studies, with approximately half of children
treated with EIBI for 20+ h/week for several years being
able to function sufficiently like their typical peers
(intellectually, socially and communicatively) to be
successfully integrated in typical school classrooms.
The other half of treated children typically exhibit
improvements as well, but less dramatic, and are
typically served in special programmes for students
with disabilities and continue to have more significant
intellectual and social limitations. Availability of the
first effective treatment for symptoms of autism gave
researchers practical reasons to more effectively identify
and begin to individualize interventions based on
patterns of genetic, brain, cognitive and behavioural
profiles (see Thompson 2011, pgs 33–39).
Diagnosis and Prevalence
John Haslam apothecary to the Royal Bethlehem
Hospital described a boy who had symptoms that
appear to have been those of autism (Leigh 1955;
Vailant 1962), but Jean Itard (1802) was the first to
characterize the three cardinal features of autism in
detail that were elaborated using clinical psychiatric
diagnostic nomenclature by Leo Kanner (1943), which
was the starting point for clinically diagnosing autism.
Hans Asperger (1944) described presence of similar
symptoms among a small subset of more linguistically
capable children in Vienna. These features included lack
of full understanding of, and effective use of
communication, lack of understanding of social cues
and use of age-appropriate social skills, and excessive
non-functional repetitive routines and behaviour,
including rigid behavioural routines. Between 1943 and
the mid-1960s, autism diagnosis was a catch-as-catch-
can enterprise. Few physicians or psychologists were
trained to differentially diagnose autism, and many
were wary of making the diagnosis because of the
profoundly negative implications of the diagnosis.
In 1963, Creak proposed a nine-point scale for more
objectively diagnosing autism, which was validated by
Clancy et al. (1969), who found no one item of Creak’s
scale was predictive in isolation. The diagnostic value of
the scale was in the grouping of the symptoms. They
found that a child had to show a minimum of 7 items
before the diagnosis of infantile autism could be
considered. These important early observations lay
dormant for two decades before a new attempt was
made in creating an objective instrument for autism
diagnosis.
Medical diagnosis has been determined by The
International Classification of Diseases (ICD) (WHO
2012) and the Diagnostic and Statistical Manual of the
American Psychiatric Association, (DSM) (American
Psychiatric Association 2012) and these have gone
through several iterations that have had the effect of
varying the number of individuals who meet the
diagnostic criteria from version to version without any
change in the base rates of autism. The ICD-8 was used
from 1964 to 75, which was revised in ICD-9 in 1976
and ICD-10 in 2007. Within the American DSM system,
© 2013 Blackwell Publishing Ltd, 26, 81–107

autism was first identified in the DSM-III in 1980 and is
now in the 10th revision created in 1994 (DSMIV) with a
new revision to be published in 2013 (DSM5). With the
introduction of the Autism Diagnostic Observation
Schedule in 1989, the first widely accepted and
validated instrument for diagnosing autism,
substantially more children were found to meet the
diagnostic criteria than in the past, leading to the
erroneous conclusion that actual autism cases were
increasing. While it is possible actual autism prevalence
has increased (see Rutter 2005a,b), most evidence points
to increased ascertainment as accounting for what had
been erroneously called an ‘autism epidemic’, especially
by the public news media (BMJ 2011). Autism
prevalence in the 1960s and 70s in the US was estimated
to be about five cases per 10,000 (Autism Society of
America) while in 2006, it was estimated by the Center
for Disease Control in the US to be1 per 110 (Rice 2009).
Studies in Canada revealed prevalence of 1 per 147
(Norris et al. 2006), and the UK to be 1161 per 10 000
(Baird et al. 2006). Numerous studies produced similar
prevalence results across countries and research
methods.
The notion that there was an autism epidemic created
a widespread belief that there must be an envi-
ronmental cause for the presumed, but non-existent,
‘outbreak’. Rampant speculation about hypothesized
environmental causes of autism spread like wildfire
within the parent community, with immunization and
diet causing greatest concern among parents. There was
Figure 4 Cumulative significant autism and related
publications 1920–2012. Related publications do not necessarily
involve people with autism but involve findings that lay
essential foundations for subsequent autism research and
practice. Publciations were selected by the author based on an
estimate of the impact on the course of research, theory and
practice.
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 91
no valid or reliable evidence that either immunization
or diet is related to autism prevalence, but it was
difficult to convince parents otherwise. Immunization
was the main focus for two reasons. First, autism
symptoms become apparent around the age at which
immunization typically occurs, so the temporal
proximity of the two events appeared suspicious to
parents. Diet became a popular issue following
publication of a factious article alleging a link between
enterogastric toxins arising from eating foods containing
gluten and autism (Wakefield et al. 1998). Although
there has never been an established link between coeliac
disease (Gluten allergy) and autism, nonetheless, many
parents subjected their children to gluten- and caseine-
free diets hoping to alleviate autism symptoms (Batista
et al. 2012).
If there was a contagion, it appears to have been the
dissemination of misinformation among parents, the
news media and some professionals who were complicit
in spreading inaccurate information, rather than an
actual autism epidemic. It now appears there was either
no actual increase in prevalence, or if there was an
increase, it was relatively small and had other
explanations (Rutter 2005a,b; Baron-Cohen 2006; Virkud
et al. 2009). A publication in the Lancet authored by a
gastroenterologist and his team proposed autism was
caused by measles–mumps–rubella vaccine that they
alleged damaged the intestinal lining, creating a
firestorm of accusations about the alleged causes of
autism, which was later expunged from the journal due
to ethical breaches. Those involved in spreading the
misinformation were later sanctioned by the General
Medical Council (Boseley 2010). Over 20 studies
conducted independently in various countries have
failed to find a connection between the MMR vaccine
and autism prevalence leading governmental agencies
and an unbiased review group to conclude that there
is no relation between MMR vaccine and autism
prevalence (US Centers for Disease Control &
Prevention 2008; Committee to Review Adverse Effects
of Vaccines (2012) and the UK National Health Service
(2007) and the Cochrane Library review (Demicheli et al.
(2005). As a result of the scare, many parents stopped
having their children immunized against measles and
mumps, with a resulting increase in cases of those
diseases in the UK (see Figure 5).
Regrettably, many in the general public seem to
have the misimpression that measles and mumps are
benign diseases, and they therefore elected to decline
to immunize their children rather than encountering
the assumed risk that the vaccine might cause autism,
92 Journal of Applied Research in Intellectual Disabilities
Figure 5 Measles cases in the UK as a function of percentage
of the population receiving measles vaccine. Reproduced with
permission from the United Kingdom Health Protection
Agency, 151 Buckingham Palace Road, London SW 1W 9SZ.
which it does not (Brown et al. 2012). Measles (Rubeola)
and mumps (Epidemic parotitis) were considered serious
disease associated with pneumonia, deafness and brain
damage before vaccines were introduced. If not treated
effectively, measles can lead to pneumonia, diarrhoea
and death and adverse effects occur most often
in developing countries. Before the measles vaccine
was introduced in the UK, approximately 100 deaths
occurred each year due to measles and this dropped
to 13 deaths a year by the mid-1980s (Medical
Research Council 2012). In the USA, prior to
introduction of the vaccine in 1963, almost everyone
got measles. Each year there were approximately three
to four million cases and an average of 450 deaths
(Schoenstadt 2007).
Rarely, measles viruses associated with a brain
condition called subacute sclerosing panencephalitis
(SSPE), a progressive and fatal neurological disease
that can be caused by high levels of infection by the
measles virus in the brain. It typically occurs 10–
15 years after initial measles (MRC Medical Research
Council 2012). More than 50% of patients with mumps
will develop meningitis, which may occur during
any period of the disease. Generally, patients make
a full recovery without permanent side effects. Until
the 1960s, when mumps vaccine was introduced,
mumps was the primary cause of confirmed viral
encephalitis. Mumps is also associated with infertility
in 13% of males and 8th cranial nerve hearing
loss. While vaccine fears are subsiding among the
general public, it will likely take an entire generation
for the population to recover from the serious
misinformation campaign regarding measles–mumps–
rubella vaccination.
Defining diagnostic features
A controversy has revolved around the degree to which
the foregoing three major features of autism vary
independently from person to person who meets the
diagnostic criteria, or whether they co-vary, that is, if an
individual exhibits a disability in one domain (e.g.
functional communication), do they also exhibit a
disability to a similar degree in the others (e.g. lack of
social skills). This issue is at the root of the
disagreement about a distinction between Autistic
disorder and Asperger disorder (DSM5). Some
prominent clinical researchers have insisted Asperger
disorder is a qualitatively different condition from
autism (Wing, Klin, Volkmar) with spared language
functioning but some disability in social skills and
repetitive compulsive routines, while others have
increasingly argued they are qualitatively the same
condition varying only in degree of expression.
Considerable evidence indicates autism and Asperger
disorder, as well as atypical autism (Pervasive
Developmental Disorder NOS) are present within the
same families far more commonly than expected by
chance (Liu et al. 2008; Constantino et al. 2010), which
should not be the case if they are qualitatively
independent conditions. Moreover, a review of a
substantial number of research studies between 1981
and 2010, shows that six possible criteria for
diagnosing Asperger disorder (the age at which signs
and symptoms related to autism become apparent,
language and social communication abilities,
intellectual abilities, motor or movement skills,
repetitive patterns of behaviour and the nature of
social interaction) overlap substantially with the criteria
for diagnosing autism and cannot be reliably
distinguished from one another (Sharma et al. 2012).
Rutter (2011) has proposed categorical and dimensional
approaches to diagnosis should be combined and
research and clinical classifications should be kept
separate. Those who are opposed to subsuming
Asperger disorder within autism point out that the
proposed DSMV diagnostic criteria which include
Asperger disorder within autism as a quantitatively
less severe form, fail to include social imagination,
differences in diagnosis in infancy and adulthood, and
the possibility that girls and women with autism may
continue to go unrecognized or misdiagnosed (Wing
et al. 2011) and point out that in some studies as many
as 40% of individuals previously diagnosed with
Asperger disorder would not be identified using the
proposed new criteria (DSM-V) (McPartland et al.
© 2013 Blackwell Publishing Ltd, 26, 81–107

2012). However, it appears inevitable that autism will
officially diagnostically become a single condition, but
the precise method for specifying severity of symptom
clusters remains unclear.
Misunderstanding diagnosis
Parents, teachers and some professionals continue to
question the validity of the autism diagnosis because
there is no definitive biological test, like a blood test, a
brain scan or genetic test for autism. Moreover, many
are puzzled by the large variability within the group of
individuals with autism. While this is understandable, it
reflects a lack of understanding about the typical nature
of medical diagnosis. That autism is variable in
expression qualitatively and quantitatively is not
unusual among medical diagnoses. The fact that no
single brain locus or gene can be identified causing
autism is actually typical among most medical
conditions. Infantile Cerebral Palsy (ICD: 343) includes
three main subtypes, spastic, ataxic and athetoid/
dyskinetic. The condition can come about in many ways
during intrauterine development (e.g. exposure to
radiation, infection), asphyxia before birth, hypoxia of
the brain and birth trauma during labour and delivery,
and complications in the perinatal period. Various parts
of the brain are often involved with varying degrees of
disability symptoms. Few suggest there is no such thing
as Cerebral Palsy because of this variability. The same is
true of Epilepsy (ICD: 345), that includes absence
epilepsy, tonic-clonic, status epilepsy and temporal lobe
epilepsy without status (which is called partial epilepsy
in the US). In some cases very specific brain loci can be
identified as the point at which seizures begin but in
many cases that is not the case. Again, the type of
symptoms and severity vary greatly, which does not
detract from the diagnosis of epilepsy. Some types of
epilepsy have strong genetic causal links and others not
at all.
The absence of a singular biological test with an
unambiguous dividing line for autism is not unusual for
many medical conditions. When the number of
millimetres of mercury on the sphygmomanometer
column exceeds a value after inflating the blood
pressure cuff, a physician may say ‘You have low grade
hypertension’, much as a psychologist might say to the
parent of a child with an ADOS score of 7 on Module 1
who exhibits hyperlexia and other mild autism signs
‘Your son has high functioning autism’. As there is no
unambiguous dividing line, some critics suggest that
raises doubts about the very concept of autism, which is
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 93
a specious argument. No one seriously doubts there is a
difference between day and night because of the
existence of twilight. Fuzzy distinctions at the border
between medical conditions is more often the norm than
not.
Standardized Assessments
Diagnosis
Until 1989 clinical observations, parent interviews and
the Childhood Autism Rating Scales (CARS) and the
Autism Behaviour Checklist (ABC) were commonly
used to determine whether a child would receive an
autism diagnosis. Depending on clinician training, the
value of observations and parent interviews may be
invaluable or not very useful, leading to great variability
in diagnoses. The CARS is a screening test not a
diagnostic test, although it is widely used for the latter
purpose in schools and other community settings. It
correlates reasonably well with more widely accepted
measures such as the ADI-R (Saemundsen et al. 2003).
In the UK the Modified Checklist for Autism in
Toddlers (M-CHAT) may be used to screen 18-24 month
old children (Robins et al. 1999). Diagnositic variability
has been reduced considerably with the introduction of
the Autism Dianostic Interview and Observation
Schedule (ADI and ADOS) (Lord et al. 1989).
Many university autism specialty clinics and some
community centres and schools require that the Autism
Diagnostic Observation Schedule (ADOS) (Lord et al.
1989) be administered, the first validated autism
diagnostic test. The ADOS consists of a series of probes
in key functional domains by a trained examiner using
a kit of specific test materials, and requires 45 min to
2 h to administer, depending on the child’s age,
functioning level and the extent of interfering
challenging behaviour. Each probe item is scored and
scores are tabulated for Communication, Socialization
and Repetitive Behaviour and total score for the two
former subscales. The ADOS is available in age and
functioning level modules. Most young children
(beginning at 2 years) suspected of having autism are
tested using Module 1. While well-trained examiners
can administer the test with reliability, some
professionals who administer the test have only
participated in a single day of hands-on training and
often only involving practice testing a single child. This
poses significant problems because it does not expose
the examiner to the wide range of symptoms and ability
levels presented by children with autism, or provide
94 Journal of Applied Research in Intellectual Disabilities
any training in differential diagnosis (distinguishing
autism spectrum disorders from language disabilities,
obsessive compulsive disorder, ADHD, or anxiety
disorder). Direct quantitative comparisons of severity
scores across test ADOS modules cannot be validly
made. In other words a score of 7 on Module 1 does not
mean the same thing as a score of 7 on Module 2. This
is troubling to parents, teachers and other practitioners
who wish to compare autism severity progress as a
child grows older, and more than one assessment
module is used. Research is underway to create a
common symptom severity metric but this complex
procedure is only available for research purposes, and
cannot not be routinely be used clinically at this time
(Gorham et al. 2012). As a result, the standard clinical
practice is to report severity according to a crude
ordinal scale: Not autism, autism spectrum, autism,
which is often useful for administrative tracking but is
of limited value to parents or intervention planners. The
greatest challenge in autism diagnosis is distinguishing
autism from other disabilities with overlapping
symptoms, such as any combination of attention deficit
hyperactivity disorder, obsessive compulsive disorder,
other anxiety disorders, speech-language disabilities and
borderline low intellectual functioning. At present, these
issues can only be addressed by considerable training in
a clinical setting that serves all of these populations.
Misdiagnosis appears to be common. Other strategies
must be used to more frequently and sensitively track
intervention progress such as criterion-referenced
assessments such as the Assessment for Basic Language
and Learning Skills-R (Partington 2006) or the Verbal
Behaviour Milestones Assessment Monitoring System
(Sundberg 2008).
Alternative Early Intervention
Approaches
Early intervention for children with disabilities began
long before such a strategy was proposed for children
autism. To understand the reasons for the very deep
divide within the field of early intervention regarding
which approach is most appropriate for young children
with autism, we first examine the roots of these
assumptions.
Developmental theory
Marie Montessori, who had studied Edouard S
eguin’s
‘physiological method’ for teaching young children with
developmental disabilities (Seguin 1866), developed
the Orthphrenic School for training teachers in
educating children with intellectual disabilities. Seguin
had argued that children with disabilities lacked skills
because of sensory and motor weaknesses that could be
strengthened with repeated practice of prescribed
activities. Seguin’s approach was much more structured
than Montessori’s, especially in her later work.
Montessori opened Casa dei Bambini, or Children’s
House for 3- to 7-year-old children with disabilities. She
provided practical activities such as sweeping and
personal care and exercises for care of the environment
and the self, including flower arranging, hand washing,
gymnastics, care of pets and cooking. She experimented
with allowing children free choice of the materials,
uninterrupted work and freedom of movement and
activity within the limits set by the environment
(Montesorri 2006). Montessori’s approach became
synonymous with early educational intervention for
children with disabilities throughout much of the world.
Philosophical and Theoretical
Foundations
Philosophical assumptions of two early developmental
theorists largely determined how early childhood
learning and education were understood and appro-
ached for most of the 20th century. Jean Piaget grew up
in post-WWI Switzerland in which there was great
national pride in the country’s autonomy from outside
influence (Chenaux-Repond 1996). Piaget studied the
philosophy of Henri’ Bergson, who was convinced that
immediate experience and intuition were more
significant than rationalism and science for
understanding reality (Lawlor & Moulard 2011). While
Piaget’s writing was filled with striking insights about
child cognitive development, the behaviour Piaget
observed, which was the basis for his theory, was that
of his own exceptionally bright children of very capable,
socially competent and highly verbal parents. In
actuality, Piaget’s children had little in common with
most children with intellectual disability or autism, to
whom his theory was subsequently applied.
Lev Vygotsky was born in Belarus in 1896 and
experienced the turmoil of the Russian Revolution. At
university, he studied law. He began to work in
psychology shortly after the Russian revolution, where
Marxism replaced the rule of the czar. For Vygotsky, the
individual child’s development was largely a result of his
or her exposure to their culture and was mainly acquired
through thought, language and reasoning. Vygotsky was
greatly influenced by Lev Shestov and Nikolai Berdyeav
© 2013 Blackwell Publishing Ltd, 26, 81–107

who became well known as existentialist thinkers during
their post-Revolutionary exiles in Paris. Shestov launched
an attack on rationalism and systematization in
philosophy as early as 1905 in his book of aphorisms All
Things Are Possible. Berdyaev, also from Kiev but with a
background in the Eastern Orthodox Church, drew a
distinction between the world of spirit and the everyday
world of objects. Human freedom, for Berdyaev, is rooted
in the realm of spirit, a realm independent of scientific
notions of causation. Not surprisingly, Vygotsky was not
an empiricist and gravitated towards knowledge through
self-reflection with emphasis on freedom of spirit. The
philosophical ideas of these two cognitive developmental
theorists formed much of the foundation of early
education and intervention throughout the 20th century
up to the 1980s. Although widely adopted throughout the
West, neither theorists’ ideas grew from foundations
familiar to Northern European or American thinkers.
Neither adopted systematic data collection nor the
rigorous methodology of the experimental method of
early 20th century physiology as practiced in most of
Europe, Canada and the USA, as a basis for establishing
knowledge claims. Piaget and Vygotsky were both
steeped in concepts of free will and autonomy and
committed to the idea that children’s early learning
occurred through a somewhat ill-defined process of
discovery, with occasional guidance from a more
experienced model. They operated from very different
epistemological traditions from those of American
psychologists who developed behaviour analytic
interventions.
John Bowlby was a physician trained in psycho-
analysis, whose writing on attachment theory became
the third pillar of development-based autism early
intervention. John Bowlby had grown up being cared
for by a nanny as a young child. He rarely saw his own
mother more than 1 h a day. At age seven, he was sent
away to boarding school. He later said, ‘I wouldn’t send
a dog away to boarding school at age seven’ (Schwartz
J, 1999, p. 225). After graduating from Cambridge
University, he enrolled at University College Hospital
London and qualified in medicine. While still in medical
school, he enrolled in the Institute for Psychoanalysis
where he trained in adult psychiatry and qualified as a
psychoanalyst. He was subsequently commissioned to
write the World Health Organization’s report on the
mental health of homeless children in post-war Europe
(Bowlby 1951). Despite his training, Bowlby rejected
some aspects of psychoanalytic theoretical explanations
for early childhood attachment difficulties, adopting
instead ideas from the emerging European ethology
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 95
(Konrad Lorenz, Niko Tinbergen and Robert Hinde).
However, it has been pointed out that in the last
analysis, Bowlby’s theory was deeply rooted in
psychoanalytic concepts (Sroufe 1986). At about the
same time, Bowlby’s former colleague, Mary Ainsworth
was completing observational studies on infant
attachment in Uganda. Her results contributed to the
subsequent evidence base of attachment theory as
presented in 1969 in Attachment the first volume of the
Attachment and Loss trilogy. The second and third
volumes, Separation: Anxiety and Anger and Loss: Sadness
and Depression followed in 1972 and 1980, respectively.
According to Bowlby and Ainsworth’s theory,
attachment in infants is primarily a process of proximity
seeking to an identified attachment figure in situations of
perceived distress or alarm for the purpose of survival.
Infants become attached to adults who are sensitive and
responsive in social interactions with the infant, and
who remain as consistent caregivers for some months
during the period from about 6 months to 2 years of
age. Unlike Piaget and Vygotsky, whose theories arose
primarily from philosophical beliefs and informal
observations of only a few typical children, Bowlby’s
theory depended on Ainsworth’s more systematic
observations on children with disrupted early childhood
experiences.
Bowlby’s writing has been of fundamental importance
in understanding the consequences of early separation
of children from adult caregivers, such as during
wartime and of child neglect and abuse (Howe et al.
1999). It is not clear that Bowlby’s attachment theory is
directly applicable to autism, although it is incorporated
in some forms of early intervention (Floortimeâ and
Relationship Development Interventionâ). Autism does
not fit the definition of an attachment disorder in the
vast majority of cases. ‘F94.1 Reactive attachment disorder
of childhood: Starts in the first 5 years of life and is
characterized by persistent abnormalities in the child’s
pattern of social relationships that are associated with
emotional disturbance and are reactive to changes in
environmental circumstances…. The syndrome probably
occurs as a direct result of severe parental neglect,
abuse, or serious mishandling’. (ICD-10 Version 2010)
(underlining added for emphasis). Indeed, there is
substantial evidence children with autism are
emotionally attached, in particular to their mothers,
although the way they express their attachment is
atypical (Sigman & Ungerer 1984) and may involve
somewhat different processes (Rogers et al. 1993).
Despite the lack of concordance of theory and empirical
reality, some continue to assume autism involves an
96 Journal of Applied Research in Intellectual Disabilities
attachment disorder and should be treated accordingly
(Gutstein & Sheely 2002; Greenspan & Wieder 2008).
When Chomsky (1959) published his critique of
Skinner’s book Verbal Behavior, many within the
cognitive developmental psychology movement viewed
that as the final nail in the Behaviourists’ coffin, and
apparently assumed the field would wither up an die,
and what few remaining practitioners of behaviour
analysis that still existed, would switch to different
approaches. It did not happen that way as it turned out,
and while Chomsky had some legitimate concerns about
Skinner’s theoretical analysis of language, over the past
two decades considerable work has been carried out
empirically fleshing out components in his analysis of
verbal behaviour (Michael 1984; Sundberg & Partington
1998). More to the point, a major focus of behavioural
intervention in young children with autism has been
teaching alternative communication and language
strategies to non-verbal children, notwithstanding
Chomsky’s admonitions that Skinner’s understanding of
language was too primitive to be useful (Chomsky,
1959).
Behavioural Approaches to Early
Intervention
Burrhus F. Skinner and O. Ivar Løvaas were largely
responsible for the emergence of a behaviour analytic
approach to autism – Skinner because he promulgated
the basic principles and Løvaas because he applied
them specifically to young children with autism. B. F.
Skinner grew up before and during WWI in
Susquahanna, PA in the USA, within a pragmatically
conservative family in a mining region. Skinner was
always drawn to technology. Although he had hoped
to be a writer as an undergraduate, at Harvard
University as a psychology doctoral student, he soon
fell under the powerful influence of W. J. Crozier and
L. J. Henderson, distinguished physiologists who were
on the forefront of the General Physiology movement.
He studied Sherrington’s reflex and developed the idea
that psychology needed a comparable unit of analysis.
Although he claimed he had not studied Claude
Bernard’s writing (Skinner, BF, pers. comm.), much of
his metatheoretical framework of experimental analysis
and single subject experimentation is drawn directly
from Bernard’s Experimental Medicine (1865), including
his notion of causality. Skinner ambitiously took it
upon himself to attempt to develop within psychology
a field comparable to General Physiology, based on
general principles that superseded any particular
subdomain of psychology (as had happened in
physiology).
Skinner attempted to discover lines along which
behaviour naturally fractured by providing consequences
for portions of behaviour, to determine if their
probability of recurrence could be selectively changed,
which was fortuitous and proved successful. Although
the behaviour Skinner initially studied was rats
depressing telegraph keys in a metal box leading to food
pellets, he almost immediately saw that the same idea
could, in principle, be applied to any behaviour in the
larger world around that box, including the behaviour of
people. For people, the consequences of interest were not
food pellets, but were largely social in nature (smiles,
successfully achieving the right answer, running faster
than yesterday or being hugged by your mother). This,
not surprisingly offended many psychologists, especially
those who believed psychology was the study of the
mind, not simply the things rats and people did and the
events around them. For Skinner to imply, as it appeared
to many, that the life work of clinical psychologists who
devoted their lives to adjusting the motivational and
emotional fittings on their clients’ mental plumbing was
actually unnecessary, and amounted to frippery was not
well received. To teachers who were very concerned that
their students not only learn, but they enjoy learning and
overcome distress they may have experienced as they
struggled to master challenges, to suggest those feelings
are unimportant, as Skinner and some of his followers
did, was understandably offensive.
So despite the quite remarkable pace of new findings
within in the field of the experimental analysis of
behaviour, and within the nascent field of applied
behaviour analysis, some of their most prominent
spokespersons were unjustifiably offending much of the
professional community and alienating lay people as
well, such as parents of children with autism and other
disabilities. For the next 20 years, the analysis of
behaviour emerged as a very complex laboratory
research field producing vast numbers of journal
articles, book chapters, and eventually handbooks
summarizing the remarkable amount of material that
had been discovered to that point (Blackman 1974;
Catania 1968; Honig & Staddon 1977; Lowe et al. 1985).
Two decades into that era, the first serious attempts
began to be made to apply Skinner’s principles in a
more sophisticated and systematic way to address very
important societal problems and went largely unnoticed
outside of the field of behaviour analysis.
Ole Ivar Løvaas was born on a farm in Lier, Norway,
not far from Oslo in 1927. He experienced first hand
© 2013 Blackwell Publishing Ltd, 26, 81–107

Nazi oppression during WWII when Norway was
occupied by Germany. He attended college in the USA
at a small Midwestern college on a music scholarship
and later switched his specialty to psychology. Working
as a psychiatric assistant at a private mental hospital in
the state of Washington, he became disillusioned with
the care provided and lack of patient improvement. His
interest shifted from psychoanalysis, the predominant
therapy approach of that time, to the embryonic field of
applied behaviour analysis (ABA) based on principles
promulgated by B. F. Skinner. After completing his
doctorate in 1958, Løvaas stayed at the University of
Washington, where he worked alongside other applied
behaviour analysis pioneers such as Sidney Bijou,
Donald Baer and Todd Risley. His perspective regarding
treatment of behavioural aspects of mental disorders
became decidedly pragmatic, very much like those of
farmers in Norway where he had grown up. You did
what worked without too much concern for exactly how
or why it worked. In 1961, Ivar Løvaas was offered a
position at the UCLA Psychology Department where he
became an assistant professor and was soon placed in
charge of an entire ward at UCLA’s Neuropsychiatric
Institute. Few professionals were familiar with autism at
the time, but Løvaas was drawn to several children with
autism who were being treated at UCLA and at the
nearby Camarillo State Hospital. Those children (Ricky,
Pamela and several others) did not speak, nor display
typical social interest, nor play. They rocked, twirled in
circles, displayed other rigid routines and – most
disturbingly – engaged in persistent and sometimes
severe self-injurious behaviour. Løvaas reasoned that if
operant learning principles could be used to teach
complex behavioural skills to laboratory rats, whose
brains weigh 2 g, surely those same principles could
apply to children, whose brains were several hundred
times larger. Perhaps, Løvaas thought that he could even
teach them to respond appropriately to adult requests,
learn basic skills and even talk. Most importantly at the
time, he sought a way of overcoming their excruciating
self-injury, for which there was no other treatment. His
initial efforts included use of punishment, which were
later eliminated from his overall treatment approach.
Unlike Piaget and Vygotsky’s developmental theories
that were philosophically driven, Løvaas’s behavioural
approach to early intervention was more narrowly based
on the assumption that young children could be taught
specific skills necessary to communicate their needs, to
care for themselves and acquire basic cognitive skills
using operant learning principles. There was no initial
consideration of the possibility a child’s attachment
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 97
difficulties were at the root of their learning and
behaviour challenges, or that it would be necessary to
follow prescribed developmental stages in implementing
early behavioural intervention. It was not so much that
Løvaas was antagonistic towards these ideas because he
did not find them necessary. Early behavioural
interventionists viewed their task as discovering how
best to teach young children who exhibited very specific
skill deficits, much as they might teach any other child
with a disability skills necessary for getting along in the
world, such as making requests, eating with a spoon or
following adult directions. Like Løvaas, others among
the first behavioural researchers had all been trained in
laboratory methods using standardized operant learning
principles. This included the standard experimental
method of data collection and graphically reporting the
results of their observations, which originally emerged
from the principles of 19th century experimental
physiology with emphasis on experimental control of
important learning variables (Thompson 1984). Their
goals were modest at first. None of them had any notion
that they were in the process of treating the condition
called autism, nor planned to normalize social,
communication and behavioural functioning of an
affected young child. They began with the naively
optimistic assumption that one response a child with
autism might learn was generally like any other
response, so if one could teach a child to follow a simple
direction ‘Come sit down’, it would also be possible to
teach the child more complex responses using the same
method, such as respond to the question, ‘Where did
your mother go?’ or ‘What is the best way to do that?’
While that turned out not always to be the case, it may
have been a fortuitous beginning place because it
guaranteed a degree of early success. Initial studies
demonstrated that children with autism could indeed be
taught relatively simple arbitrary responses using
mechanical signals like tones or lights, as well as spoken
requests (Ellis et al. 1960; Ferster, 1961; Orlando & Bijou
1960; Spradlin 1958). These first efforts were followed by
a rash of more complex studies, in which researchers
were often surprised to discover that the principles from
the animal laboratory also applied relatively well to
people. But more importantly, they also were effective
in applied settings with children and adolescents with
developmental disabilities (Girardeau & Spradlin (1964).
The methods used were directly derived from laboratory
research with non-human (Skinner 1938) and human
participants (Bijou 1955) and were very limited in scope.
The earliest operant laboratory and single subject
applied interventions were mostly conducted with
98 Journal of Applied Research in Intellectual Disabilities
individuals with developmental disabilities and often in
large public institutions. Subsequently, numerous applied
programmes emerged with school-age children and
older individuals with developmental disabilities
demonstrating efficacy of the basic principles and
techniques (e.g. reinforcement magnitude and schedules,
discrimination learning, backward chaining, reinforce-
ment of successive approximations) (Thompson &
Grabowski 1972). Some people with autism were
included within the groups receiving such services, but
separate records were not maintained of any differences
in success rates using operant methods. There were
generally no efforts to provide comprehensive skill
training across important life domains so as to engender
more typical functioning that would apply to most
aspects of daily life (See for example, Thompson &
Grabowski 1972; 1977). Much of the criticism of early
behavioural intervention with institutionalized popula-
tions (mentally ill and severely intellectually disabled)
emerged from critics within the field, such as Kazdin &
Bootzin (1972) and Kazdin (1982), who expressed concern
not so much about effectiveness or appropriateness of
behavioural targets, but generalization and dissemi-
nability of the procedures. Not surprisingly, the
psychiatric community viewed behavioural intervention
procedures purely as ways of managing psychiatric
wards of patients with schizophrenia (Martin 1972) rather
than treatments, per se, and expressed concern that they
did not change the underlying psychiatric disorder.
Cognitive developmental psychology had relatively little
to say about these early interventions because their
perspectives were based on Piaget’s and Vygotsky’s
theories which assumed cognitive and verbal skills not
present among many of the individuals involved in the
earliest behavioural intervention projects (e.g. Thompson
& Grabowski 1972). There was relatively limited
resistance to these efforts with older individuals
with intellectual disabilities by most developmental
psychologists. Where criticisms existed, they were often
incredulity and doubts that behavioural practitioners
were actually teaching skills that developmental theory
suggested were not possible (e.g. D. Zeaman, pers.
comm.). Nonetheless, those early efforts often led to
substantial improvements in the quality of life for older
people with developmental disabilities and, in at least
some cases, led to transfer of large numbers of
individuals with intellectual disabilities from large
institutions to integrated community settings (Welsch v.
Likins 1974).
Løvaas was first to develop a consistent programme
of clinical research yielding substantial enduring
behavioural improvements among children with
autism. His earliest work focused on circumscribed
skill deficits like lack of language and on reducing
self-injury. His use of aversive procedures to reduce
self-injury was controversial, creating strenuous
opposition to the entire applied behaviour analysis
approach to autism. Moreover, the first children with
autism who Løvaas treated made only modest gains
and often skill improvements were transient. This
initially dampened public support for Løvaas’s
approach. He concluded his attempts that had been
too little (several hours per week) and too late
(beginning at 7–9 years of age).
Ivar Løvaas undertook a much more ambitious
project involving 40 hours per week of therapy for
3 years with 2- to 5-year-old children with autism.
When he published the results of his longitudinal
follow-up study of EIBI with 19 2- to 5-year-old children
with autism, compared with outcomes for an untreated
group and another receiving less intensive early
intervention (Løvaas 1987), objections from the
developmental psychology world erupted. For the first
time behavioural early intervention method had been shown
to be highly effective in reducing and in some cases nearly
eliminating most autism symptoms in about half of the
treated young children, and the effects were durable and long
lasting. Løvaas’s findings sent a shock wave throughout
the developmental psychology community, which
though lip-service had been paid to alternative
approaches, had heretofore been largely assumed early
intervention methods were the exclusive province of
specialists trained in cognitive development and
attachment theory (Shonkoff & Meisels 2000).
Early intervention in the United States had been
dominated by political pressure to counteract effects
of poverty on early childhood experiences among ‘at
risk’ children with low to low average intellectual
functioning, rather than those with identified
disabilities. It was often assumed that cognitive
developmental psychologists were the experts on early
intervention (White & Casto 1985; Deutsch et al 1972;
Jordan et al. 1985; Irvine et al. 1982). Nearly all early
intervention programmes began by assuming a
Piagetian and Vygotskian perspective, or example, the
well known, High/Scope Perry Preschool Program in
Ypsilanti Michigan was built ‘on the child development
theories of Jean Piaget (Piaget & Inhelder 1969) and Lev
Vygotsky (1962/1934), the progressive educational
philosophy of John Dewey (2007/1916), and more recent
work in cognitive developmental psychology (e.g.,
Clements, 2004; Gelman and Brenneman, 2004’
© 2013 Blackwell Publishing Ltd, 26, 81–107

(Promising practices network 2009). There was relatively
little emphasis on specific teaching methods. Instead, a
constructivist model was adopted, by which children
were supposed to construct their own realities based
on guided discovery-based experiences. Tobias & Duffy
(2009, pg 4) wrote ‘… to us it would appear that
constructivism remains more of a philosophical
framework than a theory that either allows us to
precisely describe instruction or prescribe design
strategies’. More recently, other writers transformed
broad principles of developmental psychology theory
into more practical forms, such as the activity-based
preschool curriculum built around typical daily
routines, and appeared to be less concerned about
constructivist philosophy (Squires & Bricker 2006; Dunst
et al. 2001; McWilliam 2010).
Two aspects of Løvaas’s findings were especially
troubling to developmental psychology critics. First, the
effects obtained over 3 years of EIBI were clinically very
large, much more substantial than anyone could have
anticipated and had ever before been obtained. To
many, this taxed credibility. Perhaps more troubling,
Løvaas’s work did not begin with developmental
psychology theoretical assumptions. He did not assume
children with autism had failed to develop social and
communication skills because they had a flawed or
insecure attachment with their parents, or that they
required developmentally age-appropriate guided
cognitive exploration of the world around them to
develop their unique intellectual mastery, or the basic
skills he was attempting to teach. Løvaas and other
early behavioural practitioners did not find such
assumptions helpful in teaching young children with
autism skills that were intended to make their daily
lives a little better, like greetings, making eye contact
when speaking and other rudimentary social skills.
Unlike Piaget, Vygotsky and Bowlby, Løvaashad relied
hardly on any theory at all, other than the inductive
assumption that children with autism could be taught
specific skills using operant learning principles, which
when combined, began to approximate more typical
functioning. Løvaas’s proposal was based on earlier
observations that teaching them such skills in more
controlled situations was possible using such an
approach. It was not a very large leap of faith. The
pragmatic principles involved in teaching children with
autism the skills were derived from Skinner’s analysis
of operant behaviour (Skinner 1938; Skinner 1953;
Holland & Skinner 1961).
To some in developmental psychology, it seemed
incomprehensible that such a relatively simple
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 99
pragmatic and a theoretical approach had proven to be
so effective. For several years, after Løvaas 1987 paper
was published, articles appeared in professional
journals attacking Løvaas’s methods, claiming that such
dramatic findings could not be replicated (e.g. Schopler
et al. 1989; Gresham & MacMillan 1998). Subsequently,
numerous replications of Løvaas’s findings were
published, all obtaining very similar results (e.g.
McEachin et al. 1993; Remington et al. 2007; Sallows &
Graupner 2005; see also summary in Løvaas & Wright
(2006). In 2001, an expert panel of the US National
Research Council concluded that applied behaviour
analysis intervention was often effective, although it
was unclear which aspects of the service was
responsible for the main results (Lord & McGee 2001).
The National Research Council panel chaired by Lord
and McGee also noted behaviour analytic methods
other than Løvaas’s Discrete Trial Method appeared
effective as well, although there were fewer studies at
that time. Criticisms about effectiveness of the
behaviour analytic approach began to subside.
Instead, subsequent critiques focused on the specific
techniques involved in Løvaas’s Discrete Trial
Intervention, which were likened to dog training
(Kaufman 1998–2008) and some expressed concern the
training was robotic (Chew 2006). These views were
often stated within the context of a strong philosophical
commitment to developmental psychology approaches
based on Piaget, Vygotsky and Bowlby’s theories,
although typically no empirical evidence was provided
to support the claims. These critiques also reflected
wide-spread concern that the predominant discrete-trial
approach was excessively doctrinaire and probably not
appropriate for all children on the autism spectrum
(Magiati et al. 2007).
Aggravating the conflict between behavioural and
developmental practitioners, some of the early
advocates of the EIBI approach published articles
claiming the changes obtained for many of the children
with autism receiving behavioural treatment constituted
‘recoveries’, or ‘cures’ a claim, which was rejected by
psychologists and educators in the field(Gernsbacher
(2003). Others who have evaluated the evidence from
children receiving such treatment said that while the
children had clearly improved, claims of recovery were
exaggerated (Herbert et al. 2002).
Cognitive Developmental Alternatives
Eric Schopler and colleagues had developed a
cognitively based intervention that had largely been
100 Journal of Applied Research in Intellectual Disabilities
used with school age children, Treatment and Education
of Autistic and Communications-Handicapped Children
Program called TEACCH (Mesibov et al. 2005).
TEACCH is based on the relative strength of individuals
with autism in visual information processing (compared
to difficulties with auditory processing, particularly of
language) and providing cues for organizing activities
leading to increased independence. There has been one
controlled study using the TEACCH method with 11
preschool children showing pre-post improvements in
scores on standardized tests over a six month period
(Ozonoff & Cathcart 1988) although little information is
available about the longer term generalization of those
skills or functional life trajectory.
In the UK and parts of Europe, considerable emphasis
has been placed on the theory of mind (ToM), a concept
that emerged from laboratory research with a
chimpanzee and children with autism (Premack &
Woodruff 1978; Baron-Cohen et al. 1985). The authors
and others have contended that ToM is the fundamental
deficit in autism and all other deficits flow from it.
Numerous studies have been reported on ToM, cognitive
tasks and brain imaging, but few intervention studies
have been based on ToM. ToM may be a specific case of
a more general deficit, that is, lower-level domain-
specific mechanisms – for example, tracking gaze, joint
attention – interacting with higher-level domain-general
mechanisms for metarepresentation and executive
function can account for observed patterns of deficits in
both autism (Stone & Gerrans 2006). Acquiring skills in
the typical TOM task may not be relevant to everyday
functioning in the natural environment. Begeer et al.,
(2011) used a randomized controlled design to test the
effectiveness of a 16-week ToM treatment in 8- to 13-
year-old children with autism spectrum disorders and
normal IQs (n = 40). The results showed that, compared
to controls, the treated children with ASD improved in
their conceptual ToM skills, but their elementary
understanding, self-reported empathic skills or parent
reported social behaviour did not improve. Others have
raised doubts about the concept (Boucher 2012; Costall &
Leudar 2007). The adoption of the term ‘mind reading’
(Howlin et al. 1998; Baron-Cohen 2007), although
accompanied by caveats about the scientific basis for the
unique usage of that term in this context, has been
unfortunate; while it may be popular with some in the
news media and general public, it is unlikely to advance
the scientific understanding of autism.
More recently, two commercial proprietary autism
early intervention treatment methods emerged in the
USA based on developmental psychology theory,
Floortimeâ and Relationship Development Intervention
RDIâ(Gutstein & Sheely 2002; Greenspan & Wieder
2008), which emphasized emotional bonding and child
learning through guided exploration. In each case, the
authors indicated that the goal was not to teach the
child-specific skills but to build a strong emotional bond
between caregiver and child. There have been no
controlled evaluations of Floortimeâ using standardized
measures, although one article reporting outcomes using
parent ratings of their relationship with the child (rather
than based on child social and communication progress)
and claimed significant gains using a measure that has
not been validated (Solomon et al. 2007). An evaluation
of the RDIâ method by its developer in one study
claimed ‘While all children met ADOS/ADI-R criteria
for autism prior to treatment, no child met criteria at
follow-up’ (Gutstein et al. 2007). There have been no
replications of these findings by an independent
research group.
Behaviour Analytic Early Intervention
Methods
A common misunderstanding among parents and
practitioners is the assumption that ‘ABA’ intervention
for young children with autism is the same as discrete
trial training or discrete trial intervention (DTI),
basically synonymous with Løvaas 1987 method.
Applied behaviour analysis (ABA) is not a specific set of
techniques; it is a family of underlying principles and
procedures, which underlie a great many applications of
which DTI is only one example (Baer et al. 1968). ABA
is to autism intervention, as physiology is to paediatric
medical treatment. The principles underlie the treatment
but are not the same as the treatment.
Moreover, there are several variations on applied
behaviour analysis interventions that vary considerably
from those of Discrete Trial Intervention along several
important dimensions. Applied behaviour analysis
treatments include Incidental Teaching (Hart & Risley
1975; Koegel & Frea 1993, McGee et al. 1992), Pivotal
Response Therapy (Pierce & Schreibman 1995), Verbal
Behaviour (Stafford et al. 1988; Carbone 2007), Pyramid
Picture Exchange Communication System (Bondy &
Frost 1994) and Blended Intervention (Thompson 2011),
all of which are based on the principles of applied
behaviour analysis. In addition, there are more specific
behavioural techniques that are often incorporated
within overall treatment packages, such activity
schedules (Krantz et al. 1993), scripts and script fading
(Krantz & McClannahan 1998) and video modelling
© 2013 Blackwell Publishing Ltd, 26, 81–107

(Sherer et al. 2001; D’Ateno et al. 2003; Nikopoulos &
Keenan 2004). Finally, all of these methods have been
incorporated within classrooms and entire schools, as
components of positive behaviour support (Horner
1994; Carr et al. 1999), which is based on applied
behaviour analysis.
Hybrid interventions
Within the past decade, increasingly hybrid
interventions have emerged that incorporate aspects of
behavioural and developmental interventions. Pivotal
Response Treatment is an incidental teaching method
emphasizing teaching pivotal skills that leverage a wide
array of other responses spontaneously without
explicitly being taught in natural environments and
provides the child with considerable control over choice
of activities and reinforcers (Koegel et al. 1999).
Schreibman et al. 1996). Blended Intervention is a largely
behavioural model that incorporates activity-based
intervention strategies within natural environments and
emphasizes functional social and communication skills
and ecological validity (Thompson 2011; Thompson
et al. in press). The Denver Early Start Model is a
largely developmental intervention that incorporates
some behaviour analytic teaching methods, primarily
Pivotal Response Training into the method, and has
been shown to be efficacious in a random assignment
double blind assessment (Dawson et al. 2010). SCERTS
is a communication-based developmental method that
also incorporates some behavioural intervention
methods within the strategy. One controlled study of
the entire treatment package has been conducted
(Wetherby & Woods 2006), and numerous studies of
components of the approach have been published.
Differences That Matter
Much of the disagreement about differences in early
intervention approaches is philosophical at its root,
about the nature of human nature. One group is wed to
the continental philosophical approach and the other to
the American pragmatist approach. The former take
exception to procedures that appear mechanistic and are
not sufficiently mindful of the whole child, including
her/his thoughts and feelings, while the latter questions
methods for which objective, quantitative empirical
evidence is lacking and suspects the preoccupation with
the child’s cognitive processes and emotions is an
excuse for evading accountability in the comfort of their
armchair.
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 101
The various methods (developmental versus
behavioural) overlap across several significant
dimensions (Thompson 2011, page 70), including:
1. Adult versus child-directed
2. Individual versus group learning
3. High versus low intensity
4. Parents versus therapists as interventionists
5. Isolated setting versus embedded within natural
daily routines
6. Specific functional communication, social and
cognitive skills versus relationships
Some of these differences matter a great deal and
others are likely less important to outcome and reflect
philosophical preferences. Moreover, the assertion that
one end of the dimension is uniquely characteristic of
one approach and the other end, the opposite end, is
often false in practice because some blend of the two is
often used. It is no longer tenable to contend such
differences really matter to outcome without empirical
evidence to support such assertions.
Nor, it is sound to maintain that all interventions are
equally effective with all children on the autism
spectrum regardless of their individual profiles, or that
all children require the same intensity of intervention to
exhibit meaningful gains. The Autism Intervention
Responsiveness Scaleâ has been introduced which can
be used with some success to predict roughly what
combination of naturalistic and discrete trial approaches
are likely to be most effective for preschool age children
with autism (Thompson 2011; page 77). In a study with
25 preschool children on the autism spectrum, the AIRS
scores predicted accurately assignment to discrete trial
and incidental intervention but with less accuracy for
blended intervention. Of 25 children, 16 were in regular
education classrooms after receiving the AIRSâ assigned
intervention for 1–3 years, 11 without additional
support and five with paraprofessional support. Eight
were in self-contained special education classrooms.
Parent symptoms ratings of children who received EIBI
and a comparison group not receiving EIBI revealed
that those not receiving EIBI displayed more autism
socialization deficits and displayed more repetitive
behaviour and fixed routines (Thompson et al. in press).
Additional research is necessary to establish the
generalizability of these findings.
Summary
Parents and practitioners who face the day-to-day
challenges of parenting, teaching or treating children
with autism ask, ‘Why hasn’t more progress been made
102 Journal of Applied Research in Intellectual Disabilities
in understanding and treating autism?’ Frustration is
understandable, but 25–30 years ago, there were no
treatments for autism and many children were placed in
classrooms for children with severe intellectual
disabilities and then in large public institutions where
they remained the rest of their lives. It was common to
see young adults with autism lined up along the walls
of institution wards rocking and flapping their hands
aimlessly or shouting with alarm when approached too
closely. Many engaged in self-injury and aggression.
In reality, enormous progress has been made in the
scientific study of autism over the past seven decades.
We learned early on that autism is not of psychogenic
origin, such as ‘bad mothering’. Much of the impetus for
these advances arose from the availability of effective
intervention methods that changed the life trajectories of
many children with autism. Today instead of 1–2% of
individuals with autism having good outcomes as was
the case in the DeMyer et al. (1973) follow-up study,
over half are now in regular education classrooms and
many are going on to college. The other half is being
educated for vocational goals. The second major factor
making these advances possible has been emergence of
technologies in more reliable and valid psychological
assessment, brain imaging and advanced genetics. It has
become clear that autism is a heterogeneous condition
with multiple causes and multiple overlapping
neurobiological mechanisms. It is very unlikely that
there will be a single biomedical treatment for all forms
of autism. However, for a significant proportion of
affected children with autism, it appears early
intervention may promote activity-based synapse
formation in some of the affected brain areas, which
normalizes some functioning. The possibility of
combining pharmacological with behavioural
intervention to facilitate more rapid progress early in life
is currently being tested (D. Chugani, pers. comm.). The
demonstrated possibility of promoting neurogenesis in
later life, such as in constraint induced therapy in stroke
patients through intensive use of an affected limb (Taube
et al. 1999) provides a promising avenue for working
with older children as well.
The search for shared endophenotypes is an
additional promising area for further research, that is,
collections of underlying phenotypic features across
syndromes that share a common genetic error, such as
Prader–Willi syndrome and autism (Thompson 2009).
An endophenotype is a set of underlying biological
features that can be linked to a specific gene or set of
genes, which may be shared by two or more disabilities,
such as genes contributing to compulsive rituals.
A neglected area for research has been transition for
adolescence to adulthood for individuals with autism
spectrum disorders with varying degrees of disability.
While some progress has been made, the field of
vocational, residential, leisure and personal relationships
of young adults with autism has only barely begun to
be studied.
Leaders face the challenging task of training a new
generation of practitioners with sufficient skills to
individualize interventions for children with autism and
to more effectively disseminate best practices.
Engendering the political will to implement such
procedures by government agencies and in some
countries, private health insurers, continues to be a
formidable barrier, including devising ways of justifying
effective services based on cost-effectiveness as well as
humanity. Assisting parents and practitioners in
countries where outmoded and backward practices
prevail should be a global goal of international
professional organizations.
It is professionally irresponsible to make unsubstantiated
claims of recovery or cure when those terms do not
properly apply. Highly effective treatment of young
children with autism usually leaves some residual
symptoms (Sallows & Graupner 2005) making the use of
such terms misleading. Surely, it is sufficient for children
to be functioning very well alongside their peers and
leading good lives with their families, school and the
communities, even if they exhibit some differences.
Derogatory claims, such as ‘dog training’, or ‘robotic’
performance of children receiving behavioural treatment
based on philosophical or theoretical biases of the critics,
in the absence of clear evidence to substantiate those
assertions is not in keeping with professional standards.
Not only are such assertions inaccurate, they merely
serve to confuse parents and practitioners. The scientific
fields of autism research and services cannot continue to
serve a battlefield upon which self-absorbed theoretical
crusades are waged, at the expense of children with
autism and their families. We need not continue
quibbling amongst ourselves as professionals about the
philosophical issue of the nature of human nature, to
implement proven effective practices, which are available
and can meaningfully improve the lives of young
children with autism and their families.
Correspondence
Any correspondence should be directed to Travis
Thompson, PhD, 2187 Ferris Lane, Roseville, MN 55113,
USA (e-mail: thomp199@umn.edu)
© 2013 Blackwell Publishing Ltd, 26, 81–107

References
American Psychiatric Association (2012) Diagnostic and statistical
manual of Mental Disorders (DSM). http://www.psych.org/
mainmenu/research/dsmiv.aspx copyright 2012; accessed 8
February 2012
Baer D, Wolf M & Risley T. (1968) Some dimensions of applied
behavior analysis. Journal of Applied Behavior Analysis 1, 91–97.
Baird G., Simmonoff E., Pickles A., Chandler S., Loucas T.,
Meldrum D & Charman T. (2006) Prevalence of disorders of
the autism spectrum in a population cohort of children in
South Thames: the Special Needs and Autism Project
(SNAP). The Lancet 368, 210–215.
Baron-Cohen S. (2006) The hyper-systemetizing, assortative
mating theory of autism. Progress in Neuropsychopharmacology
and Biological Psychiatry 30, 865–872.
Baron-Cohen S. (2007) Mind Reading: The Interactive Guide to
Emotions. Jessica Kinglsey Publishers, London, UK.
Baron-Cohen S., Leslie A. M. & Frith U. (1985) Does the autistic
child have a ‘theory of mind’? Cognition 21, 37–46.
Batista I. C., Gandolfi L., Nobrega Y. K., Almeida R. C.,
Almeida L. M., Campos Junior D. & Pratesi R. (2012) Autism
spectrum disorder and celiac disease: no evidence for a link.
Arquivos deNeuropsiquiatria 70, 28–33.
Beeger S., Gevers S., Clifford P., Verhoeve M., Kat K.,
Hoddenbach E. & Boer F. (2011) Theory of mind training in
children with autism: a randomized controlled trial. Journal of
Autism and Developmental Disorders 41, 997–1006.
Bender L. (1947) Childhood schizophrenia. Orthopsychiatry 17,
40.
Bender L. (1959) Autism in children with mental deficiency.
American Journal of Mental Deficiency 64, 81–86.
Bender L., Goldschmidt L. & Siva D. V. (1962) LSD-25 helps
schizophrenic children. American Druggist, 146, 33.
Bernard C. (1865/1949) An Introduction to the Study of
Experimental Medicine. Translated by Henry Copley Greene.
Original copyright 1929. Henry Schuman, Inc., New York,
NY.
Bettleheim B. (1967) The Empty Fortress. The Free Press, New
York.
Bijou S. W. (1955) A systematic approach to an experimental
analysis of young children. Child Development 26, 161–168.
Blackman D. E. (1974) Operant Conditioning: Experimental
Analysis of Behaviour. Methuen, London, UK.
Bondy A. S. & Frost L. A. (1994) The picture exchange
communication system. Focus on Autism 9, 1–19.
Boseley S. (2010) Andrew Wakefield Found ‘Irresponsible’ by GMC
over MMR Vaccine Scare. The Guardian, London. Retrieved
2011-01-09.
Boucher J. (2012) Putting theory of mind in its place:
psychological explanations of the socio-emotional-commu-
nicative impairments in autism spectrum disorders. Autism
16, 226–246.
Bowlby J. (1951) Maternal care and mental health. Bulletin of the
World Health Organization 3, 355–534.
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 103
British Medical Journal (2011) How the Autism epidemic came
to be. BMJ 342, d852.
Brown P. O. (1990) Integration of retroviral DNA. Current
Topics Microbiology and Immunology 157, 19–48.
Brown K. F., Long S. J., Ramsay M., Hudson M. J., Green J.,
Vincent C. A., Kroll J. S., Fraser G., Sevdalis & N. (2012) U.
K. parents’ decision-making about measles-mumps-rubella
(MMR) vaccine 10 years after the MMR-autism controversy: a
qualitative analysis. Vaccine 30, 1855–1864.
Carbone V. (2007) Carbone Clinic. Valley Cottage, NY. Available at:
http://www.drcarbone.net/ (accessed on 17 November 2012).
Carr E. G., Horner R. H., Turnbull A. P., Marquis J. G., Magito
McLaughlin D., McAtee M. L., Smith C. E., Anderson Ryan K.,
Ruef M. B. & Doolabh A. (1999) Positive Behaviour Support for
People with Developmental Disabilities: A Research Synthesis
(American Association on Mental Retardation Monograph Series).
American Association on Mental Retardation, Washington, DC.
Catania A. C. (1968) Contemporary Research in Operant Behaviour.
Scott Foresman.
Centers for Disease Control and Prevention (2008) “Measles,
mumps, and rubella (MMR) vaccine”. Retrieved 2008-12-21.
Chenaux-Repond D. (1996) Switzerland and Europe. In: The
New Switzerland: Problems and Politics (eds Kieser R. &
Spillmann K.). The Society for the Promotion of Science and
Scholarship, Palo Alto, California.
Chew C. (2006) ABA: rote? too demanding? useful? Published
3-28-2006 Blisstree.com. http://www.blisstree.com/2006/09/
26/mental-health-well-being/aba-rote-too-demanding-useful/
accessed on 29 January 2013.
Chomsky N. (1959) A review of B.F.Skinner’s “Verbal
Behavior”. Language 35, 26–58.
Clancy H., Dugdale A. & Rendle-Short J. (1969) The diagnosis
of infantile autism. Developmental Medicine and Child Neurology
11, 432.
Clements D. H. (2004) Major themes and recommendations. In:
Engaging Young Children in Mathematics: Standards for Early
Childhood Mathematics Education (eds D. H. Clements, J.
Samara & M. DiBiase). Lawrence Erlbaum Associates,
Mahwah, NJ.
Committee to Review Adverse Effects of Vaccines. (2012)
Institute of Medicine, National Academy of Sciences. National
Academies Press, Inc., Washington, DC.
Constantino J. N., Zhang M. S., Frazier T., Abbacchi A. M. &
Law P. (2010) Sibling recurrence and the genetic
epidemiology of autism. The American Journal of Psychiatry
167, 1349–1356.
Costall A. & Leudar I. (2007) Getting over “the problem of
other minds”: communication in context. Infant Behaviour&
Development 30, 289–295.
Creak E. M. (1963) Childhood psychosis: a review of 100 cases.
British Journal of Psychiatry 109, 84–89.
D’Ateno P., Mangialpanello K. & Taylor B. A. (2003) Using
video modeling to teach complex play sequences to a
preschooler with autism. Journal of Positive Behaviour
Interventions, 5, 5–11.
104 Journal of Applied Research in Intellectual Disabilities
Dawson G., Rogers S., Munson J., Smith M., Winter J.,
Greenson J., Donaldson A. & Varley J. (2010) Randomized,
controlled trial of an intervention for toddlers with autism:
the Early Start Denver Model. Pediatrics 125, e17–e23.
Demicheli V., Jefferson T., Rivetti A. & Price D. (2005) Vaccines
for measles, mumps and rubella in children. Cochrane
Database Systematic Reviews 19, CD004407.
DeMyer M. K., Barton S., DeMyer W. E., Norton J. A., Allen J.
& Steele R. (1973) Prognosis in autism: a follow-up study.
Journal of Autism Child Schizophrenia 3, 199–246.
Despert J. L. (1971) Reflections on early infantile autism. Journal
of Autism and Childhood Schizophrenia 1, 363–367.
Deutsch M., Taleporos E. & Victor J. (1972) A brief synopsis of
an initial enrichment program for early childhood. In: A
Report on Longitudinal Evaluations of Preschool Programs (ed S.
Ryan). US Office of Child Development, Washington DC.
Dewey J. (2007/1916) Democracy and Education: An Introduction
to the Philosophy of Education. Nu-Vision Publications, LLC,
Sioux Falls, SD.
Dunst C. J., Bruder M. B., Trivette C. M., Hamby D., Raab M. &
McLean M. (2001) Characteristics and consequences of
everyday natural learning opportunities. Topics in Early
Childhood Special Education 21, 68–92.
Ellis N. R., Barnett C. D. & Pryer M. W. (1960) Operant
behavior in mental defectives: exploratory studies. Journal of
the Experimental Analysis of Behavior 1, 63–69.
Feinstein A. (2011) A History of Autism: Conversations with
Pioneers. Wiley-Blackwell, Inc., London, UK.
Gelman R. & Brennan K. (2004) Science learning pathways
to young children. Early Childhood Research Quarterly 19,
150–158.
Gernsbacher M. (2003) Is one style of early behavioral
treatment for autism ‘scientifically proven?’. Journal of
Developmental and Learning Disorders 7, 19–25.
Girardeau F. & Spradlin J. (1964) Token rewards in a cottage
program. Mental Retardation 2, 245–251.
Gotham K., Pickles A. & Lord C. (2012) Trajectories of autism
severity in children using standardized ADOS scores.
Pediatrics 130, e1278–e1284.
Greenspan S. & Wieder S. (2008) Engaging Autism: The Floortime
Approach to Helping Children Relate, Communicate and Think. De
Capo Press, Perseus Books Group, New York, NY.
Gresham F. M. & MacMillan D. L. (1998) Early intervention
project: can its claims be substantiated and its effects
replicated? Journal of Autism and Developmental Disorders 28,
5–13.
Gutstein S. & Sheely R. (2002) Relationship Development
Intervention with Young Children: Social and Emotional
Development Activities for Asperger’s, Autism, PDD and NLD.
Jessica Kingsley Publications, London.
Gutstein S. E., Burgess A. F. & Montfort K. (2007) Evaluation of
the relationship development intervention program. Autism
11, 397–411.
Haag G., Tordjman S., Duprat A., Urwand S., Jardin F.,
Cl
ement M. C., Cukierman A., Druon C., Du Ch^atellier A.
M., Tricaud J. & Dumont A. M. (2005) Psychodynamic
assessment of changes in children with autism under
psychoanalytic treatment. International Journal of Psycho-
analysis 86(Pt 2), 335–352.
Harcherik D. F., Cohen D. J., Ort S., Paul R., Shaywitz B. A.,
Volkmar F. R., Rothman S. L. & Leckman J. F. (1985)
Computed tomographic brain scanning in four
neuropsychiatric disorders of childhood. American Journal of
Psychiatry 142, 731–734.
Hart B. & Risley T. E. (1975) Incidental teaching of language in
preschool. Journal of Applied Behavior Analysis 8, 411–420.
Herbert J. D., Sharp I. R. & Gaudiano B. A. (2002) Separating
fact from fiction in the etiology and treatment of autism:
a scientific review of the evidence. Scientific Review of
Mental Health Practice. Spring-Summer Issue. 1. http://
www.srmhp.org/0101/index.html (accessed on 21 December
2012).
Holland J. G. & Skinner B. F. (1961) The Analysis of Behaviour: A
Program for Self-Instruction. McGraw Hill, Inc., New York.
Honig W. K. & Staddon J. E. R. (1977) Handbook of Operant
Behavior. Prentice Hall, Inc., New York, NY.
Horner R. H. (1994) Functional assessment: contributions and
future directions. Journal of Applied Behaviour Analysis 27,
401–404.
Howe D., Brandon M., Hingings D. & Schofield G. (1999)
Attachment Theory, Child Maltreatment and Family Support: A
Practice and Assessment Model. Lawrence Erlbaum &
Associates, New Jersey.
Howlin P., Hadwin J. & Baron-Cohen S. (1998) Teaching
Children with Autism to MindReading: Practical Guide for
Teachers and Parents. Wiley, Chichester, UK.
Irvine D. J., Horan M. D., Flint D. L., Kukuk S. E. & Hick T. L.
(1982) Evidence supporting comprehensive early childhood
education for disadvantaged children. Annals of the American
Academy of Political and Social Sciences 461, 74–80.
Itard M. E. (Jean) (1802) An historical account of the discovery
and education of a savage man: or, the first developments,
physical and moral, of the young savage caught in the woods
near Aveyron in the year 1798, London: Richard
Phillips (Google eBook). A2–152. https://google.com/books/
reader?id=E63cRcnV2hlC&printse=frontcover&output=reader
&authuser=0&hl=en&pg=GBS.PA10(accessed on 21 January
2013)
Jackson D. A., Symons R. H. & Berg P. (1972) Biochemical
method for inserting new genetic information into DNA of
Simian Virus 40: circular SV40 DNA containing lambda
phage genes and the galactose operon of Escherichia coli.
Proceedings of the National Academy of Sciences, USA 69,
2904–2909.
Jordan T. J., Grallo R., Deutsch M. & Deusch C. (1985) Long-
term effects of early enrichment: a 20-year perspective on
persistence and change. American Journal of Community
Psychology 13, 393–415.
Kaufman R. (1998–2008) Stop Trying to Turn Our Children Into
Robots The Autism Treatment Center of America.
© 2013 Blackwell Publishing Ltd, 26, 81–107

http://www.autismtreatmentcenter.org/contents/learn_more/
media_advisory-march08b.php (accessed 20 December 2012).
Kazdin A. E. (1982) The token economy a decade later. Journal
of Applied Behavior Analysis 15, 431–445.
Kazdin A. E. & Bootzin R. R. (1972) The token economy: an
evaluative review. Journal of Applied Behavior Analysis 5,
343–372.
Kleim J. A., Barbay S. & Nudo R. J. (1998) Functional
reorganization of the rat motor cortex following motor skill
learning. Journal of Neurophysiology 80, 3321–3325.
Kleim J. A., Barbay S., Cooper N. R., Hogg T. M., Reidel C. N.,
Remple M. S. & Nudo R. J. (2002) Motor learning-dependent
synaptogenesis is localized to functionally reorganized motor
cortex. Neurobiology of Learning and Memory 77, 63–77.
Koegel L. K., Koegel R. L., Harrower J. K. & Carter C. M. (1999)
Pivotal response intervention I: overview of approach. Journal
of the Association for Persons with Severe Handicaps 24, 174–185.
Krantz P. J. & McClannahan L. E. (1998) Social interaction skills
for children with autism: ascript-fading procedure for
beginning readers. Journal of Applied Behaviour Analysis 31,
191–202.
Krantz P. J., MacDuff M. T. & McClannahan L. E. (1993)
Programming participation in family activities for children
with autism: parents’ use of photographic activity schedules.
Journal of the Applied Behaviour Analysis 26, 137–138.
Langdell J. I. (1973) Childhood autism. California Medicine 118,
59–61.
Lawlor L. & Moulard V. (2011), “Henri Bergson”, The Stanford
Encyclopedia of Philosophy (Winter 2011 Edition), (ed. E. N.
Zalta), http://plato.stanford.edu/entries/bergson/ (accessed
on 1 March 2012).
Leigh D. (1955) John Haslam, MD: Apothecary to Bethlehem.
Journal of the History of Medicine and Allied Sciences 10, 17–44.
Liu X. Q., Paterson A. D., Szatmari P. & Autism Genome
Project Consortium (2008) Genome-wide linkage analyses of
quantitative and categorical autism subphenotypes. Biological
Psychiatry 64, 561–570.
Lord C. & McGee J. P. (2001) Educating young children with
autism. Committee on Educational Interventions for Children
with Autism. Division of Behavioral, Social Sciences and
Education, National Research Council. National Academies
Press, Inc., Washington DC.
Lord C., Rutter M., Goode S., Hemmsbergen J., Jordan H.,
Mawhood L. & Schopler E. (1989) Autism diagnostic
observaton schedule: a standardized observation of
communicative and social behavior. Journal of Autism and
Developmental Disorders 19, 185–212.
Løvaas O. I. (1987) Behavioral treatment and normal
educational and intellectual functioning in young autistic
children. Journal of Consulting and Clinical Psychology 55, 3–9.
Løvaas O. I. & Wright S. (2006) A reply to recent public critiques.
Journal of Early Intensive Behavioural Intervention 3, 221–229.
Lowe C. F., Richelle M., Blackman D. E. & Bradshaw C. M.
(1985) Behaviour Analysis and Contemporary Psychology.
Lawrence Erlbaum Associates, Hillside, NJ.
© 2013 Blackwell Publishing Ltd, 26, 81–107
Journal of Applied Research in Intellectual Disabilities 105
Magiati I., Charman T. & Howlin P. (2007) A two-year
prospective follow-up study of community-based early
intensive behavioural intervention and specialist nursery
provision for children with autism spectrum disorders.
Journal of Child Psychololgy and Psychiatry 48, 803–812.
Martin M. (1972) Behavior modification in the mental hospital:
assumptions and criticisms. Hospital and Community
Psychiatry 23, 287–289.
McEachin J. J., Smith T. & Løvaas O. I. (1993) Long-term
outcome for children with autism who received early
intensive behavioural treatment. American Journal on Mental
Retardation 97, 359–372.
McGee G. G., Almeida M. C., Sulzer-Azaroff B. & Feldman R.
S. (1992) Promoting reciprocal interactions via peer incidental
teaching. Journal of Applied Behavior Analysis 19, 147–157.
McPartland J. C., Reichow B. & Volkmar F. R. (2012) Sensitivity
and specificity of proposed DSM-5 diagnostic criteria for
autism spectrum disorder. Journal of American Academy of
Child and Adolescent Psychiatry 51, 368–383.
McWilliam R. A. (2010) Routines-Based Early Intervention.
Brookes Publishing Inc., Baltimore, MD.
Medical Research Council (2012) Achievements and Impact:
Measles, Copyright, MRC UK; http://www.mrc.ac.uk/
Achievementsimpact/Storiesofimpact/Measles/index.htm
(accessed 28 February 2012).
Mesibov G. B., Shea V. & Schopler E. (2005) The TEACCH
Approach to Autism Spectrum Disorders. Kluwer Academic/
Plenum Publishers Inc., New York.
Michael J. (1984) Verbal behavior. Journal of the Experimental
Analysis of Behavior 42, 363–376.
Miles J. H., Takahashi T. N., Bagby S., Sahota P. K., Vaslow D.
F., Wang C. H., Hillman R. E. & Farmer J. E. (2005)
Essential versus complex autism: definition of fundamental
prognostic subtypes. American Journal of Medical Genetics
135A, 171–180.
Montesorri M. (2006) The Secret of Childhood. Fides Publisher,
Notre Dame, IN.
MRC Medical Research Council (2012) Measles, http://www.
mrc.ac.uk/Achievementsimpact/Storiesofimpact/Measles/
index.htm) (accessed on 18 February 2012).
Mullis K. B. (1985) Porcess for amplifying nucleic acid
sequences. Patent application 791, 308 October 25, 1985;
Patent issued July 28, 1987. U.S. Patent Office, Washington,
DC.
Nikopoulos C. K. & Keenan M. (2004) Effects of video
modeling on social initiations by children with autism.
Journal of the Applied Behaviour Analysis 37, 93–96.
Norris S., Pare J.-R, & Starky S. (2006) Childhood autism in
Canada: some issues relating to behavioral intervention.
Available at: http://www.parl.gc.ca/information/library/
PRBpubs/prb0593-e.htm (accessed on 10 February 2013).
Nudo R. J., Milliken G. W., Jenkins W. M. & Merzenich M. M.
(1996) Use-dependent alterations of movement repre-
sentations in primary motor cortex of adult squirrel monkeys.
Journal of Neuroscience 16, 785–807.
106 Journal of Applied Research in Intellectual Disabilities
Oberman L. M., Hubbard E. M., McCleery J. P., Altschuler E.
L., Ramachandran V. S. & Pineda J. A. (2005) EEG evidence
for mirror neuron dysfunction in autism spectrum disorders.
Brain Research: Cognitive Brain Research 24, 190–198.
Orlando R. & Bijou S. W. (1960) Single and multiple schedules
of reinforcement in developmentally retarded children.
Journal of the Experimental Analysis of Behavior 3, 339–348.
Ozonoff S. & Cathcart K. (1988) Effectiveness of a home
program intervention for young children with autism. Journal
of Autism and Developmental Disorders 128, 25–32.
Partington J. (2006) The Assessment of Basic Language and
Learning Skills (Revised). The Behavior Analysts, Inc., Walnut
Creek, CA.
Piaget J. & Inhelder B. (1969) The Psychology of the Child. Basic
Books, Inc., New York, NY.
Pierce J. & Schreibman L. (1995) Increasing complex social
behaviors in children with autism: Effects of peer-
implemented pivotal response training. Journal of Applied
Behavior Analysis 28, 285–295.
Premack D. & Woodruff G. (1978) Does the chimpanzee have a
theory of mind? The Behavioural and Brain Sciences 1, 515–526.
Prior M. R., Tress B., Hoffman W. L. & Boldt D. (1984)
Computed tomographic study of children with classic autism.
Archives of Neurology 41, 482–484.
Promising Practices Network. (2009) Promising Practices Network
on Children, Families and Communities. Rand Corporation Inc.,
Santa Monica, CA. Available at: http://www.promising
practices.net/default.asp (accessed on 20 January 2013).
Remington B., Hastings R., Kovshoff H., degli Espinosa F., Jahr
E., Brown T., Alsford P., Lemaic M. & Ward N. (2007) Early
intensive behavioural intervention: outcomes for children
with autism and their parents after two years. American
Journal on Mental Retardation, 112, 418–438.
Rice C. (2009) Prevalence of Autism Spectrum Disorders—
Autism and Developmental Disabilities Monitoring Network,
United States, 2006. Morbidity and Mortality Weekly Report.
December 18, 2009/58(SS10);1–20, Centers for Disease Control
and Prevention, Atlanta, GA.
Rimland B. (1964) The etiology of infantile autism: the problem
of biological versus psychological causation. In: Infantile
Autism (B. Rimland), pp. 39–66. Appleton Century Crofts,
New York.
Ritvo E. R., Yuwiler A., Geller E., Ornitz E. M., Saeger K. &
Plotkin S. (1970) Increased blood serotonin and platelets in
early infantile autism. Archives of General Psychiatry, 23,
566–572.
Robins D., Fein D. & Barton M. (1999) The Modified Checklist for
Autism in Toddlers (CHAT). University of Connecticut, Storrs,
CT.
Rogers S. J., Ozonoff S. & Maslin-Cole C. (1993) Developmental
aspects of attachment behavior in young children with
pervasive developmental disorders. Journal of the American
Academy of Child & Adolescent Psychiatry 32, 1274–1282.
Rutter M. (2005a) Aetiology of autism: findings and questions.
Journal of Intellectual Disability Research 49(Pt 4), 231–238.
Rutter M. (2005b) Incidence of autism spectrum disorders:
changes over time and their meaning. Acta Paediatrica 94,
2–15.
Rutter M. (2011) Research review: child psychiatric diagnosis and
classification: concepts, findings, challenges and potential.
Journal of Child Psychology and Psychiatry 52, 647–660.
Saemundsen E., Magn
usson P., Sm
ari J. & Sigurdard
ottir S.
(2003) Autism diagnostic interview-revised and the childhood
autism rating scale: convergence and discrepancy in
diagnosing autism. Journal of Autism and Developmental
Disorders 33, 319–328.
Sallows G. O. & Graupner T. D. (2005) Intensive behavioural
treatment of children with autism: Four-year outcomes and
predictors. Journal of Mental Retardation and Developmental
Disabilities 110, 417–438.
Schoenstadt A. (2007) History of measles. eMedTV. © 2006-2012
Clinaero, Inc. (accessed on 2 March 2012).
Schopler E., Short A. & Mesibov G. (1989) Relation of
behavioural treatment to “normal functioning”: comment on
Løvaas. Journal of Consulting and Clinical Psychology 57, 162–164.
Schreibman L., Stahmer A. C. & Pierce K. (1996) Alternative
applications of pivotal response training: teaching symbolic
play and social interactions skills. In: Positive Behaviour
Support: Including People with Difficult Behaviour in the
Community (eds L. K. Koegel, R. L. Koegel & G. Dunlap), pp.
353–371. Paul H. Brookes, Inc., Baltimore, MD.
Schultz R. T. (2005) Developmental deficits in social perception
in autism: the role of the amygdala and fusiform face area.
International Journal of Developmental Neuroscience 23, 125–141.
Schultz R. T., Grelotti D. J., Klin A., Kleinman J., Van der Gaag
C. C., Marois R. & Skudlarski P. (2003) The role of the
fusiform face area in social cognition: implications for the
pathobiology of autism. Philosophical Transactions of the Royal
Society of London B Biological Sciences 358, 415–427.
Schwartz J. (1999) Cassandra’s Daughter: A History of
Psychoanalysis. Viking/Allen-Lane Publisher Inc., London,
UK, pp. 255.
Seguin E. (1866) Idiocy: And Its Treatment By The Physiological
Method, 2nd edn. William Wood & Co., New York.
Sharma S., Woolfson L. M. & Hunter S. C. (2012) Confusion
and inconsistency in diagnosis of Asperger syndrome: a
review of studies from 1981 to 2010. Autism 16, 465–486.
Sherer M., Pierce K. L., Paredes S., Kisacky K. L., Ingersoll B.
& Schreibman L. (2001) Enhancing conversation skills in
children with autism via video technology. Which is better,
“self” or “other” as a model?. Behaviour Modification, 25,
140–158.
Shonkoff J. P. & Meisels S. (eds) (2000) Handbook of Early
Childhood Intervention. Cambridge University Press,
Cambridge, UK.
Sigman M. & Ungerer J. A. (1984) Attachment behaviours in
autistic children. Journal of Autism and Developmental
Disorders. 14, 231–244.
Skinner B. F. (1938) Behaviour of Organisms. Appleton and
Company, New York.
© 2013 Blackwell Publishing Ltd, 26, 81–107

Skinner B. F. (1953) Science and Human Behavior. Macmillan and
Company Inc., New York.
Silver A. A. (1954) Diagnosis of the various syndromes
encountered in the retarded pre-adolescent child. Quarterly
Review of Pediatrics 9, 127.
Solomon R., Necheles J., Ferch C. & Bruckman D. (2007) Pilot
study of a parent-training program for young children with
autism: the PLAY Project Home Consultation program.
Autism 11, 205–224.
Spitz R. A. (1945) Hospitalism: an inquiry into the genesis of
psychiatric conditions in early childhood. Psychoanalytic Study
of the Child 1, 53–74.
Spradlin J. (1958) Effects of Reinforcement Schedules on Extinction
in Severely Mentally Retarded Children. PhD Dissertation,
Peabody College, Nashville, TN.
Squires J. & Bricker D. (2006) Activity-based Approach to
Developing Young Children’s Social Emotional Competence. Paul
H. Brookes, Baltimore.
Sroufe L. A. (1986) Appraisal: Bowlby’s contributions to
psychoanalytical theory and developmental psychology;
attachment; separation: loss. Journal of Child Psychology and
Psychiatry 27, 841–849.
Stafford M. W., Sundberg M. L. & Braam S. J. (1988) A
preliminary investigation of the consequences that define the
mand and tact. The Analysis of Verbal Behavior 8, 31–41.
Stone V. E. & Gerrans P. (2006) What’s domain specific about
theory of mind? Society for Neuroscience 1, 309–319.
Sugranyes G., Kyriakopoulos M., Corrigall R., Taylor E. &
Frangou S. (2011) Autism spectrum disorders and
schizophrenia: meta-analysis of the neural correlates of social
cognition. PLoS ONE 6, e25322.
Sundberg M. L. (2008) Verbal Behaviour Milestones Assessment and
Placement Program: The VB-MAPP. AVB Press, Concord, CA.
Sundberg M. L. & Partington J. W. (1998) Teaching Language to
Children with Autism or Other Developmental Disabilities.
Behaviour Analysts, Inc., Danville, CA.
Taube E., Uswatte G. & Pidikiti R. (1999) Constraint-induced
movement therapy: a new family of techniques with
application to physical rehabilitation- a clinical review.
Journal of Rehabilitation Research and Development 36, 237–251.
Thompson T. (1984) The examining magistrate for nature: a
retrospective review of Claude Bernard’s An Introduction to
the Study of Experimental Medicine. Journal of the
Experimental Analysis of Behaviour 41, 211–216.
Thompson T. (2005) Paul E. Meehl and B. F. Skinner: Autitaxia.
Autitypy and Autism. Behaviour and Philosophy 33, 101–131.
Thompson T. (2009) Autism and Prader-Willi syndrome:
research and clinical opportunities in neurodevelopmental
disabilities. In: Spectrum of Neurodevelopmental Disabilities (ed
B. Shapiro). Paul H. Brookes Publishing Co. Inc., Baltimore,
MD.
© 2013 Blackwell Publishing Ltd, 26, 81–107
View publication stats
Journal of Applied Research in Intellectual Disabilities 107
Thompson T. (2011) Individualized Intervention for Young Children
with Autism: Blending Discrete Trial and Naturalistic Approaches.
Paul H. Brookes, Inc., Baltimore.
Thompson T., Barsness L., Anderson C., Bohannan A., Burggraff
B. & Dropik P. (in press) Individualized intensive early
behavioural intervention for young children with autism:
predictors of type of treatment and outcomes. (under revision).
Thompson T. & Grabowski J. G. (1972) Behavior Modification of
the Mentally Retarded. Oxford University Press Inc., New
York, NY.
Thompson T. & Grabowski J. G. (1977) Behavior Modification of
the Mentally Retarded. 2nd edn. Oxford University Press Inc.,
New York, NY.
Tobias S. & Duffy T. M. (2009) Constructivist Instruction: Success
or Failure? Routledge, Inc., New York, NY.
NHS, United Kingdom. (2003) MMR the facts. NHS
Immunisation, Department of Health Publications. Available
at: http://www.dh.gov.uk/prod_consum_dh/groups/dh_
digitalassets/dh_105189.pdf (accessed on 21 January 2013).
Vailant G. E. (1962) John Haslam on early infantile autism.
American Journal of Psychiatry 119, 376.
Virkud Y. V., Todd R. D., Abbacchi A. M., Zhang Y. &
Constantino J. N. (2009) Familial aggregation of quantitative
autistic traits in multiplex versus simplex autism. American
Journal of Medical Genetics B Neuropsychiatric Genetics 150B,
328–334.
Vygotsky L. (1962) Thought and Language. Translated by E.
Hanfmann, G. Vakar & N. N. Minnic. The MIT Press Inc.,
Cambridge MA.
Wakefield A. J., Murch S. H., Anthony A., Linnell J., Casson D.
M., Malik M., Berelowitz M., Dhillon A. P., Thomson M. A.,
Harey P., Valentine A., Davies S. E. & Walker-Smith J. A.
(1998) Illeal-lymphoid-nodular hyperplasia, non-specific
colitis and pervasive developmental disorder in children. The
Lancet 351, 637–641.
Welsch v. Likins (1974) 373 F. Supp. 487 (D. Minn. 1974)
February 15, 1974.
Wetherby A. M. & Woods J. J. (2006) Early social interaction
project for children with autism spectrum disorders
beginning in the second year of life: a preliminary study.
Topics in Early Childhood Special Education 26, 67–82.
White K. & Casto G. (1985) An integrative review of early
intervention efficacy studies with at-risk children:
implications for the handicapped. Analysis and Intervention in
Developmental Disabilities 5, 7–31.
International Classification of Diseases (WHO) (2012) http://
www.who.int/classifications/icd/en/ (accessed on 25
February 2012).
Wing L., Gould J. & Gillberg C. (2011) Autism spectrum
disorders in the DSM-V: better or worse than the DSM-IV?
Research in Developmental Disabilities 32, 768–773.