INVITED COMMENT
Autism and Epistemology IV:
Does Autism Need a Theory of Mind?
Gene S. Fisch*
Department of Epidemiology and Health Promotion, NYU Colleges of Dentistry and Nursing, New York, New York
Manuscript Received: 9 January 2013; Manuscript Accepted: 2 June 2013
In their article, “Does the autistic child have a ‘theory of mind’?,”
Baron-Cohen et al. [1985] proposed a novel paradigm to explain
social impairment in children diagnosed as autistic (AD). Much
research has been undertaken since their article went to print.
The purpose of this commentary is to gauge whether Theory of
Mind (ToM)—or lack thereof—is a valid model for explaining
abnormal social behavior in children with AD. ToM is defined as
“the ability to impute mental states to oneself and to others” and
“the ability to make inferences about what other people believe to
be the case.” The source for their model was provided by an
article published earlier by Premack and Woodruff, “Does the
chimpanzee have a theory of mind?” Later research in chimpan-
zees did not support a ToM in primates. From the outset, ToM as
a neurocognitive model of autism has had many shortcomings—
methodological, logical, and empirical. Other ToM assumptions,
for example, its universality in all children in all cultures and
socioeconomic conditions, are not supported by data. The age at
which a ToM emerges, or events that presage a ToM, are too often
not corroborated. Recent studies of mirror neurons, their loca-
tion and interconnections in brain, their relationship to social
behavior and language, and the effect of lesions there on speech,
language and social behavior, strongly suggests that a neurobio-
logical as opposed to neurocognitive model of autism is a more
parsimonious explanation for the social and behavioral pheno-
types observed in autism. Ó 2013 Wiley Periodicals, Inc.
Key words: theory of mind; autism; cognition; mirror neurons;
mental states; validity
INTRODUCTION
In their seminal article, “Does the autistic child have a ‘theory of
mind’?” Baron-Cohen et al. [1985] proposed a novel paradigm to
explain a central element of social impairment of autism in chil-
dren. Specifically, the Theory of Mind (ToM), the cognitive ability
to impute beliefs to others, is lacking in children with autism. The
authors also claimed that a ToM is independent of intellectual
disability (ID) and its absence is specific to autism.
According to a PubMed search, since its publication in 1985,
there have been 486 articles published on ToM with terms related to
autism and ID in the title or abstract. Given the many articles
published on the topic, and controversies surrounding its legitima-
cy and utility, I thought it an important area to consider for
Ó 2013 Wiley Periodicals, Inc.
How to Cite this Article:
Fisch GS. 2013. Autism and epistemology
IV: Does autism need a theory of mind?
Am J Med Genet Part A 161A:2464–2480.
researchers and clinicians who may have only a passing familiarity
with the matter. In this Commentary, I shall provide a brief
overview of the historical antecedents to the ToM, the possible
philosophical and epistemological bases for a ToM, a review of
studies which examine the evidence for and against its claims, with a
specific focus of ToM in autism; and, finally, its merits as a useful
scientific endeavor in autism research.
THE BASIS FOR THEORY OF MIND
ToM has its roots in Piagetian developmental psychology, although
the linguists, Noam Chomsky and Paul Grice, also played signifi-
cant roles historically regarding the relationship between language
and ToM. As with many other theories, Piaget’s theory of
child development reflected the spirit of its times. During the
early-to-mid 20th century, pediatricians assumed that behavior
patterns in infants were outcomes of neurodevelopmental process-
es that followed an orderly sequence—maturation [Gesell and
Amatruda, 1941; McGraw, 1943]. Piaget was not trained as a
pediatrician, nor did not view himself as a child psychologist;
rather, as a genetic epistemologist interested primarily in the
conceptual development of scientific knowledge [cf. Vonèche
and Vidal, 1985; p. 137], not children. Nonetheless, his theory of
child development—the central themes of which are that children’s
cognitive abilities are innate, emerge at specific ages, appear in four
major, distinct, sequentially invariant stages—is similar to the
Conflict of interest: none.


Correspondence to:
Gene S. Fisch, Ph.D., Department of Epidemiology and Health
Promotion, NYU Colleges of Dentistry and Nursing, 250 Park Ave. S.,
6th fl., New York, NY 10003.
E-mail: gene.fisch@nyu.edu
Article first published online in Wiley Online Library
(wileyonlinelibrary.com): 16 August 2013
DOI 10.1002/ajmg.a.36135
2464
FISCH
notions of children’s growth and development among pediatricians
of that period. Even so, the mechanics of Piaget’s theory, his
definitions of terms, and, in particular, the emergence of sequen-
tially invariant stages at specific ages, have not been sufficiently well-
validated empirically. On the other hand, Piaget did not consider
empirical verification or falsification of his theory a problem, since
“brute facts are misleading.” Piaget’s concept of theory and its
construction is generally at odds with modern scientific thought, is
internally inconsistent, his terminology often nebulous and
imprecise.
Like theories of child development, theories of autism epitomize
their epochs. From Bruno Bettelheim’s “refrigerator parents” of the
psychoanalytic 1950s, to the neurobehavioral dysfunction of the
1970s and 1980s, to the neurocognitive disorder currently in vogue,
the reputed etiology of autism has changed markedly since Kanner’s
time. In their article, Baron-Cohen et al. [1985] argued that deficits
in social skills experienced by children with autism are derived from
an inability to conceive of mental states in others. As Baron-Cohen
et al. stated, the precedent for this statement, ToM, was expounded
in an article published earlier by Premack and Woodruff [1978],
“Does the chimpanzee have a theory of mind?” ToM is defined as
“the ability to impute mental states to oneself and to others” and
“the ability to make inferences about what other people believe to be
the case” [Baron-Cohen et al., 1985]. Premack and Woodruff
[1978] stated that ToM is a well-founded ability in humans, and
argue that chimpanzees are also endowed with such ability, one not
very different from humans. Their study of chimpanzees was
prompted by Köhler’s [1925] classic work, in which he showed
that chimpanzees could use simple tools to solve problems. In
Köhler’s time, the field of psychology had already divided into two
separate camps: one which followed the principles of contiguity and
associationism (behaviorism); the other, which continued to in-
corporate concepts of mind and consciousness (cognition) in
animal behavior as articulated by Charles Darwin a half century
earlier. (A more detailed historical account can be found in Fisch
[2007].)
Premack and Woodruff [1978] attempted to demonstrate
animal cognition empirically, not by directly observing the mind
but, by utilizing ToM, to make predictions of behavior. The single
subject of their study, a 14-year-old female chimpanzee named
Sarah, was shown videotapes of photographs representing solutions
to each of four problems, after which she was a pair of alternative
solutions to each of the problems and encouraged to select one or
the other. According to Premack and Woodruff, if a ToM exists in
chimpanzees, she would choose the one which provided the correct
solution to each problem. She chose correctly on all occasions.
Premack and Woodruff interpreted their findings, arguing at length
against any form of associationism (read behaviorism) that might
have produced the outcome, and in favor of ToM (read cognition).
The study was published in The Brain and Behavioral Sciences
(TBBS), which invited commentaries to their target article. One
of the commentaries, by Savage-Rumbaugh et al. [1978], observed
that, among their concerns, there was no evidence other than
anecdotal that Sarah actually looked at the videotapes, perceived
the choice as a solution, or understood the features of the problems
and their respective solutions. To resolve these issues, Savage-
Rumbaugh et al. tested two of their own chimpanzees, presenting
2465
them with pairs of objects needed to work keyboard-related tasks,
only one of which was appropriate. Their two chimps also per-
formed extremely well, without having been presented with any
formal problem to be solved. Based on their findings, these authors
doubted that the conclusions drawn by Premack and Woodruff
were justifiable. In another commentary, Beck [1978] argued that
ToM was not a logical requirement for the ability to predict
behavior in others. Similarly, Burge [1978] questioned whether
the experiments as depicted constitute a rationale to believe that
Premack and Woodruff actually had a valid theory of mental states,
since a simpler explanation could be provided without imputing
ToM to the chimp. In a later study of ToM in chimpanzees, Povinelli
and Eddy [1996] found that chimps would gesture for food from a
human even when the human was blindfolded or had his head
covered, thereby indicating that the chimps had no concept of visual
perception in others. In his target article, Heyes [1978] surveyed
studies of imitation, socialization, self-recognition, and deception,
among other “mentalizing” behaviors in which nonhuman pri-
mates were examined, and found in each instance that was inter-
preted as a function of ToM, alternate behavioral explanations were
more parsimonious. As a result, the ability of chimpanzees to
conceive of mental states in others was deemed questionable.
Subsequent studies of chimpanzees by Woodruff and Premack
involved a different aspect of ToM, the nature and understanding
of false beliefs (FBs). Wimmer and Perner [1983], who developed
the notion of “wrong belief,” now referred to as FB, sought to
determine at what age children correctly identify the location of an
object which has been moved from one location to another. The
FB task, and its many variants, became for ToM advocates the
crucial test the evidence from which confirmed their theory. As
Gallagher [2004] noted, experiments that employ the FB task
illustrate both strengths and weaknesses of ToM, as will be made
clear below.
In their study, Kaminski et al. [2008] developed a novel method
by which to test the concept of FB in eight chimpanzees, 20 3-year-
old children, and 20 6-year-old children. Their study design was
based on the prototype developed by Wimmer and Perner [1983],
in which an object is placed in Box A by Person 1. Person 1 goes away
and Person 2 comes forward. Person 2 takes the object from Box A
and places it in Box B. Person 2 goes away and Person 1 returns.
Question for the study participant: In which box does Person 1 look
for the object? According to theory, a participant with a functional
ToM would say Person 1 will look in Box A, a FB. Someone less than
4 years of age, or with a dysfunctional ToM, would say Box B. It
should be remarked, as did Gallagher [2004], that it is not obvious
that an observation by a third person—in this instance, the partici-
pant in the study—best depicts the participant’s ability to under-
stand another individual without any form of interaction with that
other individual.
The Kaminski et al. [2008] study design was a simpler variant of
the FB task. Two subjects would face each other from behind a glass
partition and on opposite sides of a table. Subjects were trained to
take turns selecting buckets from the table and removing its
contents. One subject must select one of three buckets either before
or after the other subject has made a selection. There were rewards in
some buckets, but the buckets were opaque, so that neither subject
could know in advance what the other subject had chosen. In the FB
2466
condition, the first subject watches the experimenter appear to place
a reward in one bucket, but actually places it in another. The first
subject then must “predict” the second subject’s selection. Kamin-
ski et al. [2008] found that 6-year-old children were able to
demonstrate correctly FB attribution, but chimpanzees were not.
In another ToM test 30 years earlier, Premack and Woodruff [1979]
attempted to demonstrate FB in chimpanzees by teaching their
animals to deceive a conspecific. Premack and Woodruff were only
partly successful, teaching deceptive pointing to two of four chimps,
and only after 5 months of intensive training. In a recent review of
the literature, Call and Tomasello [2008] reported that, while
chimpanzees may understand goals and intentions of others, there
is no experimental evidence to indicate that chimps have any
conception of FB.
In his commentary, Burghardt [1978] quoted the early 20th
century animal experimentalist, Margaret Washburn, as saying:
“Knowledge regarding the animal mind, like the knowledge of
human minds other than our own, must come by way of inference
from behavior. Two fundamental questions then confront the com-
parative psychologist. First, by what method shall he [sic] find out
howtheanimal behaves?Second, howshallhe interpretthe conscious
aspect of that behavior?” In a similar vein, Penn and Povinelli [2007]
suggested that, instead of arguing over equivocal experimental
findings, researchers should focus on the definition of and evidence
for ToM. These arguments are analogous to those posed to the
inferences drawn by Piaget in his theory of stages in child
development.
To summarize: The original article by Baron-Cohen et al. [1985]
on ToM as an explanation of social impairment in autistic children
attributes their model to an earlier precedent set by Premack and
Woodruff [1978], the latter of whom claimed to ascertain ToM in
chimpanzees. Results and interpretation of the findings from
Premack and Woodruff, as well as subsequent research on ToM
in monkeys, demonstrate a lack of convincing evidence for same,
casting doubt thereby as to whether inferences based on a ToM as
articulated by Premack and Woodruff have internal validity vis-à-
vis nonhuman primates. Lack of internal validity suggests that there
may well be problems establishing external validity for humans with
autism, as we shall see shortly.
FOUNDATIONS OF A THEORY OF MIND IN AUTISM
The cognitive-theoretical foundations of ToM as related to autism
are rooted in Leslie [1987]. According to Leslie [1987], the ability to
develop an internal representation, to “mentalize,” is inherent in
humans and can be identified early in infancy in the form of
pretense or pretend play. Pretend play develops from about age
2 years and becomes increasingly elaborate as children become
older, using fewer real objects as symbols, and in story sequences
that become progressively more complex. Pretend play materializes
from a “decoupling” from the real world to an imaginary (repre-
sentational) one, “acting as if” something is true when in fact it is
not [Leslie, 1987]. Moreover, the pretender knows the difference.
For Leslie, the most important aspect is not so much the develop-
ment of ToM, but the “ability to characterize and manipulate [the
mind’s] attitudes to information. In short, pretense is an early
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
manifestation of what [Premack and Woodruff] called theory of
mind.” [Leslie, 1987, p. 415]
Mental states such as pretense have three major properties. First,
mental propositions need not be logically true (“My sister thinks I am
Australian”). Second, mental propositions need not refer to the
actual existence of the referent (“This is a picture of my unicorn”).
Third, pretend representations are not accurate representations of
the natural environment but representations of representations, that
is,second-orderrepresentations,or meta-representations[Pylyshyn,
1978]. To illustrate meta-representation using Leslie’s [Leslie, 1987]
example: If a child pretends that a banana is a telephone, the child
needs to be able to demonstrate how he/she is representing how the
real banana is used to represent the non-existent telephone. Accord-
ing to Leslie, pretend play in children is necessarily constructed from
these properties, and their existence is a precursor of the child’s
typical or “folk” ToM. This ability initially allows the child to impute
mental states in oneself, then later in others, and ultimately to
anticipate future behavior in others. This constitutes what Leslie
[1987] and Premack and Woodruff [1978] refer to as a ToM.
How does this relate to autism? Autistic disorder (AD) and
related pervasive developmental disabilities (PDD) are defined
broadly by DSM-IV-TR [American Psychiatric Association,
2000] as neurodevelopmental disorders involving impaired func-
tion in three domains: communication, socialization, and restricted
interests or stereotyped behavior. The absence of pretend or
symbolic play has been noted frequently among children with
autism, but not among children whose only dysfunction may be
ID. In their study, Baron-Cohen et al. [1985] employed the previ-
ously described Wimmer and Perner [1983] FB task to determine if
children diagnosed as AD with ID exhibited ToM deficits compared
to same-aged children with Down syndrome (DS) and ID (Baron-
Cohen [1995] would later state that ToM was the sine qua non of
standard FB tasks.). Mean IQ of the children with autism was
significantly higher than those with DS (82 vs. 64). As for perfor-
mance on the FB task, only 4/20 (20%) of children with AD passed
the test, whereas 12/14 (86%) children with DS did. The authors
thus concluded that ToM deficits are independent of ID and specific
to AD.
EARLY REBUTTAL AND REJOINDER
Challenges to the results obtained by Baron-Cohen et al. [1985] first
appeared in an article by de Gelder [1987]. de Gelder focused on
three aspects of the study: the methodology itself; the verbal
interaction between experimenters and participants; and, the attri-
bution of FB. First, knowing that children with AD do not pretend
play, then embedding the FB task in a pretend play protocol, finally
testing for correctness in the FB task, is a flawed experimental
design. The logic of the argument, as might be posited by Leslie
[1987], would proceed as follows:
 If the child exhibits pretend play, then the child has a ToM.
 The child does not pretend play.
 Therefore, the child does not have a ToM.
This is a logically and scientifically invalid proposition (denying
the antecedent). Second, the FB task is part of a verbal exchange
FISCH
between experimenter and participant in which children with AD
already have a linguistic disadvantage pragmatically, and may not
completely understand the task expected of them, despite their
vocabulary. Third, and somewhat related to the first: If children
with AD did not have a ToM, they could not suitably partake in the
conversation and the experiment. Since children with AD could
participate in answering some questions correctly, they must
therefore have a ToM.
In their reply, Leslie and Frith [1987] contended that they could
find only three problems with de Gelder’s argument. First, de Gelder
did not properly understand meta-representation in ToM. On the
contrary, Boucher [1989] observed that the concept of meta-
representation had not been completely well-formulated at the
time. As Leekam and Perner [1991] pointed out, Leslie’s [1987]
interpretation of meta-representation was not the same as Pyly-
shyn’s [1978]. Second, Leslie and Frith [1987] noted that the verbal
abilities of children with AD were higher than those with DS, so
language should not be an issue. On the other hand, as Boucher
[1989] also indicated, language skills evaluated by Baron-Cohen
et al. [1985] were assessed using the British Picture Vocabulary
Scale, a vocabulary comprehension test; whereas, ToM experiments
assume a grammatical proficiency unrelated to vocabulary com-
prehension that is likely beyond the ability of children with AD.
Finally, Leslie and Frith [1987] argue there was no evidence in the
literature to suggest that a lack of ToM would prohibit participation
in any conversation. This is a peculiar response given that one could
argue analogously that a person with no legs could enter a foot race
since no one without legs had been prohibited from participating in
such a race before. Nevertheless, Baron-Cohen [1988] suggested
that de Gelder’s conjecture, which is based on a model of conver-
sation developed by Grice [1975], should be examined. In addition,
he acknowledged that de Gelder’s claim may be correct.
Boucher [1989] also raised separate concerns about the Baron-
Cohen et al. [1985] study, also at the epistemological level, and
having to do with the proper definition of meta-representation and
the scope (broad or narrow) of ToM. If, as Leslie [1987] stated, the
absence of pretend play (meta-representation) is the behavioral
marker for an impaired ToM, then, although it is not clear why,
functional (appropriate) play should be not be impaired in children
with AD compared to children with ID only. However, Lewis and
Boucher [1988] found that, in a free play situation, functional play
was as impaired as pretend play in children with AD, and occurred
at significantly lower levels than among control subjects. Interest-
ingly, they also found that, in an elicited play situation, children
with AD could, in fact, generate pretend play [Boucher and Lewis,
1989]. Consequently, Boucher [1989] suggested that meta-repre-
sentation in autism is probably a secondary manifestation of
impairment that occurs initially at the biological level, and therefore
is not the primary deficit in autism. If, on the other hand, an
impaired ToM is to be considered the primary deficit in autism,
then it needs to explain how other aspects of the disorder, for
example, repetitive behaviors, are a function of impaired meta-
representation.
Baron-Cohen [1989a] took issue with Boucher [1989], suggest-
ing alternate interpretations of her results, and adding that his more
recent findings show children with AD failed three types of FB tasks,
including the Mental-Physical (MP) test [Baron-Cohen, 1989b].
2467
The MP distinction consisted of a child’s comprehension of mental
phenomena, for example, dreams, and physical phenomena, for
example, food. He found only 4/13 (24%) children with AD passed
the MP test, while a significantly higher proportion, 11/16 (69%), of
children with ID passed the same test. Baron-Cohen [1989b] also
administered a third variant of the FB task: the Appearance-Reality
(AR) paradigm. An example of an AR task might be as follows: A
child is given an object, such as a sponge, but made to look like
something else, such as a candy bar. The child is then asked: what is it
(appearance vs. reality)? In both of Baron-Cohen’s studies, 20–35%
of children with AD passed any of these three ToM tests, while 16–
30% of children with ID only fail them.
In contrast to Baron-Cohen’s results, other researchers employ-
ing similar FB tasks found much higher success rates among
children with AD, and lower rates of success among children
with ID only. In their study, Prior et al. [1990] found 60% of his
participants with AD passed the FB task. Grant et al. [2001] assessed
22 children with AD, ages 7–18 years, with four standard FB tasks,
and found 12/22 [56%] were able to complete all tests successfully.
Dahlgren and Trillingsgaard [1996] examined 20 high functioning
children with AD, 20 with Asperger syndrome—both groups of
which had mean IQ scores in the normal range—and 20 TD
children, ages 6–151/2 years, and tested them with first-order and
second-order FB tasks. Nearly all children with AD and Asperger
passed the first order FB task, and 60% of each of these two groups
passed the second-order FB task. Conversely, Zelazo et al. [1996]
examined 12 adolescents and adults with DS, 16–31 years, who were
severely ID, and found that they had marked difficulty performing
the FB and AR tasks. In their meta-analysis of 24 separate studies
that administered a variety of ToM tasks to TD children, children
with AD, or children with ID, Yirmiya et al. [1998] reported that
there were studies in which children with AD or ID only had
impaired ToM abilities. They also noted that, when known, the
disorder’s etiology was a significant moderating factor. Yirmiya
et al. [1998] thus concluded that ToM impairment severity, rather
than impairment in and of itself, was associated with AD. In
acknowledging these anomalies earlier on, Baron-Cohen [1989b]
retreated from his original assertions and proposed that ToM
deficits in children with AD may not be completely obliterated,
but may result from a more specific severe developmental delay
unrelated to general developmental delay.
To examine the hypothesis of specific developmental delay,
Baron-Cohen [1989c] conducted a follow-up study in which
children with AD who passed his first FB test were then adminis-
tered another, more complicated (“second-order”) test of FB.
Second-order FB tests are typically of the form, “Jane believes
that John believes that …” None of these children passed, from
which Baron-Cohen [1989c] concluded that AD may be a case of
specific developmental delay. This concession is markedly different
from the original supposition, that children with AD lack a ToM.
Burack [1992] presented an alternate interpretation of the results
obtained by Baron-Cohen. He suggested that the behaviors ob-
served by Baron-Cohen [1989c] could have been developmentally
deviant, not delayed, to which Baron-Cohen [1992] replied that
there was evidence for both delay and deviance. He referred to the
theory promulgated by Fodor [1983], that there is an innate
“module” for development, comparable to the innate module
2468
posited by Leslie [1987]. Baron-Cohen [1992] proposed a modified
ToM in which the developmental module could have two
“switches”: one which would, if turned off, elicit developmental
delay; the other, which if turned off, would produce deviant
behavior. Obviously, these additions make the innate module
ToM model more complex than originally conceived. Then again,
the innate module ToM is but one of three types of ToM theories, to
which I will return later.
An alternate approach to how FB tasks could be successfully
completed was pursued by Sharrock and Coulter [2004]. They
thought that the ability to respond correctly to FB tasks may be a
function primarily of acquired language. To test this hypothesis in
children with AD, Perner et al. [1989] examined 10 children with
AD and 12 MA-matched children with speech-language im-
pairment (SLI), and found that children with SLI performed
significantly better on the FB task than children with AD. Perner
et al. concluded that language impairment and, therefore, language
ability was unrelated to ToM. A decade later, Astington and Jenkins
[1999] examined 59 TD children, mean age 3 years, at three
different time points, to determine if language competence pre-
dicted ToM development; or, whether ToM development predicted
language competence. Their results show that language proficiency
predicted ToM development, not the other way round.
Although Perner et al. [1989] matched children according to
MA, mean chronological age (CA) in the SLI group was almost 9
years, while mean CA among children with AD was significantly
older—15 years. Given the “Verbal MA” presented in their Table 2,
children with AD likely tested in the mild-to-moderate ID range;
whereas, children with SLI likely tested significantly higher, in the
borderline-to-low normal range. Despite this marked difference in
intellectual levels, Perner et al. [1989] concluded that poor perfor-
mance was not a function of general ID.
Miller [2001] noted that children with SLI lag in their ability to
perform on FB tasks compared to same-aged typically developing
(TD) children. Considering the mean CA of children in the SLI
group in Perner et al. [1989] was 9 years, they probably were old
enough to have acquired sufficient language skills to perform as well
as younger, TD children. To examine the effect of CA on SLI, Miller
[2001] examined three younger age cohorts diagnosed with SLI,
whose ages ranged from 41/2 to 7 years, and compared them to TD
children with limited language comprehension, and to TD children
without limited language skills. Miller [2001] found that children
from both the SLI group and the limited language group had
difficulty in passing the FB tests administered to them, but TD
children performed quite well and significantly better than either of
the two language-impaired groups. Earlier, Sparrevohn and Howie
[1995] examined FB in children whose CA was comparable to those
recruited for the Perner et al. [1989] study. Sparrevohn and Howie
[1995] administered five FB tests of increasing difficulty, the first of
which examined “inferred belief.” Inferred belief is a FB-like task
that presages FB developmentally in TD children. The fifth task was
the most complex verbally, a “second-order” FB test (“Jane believes
that John believes that …”). The tests were administered to two
groups of children with AD: one with low verbal ability, the second
with high verbal skills. Sparrevohn and Howie [1995] found that
100% of participants in each group passed the inferred FB task
correctly; but, as tasks grew increasingly complex, the numbers
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
from each group who passed diminished. The most difficult
(second-order) FB task was passed by only 1/15 (7%) from the
low ability group, while 8/15 (53%) passed from the high ability
group. Contrary to Baron-Cohen [1989c], these researchers con-
cluded that acquiring ToM and its related skills follows a general
developmental sequence in children with AD as it does with TD
children. Moreover, since verbal ability affects performance on FB
tasks, linguistic proficiency is a necessary prerequisite to satisfactory
performance on ToM tasks. Indeed, Gernsbacher and Frymiare
[2005] reported findings that also show successful performance on
ToM tasks are a function of linguistic ability. They noted further
that children with AD often fail ToM tasks because of a qualitative
impairment in communication, one of the three criteria deemed
essential for a diagnosis of AD. In effect, failure on ToM tasks among
children with AD begs the question.
Linguistic ability of another sort has also been shown to affect
facility in completing FB tasks successfully—deafness. Peterson and
Siegal [1999] examined three groups of deaf children (severely and
profoundly native deaf signers, oral deaf who had grown up with
spoken language, and severely and profoundly deaf signers from
hearing homes) along with TD children and children with AD.
Verbal abilities and ages of the three groups of deaf children were
not significantly different. Children were tested using three stan-
dard FB tasks. These researchers found that native signers per-
formed no worse than TD children, but signing deaf children and
children with autism performed significantly worse. Interestingly,
children with autism passed 50–68% of the three FB tasks. Peterson
and Siegal [1999] suggested that there may be a neurobiological
basis as well as a cultural deficit that could account for the failures in
FB tasks among deaf children.
To summarize: As related to autism, ToM has come under attack
from several fronts. First, as a methodology which embeds pretend
play in an FB task, it begs the question since children with AD do not
pretend play spontaneously. Second, the linguistic sophistication
needed to provide a correct response to the FB task is beyond the
pragmatic language skills of most children with AD. Third, without a
ToM, how could such a child possibly participate in a ToM experi-
ment, a problem related to the first point. Baron-Cohen, Leslie, and
Frith countered these concerns, first by suggesting that their detrac-
tors did not understand the concept of meta-representation suffi-
ciently well, although meta-representation was not only not a
particularly well-formulated construct at the time, but there existed
different definitions of same. Second, despite its reputation as the
“litmus test” for a ToM, the FB experiment contains serious logical
and design flaws. Baron-Cohen, Leslie, and Frith also tried to show
that linguistic ability was unrelated to ToM, but researchers have
demonstrated otherwise, noting a high proportion of failures on
ToM-related tasks among speech-language impaired and deaf chil-
dren. The matter of whether one needed a ToM to participate in a
ToM experiment remained unresolved, although this too seems to
beg the question.
BASIC ASSUMPTIONS FOR THEORY OF MIND
As stated earlier, the argument for applying ToM—or lack thereof
—to autism is based on the thesis presented by Leslie [1987], in
which he asserted the following: (1) ToM is innate; (2) it is presaged
FISCH
by pretend play which appears at age 18–24 months; and (3) that the
“decoupling” of mental representations from real world phenom-
ena—forming meta-representations (the banana representing the
absent telephone)—is the mechanism by which ToM emerges.
Hobson [1990] took issue with each of Leslie’s premises. First,
infants’ understanding of other people’s minds comes about from
their reciprocal social relations with other humans, that is, it is not
innate. Second, this knowledge appears much earlier in the infant’s
development—9 months as opposed to 18 months. As these
phenomena relate to autism, Leslie postulated that children with
AD inherently lack a ToM; whereas, Hobson [1990] would argue
that, in Kanner’s original description [Kanner, 1943], they lack the
inborn biological ability to form reciprocal affective relationships
with others. Klin et al. [1992] tested these two hypotheses by
examining 58 children, 29 of whom were diagnosed with AD
and 29 were diagnosed with ID only. Mean age in both groups
was about 4 years. Klin et al. found that social deficits in AD
included adaptive behaviors that were fundamental and emerged
early in infancy, and are usually present in children at an age prior to
when putative meta-representational abilities appear, as Hobson
[1990] noted. Klin et al. concluded that their findings were consis-
tent with Kanner’s conjecture, not Leslie’s.
In their reply to Hobson [1990], Leslie and Frith [1990] quoted
him as saying “Leslie’s nondevelopmental, nonsocial, and restric-
tively cognitive account (p. 114) … (a)ll three of these epithets are
inappropriate” [Leslie and Frith, 1990, p. 122]. In fact, no such
remark was made by Hobson on p.114. In comparing Kanner’s view
of autism to Leslie’s ToM, what Hobson did say was that Kanner’s
“account seems to offer a more coherent view of impairments in
symbolic play and social understanding among autistic … children
than does Leslie’s [1987] nondevelopmental, essentially nonsocial
explanation” [Hobson, 1990; p. 119]. Leslie and Frith [1990]
counter Hobson’s “nondevelopmental” remark by stating that
all theories of development are, at their core, concerned with innate
features which unfold as the child ages. This is certainly true of
Piaget’s theory, but not necessarily that of Albert Bandura, or
Dollard and Miller, or Vygotsky for that matter, for whom the
interbehavioral, cultural, social, and linguistic factors affecting
child development were of greater concern. Leslie and Frith
[1990] argued further that ToM could hardly be considered non-
social, since pretending is a special case of understanding pretense
in others. Sadly, Leslie and Frith [1990] never demonstrate how
pretend play relates to social understanding, nor do they provide
empirical evidence to support their conjecture about understand-
ing pretense in others.
Other researchers who did examine pretense in children could
not establish those presumed deficits among children with AD.
Jarrold et al. [2010] examined true and false pretense in 34 children
with AD, ages 10–17 years, compared to 37 TD children, 3–5 years.
True and false pretense tasks are similar to the Wimmer and Perner
[1983] FB tasks, but in Jarrold et al. [2010], involved the use of red or
green paint as the object of belief (cf. Jarrold et al. [2010], for a more
complete description). Among children with AD, 21/34 (62%)
passed the FB tasks presented, while 17/37 (46%) of TD children
passed. Those who passed had significantly higher verbal MA, in
both the AD and TD groups, compared to those who failed. Both
TD and AD groups performed significantly better on true pretense
2469
tasks compared to false pretense tasks. Previously, Jarrold et al.
[1994] had examined pretend play in three groups: children with
AD; children with learning disabilities; or TD children. These
researchers found no significant differences among the three groups
regarding their success on the pretend play tasks presented, nor did
they find impairment in the ability to comprehend pretense by
children with AD. Bloom and German [2000] also cite several
studies in which children younger than 2 years are able to initiate
pretend play and understand pretense in others.
Social development has also been shown to materialize prior to
the age at which pretending appears, as Hobson [1990] noted. In his
review of social behavior in children with autism, Volkmar [2011]
reported that newborns are more attentive to face-like movements
than inanimate objects. And, at 4–5 months of age, infants can
detect changes in gaze direction by others. Carpenter et al. [1998]
examined social cognition via shared (joint) attention and gaze-
following tasks in 24 infants, 9–15 months old, and found the
number of infants passing attention-following, point-following,
and gaze-following tests increased from age 9 months to age 15
months. Language learning and development, which begins
with infants’ prelinguistic babbling and vocalizations, can be
modified by social feedback from their caregivers [Goldstein and
Schwade, 2008]. On the other hand, children with AD have
difficulties recognizing faces and identifying facial expressions,
and have difficulty using gaze in activities that involve joint atten-
tion. Osterling and Dawson [1994] examined videotapes of
22 infants less than 1 year, 11 who were later diagnosed with
autism, and 11 TD children. Osterling and Dawson found infants
subsequently diagnosed with AD displayed significantly fewer
social and joint attention behaviors and significantly more autistic
symptoms.
Another cornerstone of Leslie’s [1987] thesis is that the mecha-
nism that permits a ToM to emerge is contained in an innate
module. With age, the child reaches a distinct, inborn develop-
mental stage at which point he/she is able to marshal a “folk
psychology” to create a ToM. By folk psychology is meant a
commonsense psychology that typically embraces concepts such
as “belief,” “desire,” “fear,” “hope,” and “intent.” On the other
hand, there are those like Perner [1991] who argue that, at a certain
age, children begin to cultivate theories about themselves and
others, in order to better understand themselves and others. This
theory development in children parallels theory development in
science and is analogous to the genetic epistemology posited by Jean
Piaget [Lillard, 1998b]. The difference in the set of assumptions
made by Leslie compared to those by Perner indicates that there is
more than one ToM, which we shall now consider.
In his review of the field, Flavell [1999] noted that three major
ToMs have been proposed. One model is that proposed by Leslie, in
which an innate mechanism or module exists in brain, and that a
ToM develops in concert with neurological maturation. The mod-
ule contains three mechanisms: a Theory of Body mechanism
(ToBM) and two Theory of Mind mechanisms (ToMM1 and
ToMM2). The ToBM develops in the first year of life and allows
the neonate to explore the environment. ToMM1 comes into being
at the end of the first year, allowing the infant to relate to other
people and things. ToMM2 develops in year 2, and allows the
toddler to draw inferences about other individuals, what Flavell
2470
[1999] referred to as propositional attitudes, for example, pretend-
ing, believing, desiring, imagining.
The second model, put forth by Perner [1991], is referred to as
“Theory–Theory.” That is, our knowledge of other’s minds comes
about from how we “frame” our daily experience and interactions
into a ToM. Knowledge of other’s minds consists of three essential
elements: First, it must be specific to a particular domain of
information and no other; second, the notion of cause and effect
is specific to the domain in question; and third, this knowledge is
part of a network of related concepts and beliefs. A third major
ToM, Simulation Theory, assumes that an influential role is played
by experience. By way of repetition, children simulate what they
would think if they were in someone else’s place. However, it has
been Leslie’s ToM module and Perner’s Theory–Theory that have
monopolized studies of ToM in autism, and it is these that will be
examined in greater detail.
According to Astington and Dack [2008], Leslie’s innate modu-
larity ToM has two major features: First, it is universal among all
humans; and second, it is not subject to modification based on
interactions with the environment. Alterations in the ToM results
from the individual’s maturation, not experience.
The concept of an innate module in brain implies there is some
localization of function or neural network the specific purpose of
which is to produce a ToM. However, Stone and Gerrans [2006]
note that, although certain neural substrates may be necessary to
produce behavior, it does not therefore imply that that substrate is
specific to a ToM. (Impaired performance on FB tasks will be
revisited in a later section.) For example, Brüne and Brüne-Cohrs
[2006] cite several studies in which patients with brain lesions not
present in early development demonstrated impaired perform-
ances on FB tasks as adults. However, these lesions were not
localized to any one area in brain but were found in many different
regions—left-hemisphere, frontal cortex, left amygdala, and pre-
frontal cortex. Stone and Gerrans [2006] also found that individuals
with damaged orbitofrontal cortices make impaired responses to
ToM tasks. Stone and Gerrans proposed two model systems: One
which processes sensory information via domain-specific input
systems—visual, auditory, etc.—which includes a ToM module
to draw inferences about the physical world (their Fig. 1); and a
second model identical to the first, except that it does not
include the ToM module (their Fig. 2). In discussing both models,
Stone and Gerrans [2006] indicate how a ToM module is not
needed to draw inferences about the physical world or other
individuals. Specifically, they note that children with AD have
deficits in these lower-level, domain-specific, input systems, for
example, face recognition, gaze direction, and joint attention, as
reported previously by Volkmar [2011]. Therefore, an input–
output system devoid of a ToM module more parsimoniously
explains the inability of children with AD to draw inferences about
their environment in general and the behavior of other individuals
in particular.
To return to the two other basic features in Leslie’s [1987]
modular ToM: Specifically, that it is universal in every child; and
that changes in ToM results from maturation and not experience.
That is to say, all cultures should have some common form of ToM;
and sociological and cultural differences should not significantly
affect the development of a ToM among different nationalities. To
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
test the second of these hypotheses, Wahi and Johri [1994] assessed
42 Indian children, ages 3–8 years, from two distinctly different
socioeconomic strata, using a FB task to distinguish between real
and mental items (toys and concrete items vs. stories). As expected,
age made a significant difference in the percent correct responses
made. However, they also found that socioeconomic factors made
for significant differences in percent correct. Shahaeian et al. [2011]
recruited 135 Australian and Iranian children ages 3–6 years and
examined their performances on a variety of ToM tasks. These
researchers found that, on average, both nationalities passed the
same number of tasks, but for three types of tasks—FB, Diverse
Beliefs, Knowledge Access—the two groups differed significantly
on percent correct. Tardif et al. [2004] tested Cantonese- and
Mandarin-speaking Chinese children, ages 3–5 years, using three
FB tasks: change in location (the Sally–Anne paradigm), the
deceptive object task (A pen that looks like a lollipop: what is it
really?); and an unexpected contents task (a candy box that contains
pencils instead). Results again show an expected age effect: Older
children from both language groups perform better than younger
ones. However, Tardif et al. [2004] also noted that Cantonese
children performed significantly better on the deceptive object
task than did same-aged English-speaking children reported by
Gopnik and Astington [1988]. Kobayashi et al. [2007] approached
the cultural dissimilarity question from a different perspective.
These researchers used fMRI to examine neural correlates in
12 monolingual American and 12 bilingual Japanese children,
ages 8–11 years, on both ToM and non-ToM tasks, and found
significant differences in brain function between groups for both
sets of tasks. Kobayashi et al. [2007] concluded there were both
language- and culture-dependent neural bases for ToM develop-
ment. Guajardo and Watson [2002] manipulated children’s expo-
sure to social communication with story-telling and discussion of
episodes involving mental concepts, and found that children in the
story-telling group performed better on post-test FB and AR ToM
tasks than non-trained controls.
As for ToM’s universality: In her review of ethnopsychologies,
Lillard [1997, 1998a] noted that the concept of mind among
Europeans and Americans is likely culture specific, and that there
are other cultures which do not identify mind with brain that is
inherent in Cartesian dualism. Moreover, some cultures do not
even have a specific lexicon for mind, and its members consistently
fail ToM tasks [cf. Garfield et al., 2001]. So, despite assumptions to
the contrary, cultural differences are a significant factor in deter-
mining a successful outcome on ToM tasks, and the concept of
mind is not universal across cultures.
According to the other major ToM variant, Theory–Theory (T-
T), children use their intellectual abilities to develop a “folk
psychology” or commonsense theory of the mental states of others
in a manner similar to what scientists do when testing hypotheses
from data collected from an experiment [Perner, 1991]. This ability
may either be innate or acquired by early experience, emerging at
about age 4 years; and children are constantly upgrading and
revising their ToMs with respect to others. Finally, as the child
grows, he/she also explores and interacts with the environment
incorporating this information and revising its ToM. These three
components—an innate conception of ToM, the innate ability to
modify this conception, and the ability to incorporate information
FISCH
from the environment to further modify the ToM—are essential to
T-T.
The central thesis of T-T consists of the ability of one child’s mind
to form a theory to understand representations of others’ minds,
that is, to “mentalize.” Those who cannot form a theory of
representations cannot understand the thoughts, beliefs, desires,
or intentions of others. Also as noted above, the attainment of a
ToM does not develop until age 4 years [cf. Bloom and German,
2000; Gallagher, 2004], at which time it empowers children in their
ability to deceive others by keeping secrets, lying and by other forms
of deception. However, many studies have shown that children are
capable of deception prior to age of 4 years [Chandler et al., 1989;
Hala et al., 1991; Reddy and Morris, 2004; Melis et al., 2010].
The assumption that ToM does not develop until age 4 years has
been a point of contention among different factions of T-T adher-
ents. In an attempt to resolve the issue, Chandler et al. [1989]
proposed to examine the Wimmer and Perner [1983] FB prototype
by employing a novel paradigm of “hide-and-seek” which allowed
participants to make use of five levels of deceptive strategies:
withholding evidence (the simplest level), destroying evidence,
lying, making false trails, destroying evidence to produce false trails
(the most complex). They recruited 56 children, ages 2–5 years.
Although there were modest age differences in outcomes across
tasks, the differences were not statistically significant. Interestingly,
children from all age groups made greater use of the more complex
deceptions than the simpler ones. From these results, Chandler et al.
[1989] concluded that children as young as 21/2 years were capable of
utilizing any number of deceptive techniques in order to instill FBs in
others. In their follow-up study, Hala et al. [1991] also employed
protocols involving deceptive hiding strategies by 33 children, ages
3–41/2 years, and found no significant difference in correct responses
by age for tasks that involved hide-and-seek or FB predictions. What
was found associated with age was the increased frequency and
intricacy of the lies [Reddy & Morris, 2004].
According to Reddy and Morris [2004], the main problem with T-
T is its central canon; that the innate conception of mind begins and is
maintained at the level of thought, without acknowledging the effects
of the child’s constant interaction with the environment and with
other individuals. T-T supporters challenge any such behavioral
account, even though the latter may be the more parsimonious
explanation for the child’s responses. By rejecting empirical data that
areatvariancewith T-T beliefs,theorists againdenytheapplication of
modern scientific thought to hypothesis-testing.
At its core, experiments are used to demonstrate ToM, and the
several types of tasks that have been developed are administered to
affirm or refute ToM capability in the participants assessed. The
classic experiment, the Sally–Anne FB designed by Wimmer and
Perner [1983], has been described previously. Also noted briefly
were the AR task, the deception task, and the object removal task.
Central to any experiment must be the validity and reliability of the
tasks employed to test a ToM hypothesis and infer the conjecture
from the results obtained. We have already noted that language used
to tell the Sally–Anne story may be too difficult for children with
limited linguistic skills to pass such a test with any regularity. Bloom
and German [2000] cite several studies in which modified, simpler
and pragmatically neutral FB tasks are passed by 3-year olds,
although Gopnik [1993], a supporter of T-T, believes that this is
2471
evidence of “fragmentary FB understanding.” Gopnik’s comments
notwithstanding, other researchers found evidence that children
younger than age 4 years pass FB tasks. In their review, Baillargeon
et al. [2010] noted various studies in which the ability to attribute FB
correctly is present at an earlier age. Onishi and Baillargeon [2005]
tested toddlers, age 15 months, using a “violation-of-expectations”
protocol, and found infants’ behavior consonant with what one
would expect from an older child’s response to a FB task. In a similar
experiment, Surian et al. [2007] tested 13-month-old infants, and
obtained comparable results. And, curiously, even Gopnik found
that 18-month olds use emotional cues to infer desires on the part of
others, despite the absence of behavioral cues [Repacholi and
Gopnik, 1997]. Bloom and German [2000] observe quite acutely
that, when examining children using the FB task, TD 3-year olds are
inherently different from older children with autism. TD 3-year
olds have substantially greater communication and socialization
skills than do older children with autism. In accord with that
remark, Abbeduto et al. [2004] found that individuals with ID
and limited language skills perform less well on FB tasks than do
matched TD controls. Therefore, the inability to perform success-
fully on a ToM task calls into question what it is that the standard FB
task is actually assessing.
Another important methodological consideration is the test–
retest reliability of ToM tasks. Mayes et al. [1996] presented video-
tapes demonstrating three different FB tasks to children ages 4–5
years, testing for correctness. Three weeks later, the children were
assessed again on all three FB tasks. The kappa coefficient was used
to assess agreement from Time 1 to Time 2. The kappa statistic
adjusts for the possibility of chance agreement. For one Sally–Anne
task, kappa coefficients were moderately high. For the second Sally–
Anne task, however, kappa coefficients ranged from 0.25 to 0.47.
Mayes et al. [1996] concluded that performance on FB tasks may
not be stable in children 4–5 years old; and consequently, that the FB
protocol employed may not be a reliable indicator of children’s
ToM abilities. In their study of reliability, Charman and Campbell
[1997] tested 36 children with learning disabilities, 71/2 to 191/2 years
of age, on three FB tasks and two belief-desire tasks administered on
two different occasions, 3 weeks apart. Kappa coefficients for the FB
tasks ranged from 0.26 to 0.49, similar to the results obtained by
Mayes et al. [1996]. For the belief-desire tasks, kappa ranged from
0.48 to 0.78. Although there are no precise kappa values for what is
considered acceptable agreement, Shrout [1998] suggested that
kappa < 0.80 should not be considered satisfactory. Consequently,
the reliability of FB tasks as the “litmus test” for ToM should not be
thought of as convincing.
Another facet of mentalizing reflects empathy, and researchers
have developed ToM tasks that examine empathic ability (EA), the
capacity to put oneself in another’s shoes. Dyck et al. [2001]
examined 174 children, ages 9–16 years, from one of five groups:
AD; Asperger syndrome; ADHD; mild ID; and TD children, testing
them for EA, among other assessments. These researchers found
that children with AD showed the greatest deficits in EA, but that
children with ID also performed similarly poorly. The correlation
between IQ and EA was r ¼ 0.84, as was the correlation between IQ
and a ToM metric (r ¼ 0.77). In a related and complementary
study, Williams et al. [2012] examined whether children diagnosed
with AD could be trained to develop skills to identify emotions.
2472
These researchers recruited 55 children, ages 4–7 years, and assigned
them to an intervention or control group. The intervention con-
sisted of the presentation of an animated children’s series—Trans-
porters—designed to develop emotional recognition in children in
this age group with AD. Tests of identification and matching of four
emotions—happiness, sadness, anger, and fear—were adminis-
tered to both groups. Results showed small to moderate increases
in the intervention group in identifying all four emotions. Control
participants showed smaller increases for two emotions, and de-
creased ability in two others. Williams et al. [2012] concluded that
Transporters could improve recognition of emotions. However,
this improvement did not generalize to improved ToM skills that
were also assessed at the time.
Moral understanding is another aspect of development related to
communication and socialization. Therefore, impaired moral un-
derstanding would be related to impaired socialization. Grant et al.
[2005] examined 56 children, mean age 12–13 years, and their
ability to understand the importance of motive and intention in
judging others’ behavior. Three groups were assessed: children with
AD, children with mild LD, and TD children. Participants were
administered six pairs of stories involving motives and outcomes.
Results showed that children with AD were able to demonstrate
moral understanding and judgment, comparable to that of children
from the other two groups, and of judging damage to people as
more serious than damage to property. Therefore, despite their
impaired socialization, children with AD are capable of moral
understanding.
In summary, basic assumptions regarding ToM, its universality
in all children, unaffected by exogenous factors such as culture,
ethnicity and socioeconomic factors, are not well-supported by
empirical findings. Differences in ToM theories related to suppo-
sitions regarding its innateness, whether as a module or as theory–
theory, the age at which a ToM emerges or events that presage the
emergence of a ToM, are likewise not validated empirically. Specific
features, such as the age at which pretend play or social interactions
are supposed to materialize, or the earliest age at which children can
practice deception using ToM or understand FBs, are also not well
corroborated by research findings. The inability to incorporate the
effects of social interaction into the model as they influence
behavior is another weakness in ToM paradigms. Differences on
FB tasks between children with AD compared to those with ID only
have been found to be insignificant in many studies. Test–retest
reliability of various FB tasks, the “litmus test” for ToM [Baron-
Cohen, 1995], have not been shown to be consistent. Other features
of behavior that are limited in children with AD, such as lack of
empathy, are related to intellectual ability and not specific to AD,
while morality can be made more manifest in children with AD.
THEORY OF MIND IN NON-AUTISTIC POPULATIONS
ToM took a curious turn recently as researchers began to exploit the
model to examine disorders other than autism. Given the “autistic-
like” behaviors in fragile X syndrome, Cornish et al. [2005] admin-
istered the FB and AR tasks to 54 children, 7–15 years, 28 males with
the FMR1 full mutation and 26 males with DS, matched for CA and
verbal age. Results showed that pass rates were about 75% and
comparable in both groups. That is, about 25% of each group failed
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
FB and AR tasks, results similar to those obtained initially by Baron-
Cohen et al. [1985] for children with DS. Grant et al. [2007]
recruited 3 groups of CA- and MA-matched adolescent males: 2
groups of males with the FMR1 mutation, 15 with few autistic
features and 15 with sufficiently many to be in the range for a
diagnosis of autism according to the SCQ, and 15 males with ID
only etiology unknown. Grant et al. [2007] found that a significantly
greater number of correct responses were produced by the ID only
group compared to either FMR1 group on one ToM task (location
change), but no significant differences between the number correct
in the “non-autistic” FMR1 group (6/15) and the ID group (9/15)
on another ToM task (deceptive box). Porter et al. [2008] examined
31 individuals with Williams–Beuren syndrome (WBS), ages 5–44
years, compared to CA- and MA-matched controls, and found
significant differences between groups on FB, pretense, and inten-
tion tasks. Despite the variability of passing rates within the WBS
group, Porter et al. [2008] concluded that there were ToM deficits in
WBS.
Individuals with neurodegenerative disorders have also been
assessed for ToM. Allain et al. [2011] administered three ToM tasks
to adults, ages 36–70 years, 18 with Huntington disease (HD) and 18
controls. Results showed significant impairment in the HD group
on motor tasks and executive function (EF) (frontal lobe) tasks, as
well as significantly lower scores on two of the three ToM tasks
given. Kobayakawa et al. [2012] examined 9 middle-aged men and
women with adult-onset myotonic dystrophy (DM), and compared
them to 12 controls. Unlike the study by Allain et al. [2011], these
researchers excluded individuals who demonstrated cognitive de-
terioration at the time of recruitment. Participants were adminis-
tered two ToM tasks. Results indicate significantly lower scores on
both ToM tasks for individuals with DM compared to controls.
Poletti et al. [2011] reviewed 10 studies in which ToM was examined
in patients with Parkinson Disease (PD). Typical ToM tasks
presented included a faux pas test, other’s beliefs, and the “Reading
of Minds in the Eyes” (RME), another ToM task developed by
Baron-Cohen et al. [2001]. The RME task was also employed by
Allain et al. [2011] and Kobayakawa et al. [2012] as part of their
ToM battery of tests. Patients with PD performed poorly although,
according to Poletti et al. [2011], working memory may have played
an important role in the execution of each of these undertakings in
the PD group.
The basic format of the RME task is to show the participant a
photograph of the region around the eyes, then ask the respondent
to select which mental-state descriptor the eyes best exhibit. Var-
iations of the RME task have been validated by Calder et al. [2002]
and Peterson and Slaughter [2009], although Hallerbäck et al.
[2009] found test–retest reliability only moderately correlated
(r ¼ 0.6); and, of the 28 items in the task, 12/28 (42%) were
correctly responded to by less than 75% of the non-clinical adult
sample tested, while as many as 6/28 (21%) show chance correct
agreement.
Children with other disabilities have also been assessed using
ToM tasks. Buitelaar et al. [1996] administered a series of ToM tasks
to a non-autistic 9-year-old boy with a diagnosis of Non-Verbal
Learning Disability. He passed only 50% of the first-order ToM
tasks, and failed all second-order tasks. Based on their results,
Buitelaar et al. [1996] proposed that social-cognitive abilities in
FISCH
children should be examined with respect to their neuropsycho-
logical profiles. Peterson and Siegal [1995] examined 26 deaf
children, ages 8–13 years, who grew up in homes where sign
language was not used, therefore they had communication expe-
riences similar to those of autistic children. Children were assigned
to one of two groups: Those administered the standard FB task; and
those who were administered a conversationally modified FB task.
Of the 12 children administered the standard FB task, only 2/12
(16%) passed; whereas, 7/14 (50%) passed the conversationally
modified task. Consequently, Peterson and Siegal [1995] concluded
that ToM deficits were not specific to autism. Minter et al. [1998]
administered an FB task and a second ToM task to 42 CA- and IQ-
matched visually impaired and sighted children, mean age 6 years,
and found that visually impaired children performed significantly
worse than sighted children on both tasks. To examine the role of
language in the development of ToM, Dahlgren et al. [2010]
administered a FB task and a second ToM task to 28 children,
ages 5–13 years. Fourteen children were diagnosed with cerebral
palsy and had severe speech/language impediment; 14 were TD
children. Groups were matched on linguistic-age and MA. Results
showed that children with cerebral palsy performed significantly
less well on the standard Sally-and-Anne FB task but not on the
“thought picture” ToM task.
Several researchers have gone so far as to examine ToM in
individuals with traumatic brain injury (TBI). Changes in social
behavior have been observed frequently in individuals with TBI. An
early article by Bibby and McDonald [2005] examined 15 adults
with TBI to either their frontal, temporal, parietal, or occipital brain
regions. Compared to CA-matched controls, TBI individuals per-
formed significantly less well on first- and second-order ToM tasks.
Muller et al. [2010] explored ToM in individuals with severe TBI to
the same regions of brain as found in participants in Bibby and
McDonald study. However, the participants in Muller et al. [2010]
were significantly more impaired cognitively (mean FSIQ ¼ 70).
Individuals in the Muller et al. [2010] study performed significantly
worse than controls on four of the ToM tasks administered,
although curiously not on the FB task. In their meta-analysis of
studies examining ToM in TBI, Martı́n-Rodriguez and León-Car-
rión [2010] found large effect size differences (about 1 SD) on four
ToM tasks between subjects with TBI and unaffected controls.
The problem with all these studies is that a core component for
ToM seems to have been circumvented. For Piaget, ToM appears at
one phase of a developmental sequence of discrete stages as the child
ages, and which emerges early in the child’s life. And, in accordance
with Piaget’s theory of child development, whether one invokes
Leslie’s [1987] innate module or Perner’s [1991] T-T, it is the ability
to form a mental representation at age four which emerges as
pretend play at age 2 years in the TD child. In addition, its
manifestation is universal among TD children. Thus, one conclu-
sion from the results obtained by Cornish et al. [2005] is “autistic-
like” behaviors that appear as part of a fragile X syndrome are not
sufficient for, nor are they specifically associated with, a ToM deficit
in male children with the FMR1 full mutation who have not been
diagnosed as autistic, though results obtained by Grant et al. [2007]
seem to produce a somewhat more mixed picture. On the other
hand, from the results obtained by Porter et al. [2008], Peterson and
Siegal [1995], and Minter et al. [1998], there were non-autistic
2473
children with a genetic or congenital abnormality who failed the
ToM tasks administered to them. Therefore, it is the not necessary
to have a diagnosis of autism to show ToM deficits. That is, ToM
deficits are neither necessary nor sufficient to produce autism. As
for research among individuals with TBI, these researchers seem to
conclude that ToM tasks used to identify ToM in children can now
be used to detect ToM deficits produced by various damaged
regions or lesions in brain in adults as a consequence of their
inability to perform certain types of tasks, particularly tasks
that require a good working memory. Considering the respective
ages of their participants, it is likely not known whether any of the
adults would have successfully completed the ToM tasks had they
been administered in childhood. Since PD, HD, and adult-onset
DM are neurodegenerative disorders that occur in adults, it is not
clear what ToM as a model of childhood development has to do with
failure on ToM tasks that result in neurological deterioration in
adulthood.
MODIFYING DYSFUNCTIONAL BEHAVIOR IN AUTISM
Another problem left unresolved by ToM regards the effect of
behavioral interventions on children with AD. If, as ToM models
suggest, some innate module or brain component is obliterated or
at best, severely damaged in children with AD, and is unaffected by
exogenous factors such as culture and socioeconomic status, what
could possibly be the effects of behavioral mediation to ameliorate
the disorder? To examine the effects of behavioral intervention,
Dawson et al. [2010, 2012] employed the Early Denver Start Model
(EDSM), a comprehensive behavioral program to improve a variety
of behaviors in children with AD. After 2 years’ intensive treatment,
Dawson et al. [2010] found that children with AD showed signifi-
cant improvements in adaptive behavior and language compared to
controls. Dawson et al. [2012] later examined brain activity in
children who received EDSM intervention compared to an IQ-
matched group of children with AD who did not. These researchers
found children with AD showed EEG responses to faces similar to
that of TD children, and significantly better than the IQ-matched
AD controls. That is to say, intensive behavioral interventions in
young children with AD can improve neurological function.
AUTRES TEMPS, AUTRES THEORIES
From its inception, theories about the etiology of autism have been
proposed. However, in the past 30 years these theories have
increased in number, one might be inclined to say, in an exponential
fashion much as the putative prevalence of autism. Kanner’s earliest
account of autism was as an inborn error of affect, later described as
“infantile autism” [1949]. Asperger referred to the disorder he
observed in his patients as a “personality disorder” [1944]. These
humble beginnings have proliferated into the raft of theories in
vogue currently: Theory of Mind, Simulation, Executive Function,
Central Coherence, the Social Brain, Sensorimotor Theory, among
the most widely recognized. EF theory argues that there are areas in
brain, primarily the prefrontal cortex, which are involved with goal-
setting, focused attention, and decision-making; and, these skills
are deficient in individuals with autism [Ozonoff et al., 1991]. Yet,
deficits in EF are not specific to AD [cf. Gallagher, 2004; Volkmar,
2474
2011]. Central coherence (CC) theory argues that individuals with
AD attend to detail rather than global assessment more so than do
TD individuals; and they are unable to switch easily from figure to
global perception, and vice-versa. Unfortunately, ToM, EF, and CC
theory all come up short as cognitive models for autism, the
consequence of conflicting results in studies which attempt to
examine the empirical basis for each theory. Of late, ToM has
evolved into “mind-blindness” [Baron-Cohen, 1995], with addi-
tional innate mechanisms such as an “eye direction detector” and an
“intentionality detector.” To address issues that arose from studies
that challenged the original ToM article, Baron-Cohen [2009]
proposed a revised model referred to as “Empathizing–Systematiz-
ing Theory” (EST), in which a second factor is incorporated to
account for non-social deficits in AD. ToM was expanded to include
a dimension to assess emotional reactivity. Baron-Cohen [1995]
also put forward a two-factor theory to distinguish AD from other
disorders, with disappointedly mixed results. Finally, two core
deficits associated with AD were dimensionalized to account for
the fact that there are degrees of impairment in AD that “blend in”
to the general population. EST also incorporated Baron-Cohen’s
Extreme Male Brain (EMB) theory of AD [Baron-Cohen, 2009].
Unfortunately for Baron-Cohen’s EMB theory, Voracek and Dress-
ler [2006] found that when they examined the second-to-fourth
digit ratio—an established biomarker for sexual differentiation
between males and females—they found individual differences
to be unrelated to EST and autistic-like characteristics in the general
population.
The modifications and additions to the original model proposed
by Baron-Cohen et al. [1985] are reminiscent of the efforts by
the Ptolemaicists and neo-Aristotelians to salvage the geocentric
theory of the universe composed of concentric spheres. The geo-
centric theory was rescued—for a time—by adding epicycles to
celestial objects in the spheres which did not conform to the
original theory, a line of reasoning noted by Stone and Gerrans
[2006] regarding ToM. When the first set of epicycles still did not
conform to the data, more epicycles were affixed to the model.
Curiously, and in a similar vein, despite the wealth of data which
demonstrate that ToM is neither necessary nor sufficient as a model
to depict AD, Frith [2012] continues to assert that, while we can
observe and assess autistic behavior, and find and measure the
concomitant neurological phenomena associated with those behav-
iors, we must somehow insert another level of explanation, a
cognitive model between brain and behavior, in order to explain
behavior already accounted for by brain [cf. Stone and Gerrans,
2006]. Cromwell and Panksepp [2011] note that this is precisely the
problem with much of cognitive theory: Cognitive-behavioral
concepts that are but hypothetical constructs which simply do
not correspond to specific neurological mechanisms that generate
behavior.
EVERYTHING OLD IS NEW AGAIN
Any intelligent fool can make things bigger, more complex,
and more violent. It takes a touch of genius—and a lot of
courage—to move in the opposite direction.
Albert Einstein, (attributed)
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
Everything should be made as simple as possible, but not
simpler.
Albert Einstein, (attributed)
Less is more.
Ludwig Mies van der Rohe
In his landmark article, Kanner [1943] thought that social
deficits were primary in autism and resulted from an inborn deficit.
More than 40 years later, Fein et al. [1986] restated Kanner’s original
position, that autism is a neurological disorder that primarily
disrupts social and affective development. Although Fein et al.
also argued the case that social deficits were primary, they main-
tained that children with AD had some specific neurological
dysfunction subserving attachment and social behavior, even
though no single anatomical or physiological locus of dysfunction
had been found at that time.
For much of the past 40 years, the neurobehavioral paradigm of
autism has been at the forefront of theories regarding the etiology of
autism, and ToM has been the leading neurocognitive model for the
past generation. Recently, however, Minshew et al. [2011] have
found a broad range of sensory-perceptual, sensorimotor, and
memory deficits associated with AD which suggests that the nature
and degree of involvement of neurological functions have not been
appropriately dealt with by ToM, EF, or CC, or any of the other
neurobehavioral theories extant. In her earlier work, Minshew et al.
[2004] found neurological impairments in vestibular, visual and
postural senses in children with autism. Rogers [2009] examined
infants who were the younger siblings of children diagnosed with
AD and therefore at a higher risk of developing AD, and found the
earliest signs of autism were not social impairment, but unusual
responses to sensory stimulation and unusual motor activities that
heralded the disorder. Consequently, Minshew et al. [2011] pro-
posed shifting the etiological paradigm for autism, conceptualizing
it as a neurological and neurobiological disorder, as opposed to a
neurobehavioral or neurocognitive one.
In support of a neurobiological hypothesis, Courchesne et al.
[2011] found substantial evidence that children diagnosed with AD,
irrespective of etiology, exhibit a too-rapid growth in brain prior to
age 2 years, followed by a too-steep decline in growth afterward,
comparedtoTDchildrenofthesameage.Frontalandtemporallobes,
and the amygdala, were brain areas primarily affected. Levy et al.
[2009] noted that damage in these regions have been linked to motor
difficulties, as well as problems associated with communication and
socialization. As noted earlier, Brüne and Brüne-Cohrs [2006]
reported that patients with brain lesions in these regions—left-
hemisphere, frontal cortex, left amygdala, and pre-frontal cortex—
demonstrated impaired performances on FB tasks as adults. Zielinski
et al. [2012] examined structural features in brain regions containing
network nodes. In particular, they examined the salience network
(SN) and default mode network (DMN). The SN contains, among
other areas, the frontoinsular and orbitofrontal cortex, both involved
with social functioning. The DMN is comprised of, among other
regions, the medial and ventral prefrontal cortex, anchored by the
posterior cingulate cortex. The DMN is believed to regulate internal
FISCH
processes such as attention. Zielinski et al. [2012] found the SN to be
underdeveloped in volume, while the DMN exhibited both over-
developed and underdeveloped regions in children and adolescents
with AD compared to controls. It should be noted that neither the SN
nor DMN are modules in the usual sense, if by module is meant one of
a set of standardized parts or independent units used to construct a
more complex structure.
In a somewhat parallel development, action recognition, a basis
upon which social behavior is understood, was found in the neural
substrates of primates. So-called “mirror neurons” are triggered
when a primate observes a conspecific performing a goal-directed
action using its hand, mouth or foot. And, according to Buccino
et al. [2004], there are neurophysiological, behavioral, and brain-
imaging studies that also demonstrate the existence of mirror
neurons in human brains. Sato et al. [2012b] presented dynamic
and static facial expressions to high-functioning adults diagnosed
with ASD, and to age- and sex-matched controls, and examined
their brain activity. These researchers found regions in the social
brain network show lower activity in ASD subjects compared to
controls. Fadiga and Craighero [2003] observed that action-related
neural responses are not only a function of visual stimuli but
acoustical stimuli as well. In effect, mirror neurons allow humans
to represent in one’s brain other humans’ behavior. Bolling et al.
[2011] found neurobiological differences in processing social ex-
clusion and rule violation in a game of Cyberball in a group of TD
children compared to children with AD. As noted earlier, problems
of social processing have been a hallmark of dysfunction in AD from
Kanner’s time to the present. Thus it has been demonstrated that
neural material in brain regions directly involved in social process-
ing have been identified, that neural activity in these regions differs
in individuals with AD compared to non-AD controls, and can now
be studied in greater detail.
As remarked earlier, the concept of intentionality is rooted in the
folk psychology inherent in ToM. To address the issue of inten-
tionality in mirror neurons, Iacoboni et al. [2005] used fMRI to
study 23 human subjects exposed to three different film clips: a hand
grasping a cup (no context); a tea setting (context but no hand
grasping); and a hand grasping a cup in the tea setting. Results
showed increased signals in the premotor motor areas during the
third (embedded context) condition suggested that neural mech-
anisms are involved in the intentionality of the action. Fogassi et al.
[2005] examined inferior parietal lobule (IPL) neurons in monkeys
when they performed various motor activities, and when they
observed the experimenter performing similar actions. These
researchers found that IPL neurons fired only when embedded
in an activity was associated with some forthcoming goal. Their
results suggest that in addition to the recognition of a motor
activity, mirror neurons can anticipate the goal of the activity,
that is, its “intention.” That is, cognitive functions typically ascribed
to a ToM could be explained more pragmatically by the triggering of
a related sequence of mirror neurons in brain.
Mirror neurons were first found in the monkey’s ventral premotor
cortex, area F5, the latter of which is considered the homologue of
Broca’s area in humans [Rizzolatti et al., 1996; Rizzolatti and Arbib,
1998]. Other brain regions in monkey, such as the superior temporal
sulcus (STS), also contain neurons responding to biological actions.
Both F5 and STS are linked to the IPL, area PF, and are referred to as
2475
“PF neurons” [Rizzolatti et al., 2001]. It is thought that other areas of
brain, for example, the amygdala and orbitofrontal cortex, are also
part of the mirror neuron network. Fogassi and Ferrari [2007]
determined that language is also part of the complex. Thus, language
development, social behavior, and the understanding of intention-
ality appear to be related to a particular type of neuron and located in
well-defined interconnected brain regions.
As for Kanner’s impression that autism was inborn: AD is now
considered as a highly heritable disorder, mostly multi-monogenic
but possibly polygenic in nature; and it is increasingly the case that
genetic mutations associated with AD have been found to have a
known neurobiological effect. Recent estimates are that 15% of
individuals diagnosed with AD have a known genetic cause [Carter
and Scherer, 2013]. Creak [1963] was probably the first to note a
genetic disorder, tuberous sclerosis complex (TSC), associated with
AD. Phenylketonuria (PKU) was later shown associated with AD
[Friedman, 1969]. Later still, the FMR1 full mutation was discov-
ered in young males with autism [Brown et al., 1982]. TSC, the
FMR1 mutation, and more recently discovered mutations in the
PTEN gene, probably account for more than 10% of the known
genetic causes for autism [Smalley, 1991]. As it happens, TSC,
PTEN, and FMRP—the protein produced by the FMR1 gene—
form part of the mTOR complex in brain, the pathways for which
dovetail to inhibit mTOR signaling. Genetic mutations in TSC and
FMR1, PTEN, as well as STRADa and other regulatory genes, have
known adverse consequences on the structure of the neocortex
[Crino, 2011]. As importantly, even among known genetic abnor-
malities, such as the FMR1 mutation, TSC and PTEN, in which the
probability that a child born with one or the other mutation will
develop autism is markedly increased, variability in the behavioral
features of AD has also been reported.
More recently, mutations in members of the neuroligin family,
NLGN3 and NLGN4, have been found in children with AD [Jamain
et al., 2003; Laumonnier et al., 2004; Yanagi et al., 2012]. Members
of the neurexin family, from the beta-neurexin complex [Feng et al.,
2006], CNTNAP2 [Alarcón et al., 2008], NRXN1 [Ching et al.,
2010], as well as the SHANK3 gene [Sato et al., 2012a], have also
been found in individuals with AD. Neuroligins have been shown to
affect synapse formation, while NXRN protein is associated with
presynaptic binding with NLGN and CNTNAP2, and shows ho-
mology to SHANK3, the latter of which regulates the structure of
dendritic spines [Bourgeron, 2009].
Chromosomal regions in which microdeletions or duplications
were found among individuals diagnosed with AD have become
hotspots for candidate genes. Bundey et al. [1994] and Koochek
et al. [2006] reported instances in which duplication in 15q11-13
were found in individuals diagnosed with AD. Depienne et al.
[2009] examined 522 individuals diagnosed with ASD and found 4
with 15q11-13 abnormalities. In an earlier report using linkage
disequilibrium mapping, Cook et al. [1998] found a candidate gene,
GABRB3, in the 15q11-13 region associated with AD. Hogart et al.
[2007] showed that MeCP2 binds to sites with GABRB3 and
organizes GABRB3 in neurons.
Other researchers have found higher than expected rates of AD in
the many genetic disorders they have studied. Vorstman et al.
[2006] examined 60 children and adolescents with deletion 22q
and found 50% of those assessed with standard protocols were
2476
diagnosed with AD. Fisch et al. [2010] examined children with
one of four subtelomeric deletions—2q37, 4p16, invdupdel8p22-
23, or 11q24-25—and found 11/43 (30%) of children met
criteria consistent with a diagnosis of AD, although none of the
children with 4p16 exhibited autistic behaviors. In their review
of genetic disorders that produce developmental disabilities,
Vorstman and Ophoff [2013] highlight a number of known genetic
abnormalities in which individuals with AD have been identified.
Although candidate genes have yet to be discovered in many of
these regions, current technologies using genome-wide association
studies will likely identify the genetic variants associated with
AD.
These findings demonstrate that there are numerous genetic
mutations associated with AD, which in turn appear to disrupt
various neurobiological processes. If these neurobiological process-
es are located in, or in some way influence, the mirror neuron
complex, the consequence of which would disturb normal com-
munication and socialization, we may well be on the way to
establishing neurobiological markers for AD. One step toward
that end has been provided by Skafidas et al. [2012], who examined
SNPs in 2,609 probands with ASD. Using pathway analysis, these
researchers identified 775 SNPs that were significantly modified in
the presence of ASD. Of these, 237 were used to discriminate
between ASD and non-ASD controls with prediction accuracy of
about 85%.
As novel neurobiological and neurophysiological studies are
begun, progress, and results obtained, brain–behavior and gene–
brain–behavior pathways associated with AD will become more
clearly delineated and the underlying neurological phenomena
elucidated. All of which is to say that by establishing brain–
behavior relationships in this fashion, a ToM, or any other
metaphysical neurobehavioral entity, will be found redundant.
To paraphrase Searle [1990], it is one thing to speak of inten-
tions metaphorically, as “as-if” ascriptions. It is quite another to
take them literally.
SUMMARY AND CONCLUSION
A belief in dialectical materialism necessitates that one also
believe in the omnipotence of thought.
-Anonymous
ToM has its roots in Piagetian developmental child psychology.
Although Piaget did not consider himself as a child psychologist, his
theory of child development became widespread during the 1960s
and was adopted by cognitive psychologists seeking to oust behav-
iorism from its prominent position in psychology. The central
themes of Piagetian theory are that children’s cognitive abilities are
innate, emerge at specific ages, and appear in four major, distinct,
sequentially invariant stages. However, the methodological aspects
of the theory, particularly the emergence of sequentially invariant
stages at specific ages, have not been well-validated empirically. As
formulated, Piaget’s theory of child development lacks construct
and predictive validity, his terminology often murky and lacking in
precision. Despite these concerns, Piaget did not consider empirical
verification or falsification of his theory problematic, since he
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
believed his theory fell outside the purview of the modern scientific
explanation.
The original article by Baron-Cohen et al. [1985], in which
the authors account for social impairment in autistic children
because they lack a ToM, ascribes the source of their model to
Premack and Woodruff [1978], the latter of whom claimed to
have ascertained ToM in a chimpanzee. The methodology used
by Premack and Woodruff [1978] was not without its short-
comings, its findings open to question and conclusions criti-
cized. Ensuing research found a lack of evidence for a ToM in
primates, which suggested strongly that the research design
employed and results obtained by Premack and Woodruff lacked
both internal and external validity. The consequences stemming
from the many weaknesses identified by the empirical outcomes
of studies of ToM in primates should have forewarned future
researchers of problems that might arise in attempting to
implement a ToM in children with autism.
From the outset, ToM has had many shortcomings as a neuro-
cognitive model of autism. From a methodological perspective, a
research design that embeds a pretend play component in a FB task
is illogical since children with AD do not pretend play spontane-
ously. Second, the linguistic sophistication needed to provide a
correct response to the FB task is beyond the pragmatic language
skills of all too many children with AD whose impaired communi-
cative ability is embedded in the diagnosis of AD. Third, without a
ToM, how was it possible for a child to participate actively in a ToM
experiment? Although the FB test was supposed to the “gold
standard” for a ToM, the experiment itself contains many serious
logical and design flaws. Leslie and Frith [1987] argued that
linguistic ability was unrelated to ToM, but many researchers
subsequently showed otherwise. The matter of whether one needed
a ToM to participate in a ToM experiment remained unresolved,
although this too seems to beg the question.
Other assumptions that form the basis for a ToM, its universality
in all children in all cultures and socioeconomic conditions, are not
supported by empirical findings. Differences in versions of ToM
related to underlying assumptions about innateness, whether as a
module or as a theory, the age at which a ToM emerges, or events
that herald the emergence of a ToM, are likewise not often validated
empirically. Specific model features, such as the age at which
pretend play or social interactions are supposed to materialize,
or the earliest age at which children can practice deception using
ToM or understand FBs, are at variance with many research
findings. Other weaknesses in ToM include the inability to utilize
the early acquisition social skills in the life of the infant to explain
interbehavioral interactions. Differences on FB tasks between chil-
dren with AD and those with ID only are insignificant in many
studies. Test–retest results from various FB tasks, the “litmus test”
for ToM [Baron-Cohen, 1995], do not have good reliability. Other
features of behavior that are limited in children with AD, such as
lack of empathy, are correlated with intellectual ability and not
specific to AD.
Recent findings regarding mirror neurons, their location and
interconnections in brain, their relationship to social behavior,
intentionality, and language, and the effect of lesions in these areas
on speech, language and social behavior, strongly suggests that a
neurobiological as opposed to neurocognitive model of autism is a
FISCH
more parsimonious explanation for the social, linguistic and be-
havioral phenotypes observed in autism.
All of which is to say: Does autism really need a Theory of Mind?
ACKNOWLEDGMENTS
I thank Miriam S. Grosof, Irv Gottesman, and an anonymous
reviewer for their comments on an earlier version of this manu-
script. Any errors contained herein are solely my own.
REFERENCES
Abbeduto L, Short-Meyerson K, Benson G, Dolish J. 2004. Relationship
between theory of mind and language ability in children and adolescents
with intellectual disability. J Intellect Disabil Res 48:150–159.
Alarcón M, Abrahams BS, Stone JL, Duvall JA, Perederiy JV, Bomar JM,
Sebat J, Wigler M, Martin CL, Ledbetter DH, Nelson SF, Cantor RM,
Geschwind DH. 2008. Linkage, association, and gene-expression analyses
identify CNTNAP2 as an autism-susceptibility gene. Am J Hum Genet
82:150–159.
Allain P, Havet-Thomassin V, Verny C, Gohier B, Lancelot C, Besnard J,
Fasotti L, Le Gall D. 2011. Evidence for deficits on different components
of theory of mind in Huntington’s disease. Neuropsychology 25:741–751.
American Psychiatric Association. 2000. Diagnostic and Statistical Manual
of Mental Disorders (4th Ed.): Text Revision. Washington, DC: The
American Psychiatric Association.
Asperger H. 1944. Die “Autistischen Psychopathen” im kindesalter. Arch
Psychiatr Nervenkr 117:76–136.
Astington JW, Dack LA. 2008. Theory of mind. In: Haith MM, Benson JB,
editors. Encyclopedia of infant and early childhood development, Vol. 3.
San Diego, CA: Academic Press. pp 343–356.
Astington JW, Jenkins JM. 1999. A longitudinal study of the relation
between language and Theory-of-Mind development. Dev Psychol
35:1311–1320.
Baillargeon R, Scott RM, He Z. 2010. False-belief understanding in infants.
Trends Cogn Sci 14:110–118.
Baron-Cohen S, Leslie AM, Frith U. 1985. Does the autistic child have a
“theory of mind?” Cognition 21:37–46.
Baron-Cohen S. 1988. Without a theory of mind, one cannot participate in
a conversation. Cognition 29:83–84.
Baron-Cohen S. 1989a. The theory of mind hypothesis in autism: A reply to
Boucher. Br J Disord Commun 24:199–200.
Baron-Cohen S. 1989b. Are autistic children “Behaviorists”? An examina-
tion of their mental-physical and appearance-reality distinctions. J
Autism Dev Disord 19:579–600.
Baron-Cohen S. 1989c. The autistic child’s theory of mind: a case of specific
developmental delay. J Child Psychol Psychiat 30:285–297.
Baron-Cohen S. 1992. Debate and argument: On modularity and develop-
ment in autism: A reply to Burack. J Child Psychol Psychiatry 33:623–629.
Baron-Cohen S. 1995. Mindblindness: An essay on autism and theory of
mind. Cambridge, MA: MIT Press.
Baron-Cohen S. 2009. Autism: The Empathizing-Systematizing (E-S)
Theory. Ann NY Acad Sci 1156:68–80.
Baron-Cohen S, Wheelwright S, Hill J, Raste Y, Plumb I. 2001. The
“Reading the Mind in the Eyes” Test revised version: A study with
normal adults, and adults with Asperger syndrome or high-functioning
autism. J Child Psychol Psychiatry 42:241–251.
2477
Beck BB. 1978. Talkers and doers. Behav Brain Sci 4:557.
Bibby H, McDonald S. 2005. Theory of mind after traumatic brain injury.
Neuropsychologia 43:99–114.
Bloom P, German TP. 2000. Two reasons to abandon the false belief task as a
test of the theory of mind. Cognition 77:B25–31.
Bolling DZ, Pitskel NB, Deen B, Crowley MJ, McPartland JC, Kaiser
MD, Wyk BC, Wu J, Mayes LC, Pelphrey KA. 2011. Enhanced neural
responses to rule violation in children with autism: A comparison to
social exclusion. Dev Cogn Neurosci 1:280–294.
Boucher J. 1989. The theory of mind hypothesis of autism: Explanation,
evidence and assessment. Br J Disord Commun 24:181–198.
Boucher J, Lewis V. 1989. Memory impairments and communication
in relatively able autistic children. J Child Psychol Psychiatry 30:99–
122.
Bourgeron T. 2009. A synaptic trek to autism. Curr Opin Neurobiol
19:231–234.
Brown WT, Friedman E, Jenkins EC, Brooks J, Wisniewski K, Raguthu S,
French JH. 1982. Association of fragile X syndrome with autism. Lancet
1:100.
Brüne M, Brüne-Cohrs U. 2006. Theory of mind—Evolution, ontogeny,
brain mechanisms, and psychopathology. Neurosci Biobehav Rev
30:437–455.
Buccino G, Binkofski F, Riggio L. 2004. The mirror neuron system and
action recognition. Brain Lang 89:370–376.
Buitelaar JK, Swaab H, van der Wees M, Wildschut M, van der Gaag RJ.
1996. Neuropsychological impairments and deficits in theory of mind
and emotion recognition in a non-autistic boy. Eur Child Adolesc
Psychiatry 5:44–51.
Bundey S, Hardy C, Vickers S, Kilpatrick MW, Corbett JA. 1994. Duplica-
tion of the 15q11–13 region in a patient with autism, epilepsy and ataxia.
Dev Med Child Neurol 36:736–742.
Burack JA. 1992. Debate and argument: Clarifying developmental issues in
the study of autism. J Child Psychol Psychiatry 33:617–622.
Burge T. 1978. Concept of mind in primates? Behav Brain Sci 4:560–562.
Burghardt GM. 1978. Closing the circle: The ethology of mind. Behav Brain
Sci 4:562–563.
Calder AJ, Lawrence AD, Keane J, Scott SK, Owen AM, Christoffels I, Young
AW. 2002. Reading the mind from eye gaze. Neuropsychologia 40:1129–
1138.
Call J, Tomasello M. 2008. Does the chimpanzee have a theory of mind? 30
years later. Trends Cogn Sci 12:187–192.
Carpenter M, Nagell K, Tomasello M. 1998. Social cognition, joint atten-
tion, and communicative competence from 9 to 15 months of age.
Monogr Soc Res Child Dev 63:1–174.
Carter M, Scherer S. 2013. Autism spectrum disorder in the genetics clinic:
A review. Clin Genet 83:399–407.
Chandler M, Fritz AS, Hala S. 1989. Small-scale deceit: Deception as a
marker of two-, three-, and four-year olds’ early theories of mind. Child
Dev 60:1263–1277.
Charman T, Campbell A. 1997. Reliability of Theory of Mind task perfor-
mance by individuals with a learning disability: A research note. J Child
Psychol Psychiatry 38:725–730.
Ching MS, Shen Y, Tan WH, Jeste SS, Morrow EM, Chen X, Mukaddes NM,
Yoo SY, Hanson E, Hundley R, Austin C, Becker RE, Berry GT, Driscoll K,
Engle EC, Friedman S, Gusella JF, Hisama FM, Irons MB, Lafiosca T,
LeClair E, Miller DT, Neessen M, Picker JD, Rappaport L, Rooney CM,
Sarco DP, Stoler JM, Walsh CA, Wolff RR, Zhang T, Nasir RH, Wu BL,
2478
Children’s Hospital Boston Genotype Phenotype Study Group.
2010. Deletions of NRXN1 (neurexin-1) predispose to a wide
spectrum of developmental disorders. Am J Med Genet Part B
153B:937–947.
Cook EH Jr, Courchesne RY, Cox NJ, Lord C, Gonen D, Guter SJ, Lincoln
A, Nix K, Haas R, Leventhal BL, Courchesne E. 1998. Linkage-disequi-
librium mapping of autistic disorder, with 15q11-13 markers. Am J Hum
Genet 62:1077–1083.
Cornish K, Burack JA, Rahman A, Munir F, Russo N, Grant C. 2005. Theory
of mind deficits in children with fragile X syndrome. J Intellect Disabil Res
49:372–378.
Courchesne E, Webb SJ, Schumann CM. 2011. From toddlers to adults: The
changing landscape of the brain in autism. In: Amaral DG, Dawson G,
Geschwind DH, editors. Autism spectrum disorders. Oxford: Oxford
University Press. pp 611–631.
Creak EM. 1963. Childhood psychosis: A review of 100 cases. Br J Psychiatry
109:84–89.
Crino PB. 2011. mTOR: A pathogenic signaling pathway in developmental
brain malformations. Trends Mol Med 17:734–742.
Cromwell HC, Panksepp J. 2011. Rethinking the cognitive revolution from
a neural perspective: How overuse/misuse of the term ‘cognition’ and the
neglect of affective controls in behavioral neuroscience could be delaying
progress in understanding the BrainMind. Neurosci Biobehav Rev
35:2026–2035.
Dahlgren SO, Trillingsgaard A. 1996. Theory of mind in non-retarded
children with autism and Asperger’s syndrome. A research note. J Child
Psychol Psychiatry 37:759–763.
Dahlgren S, Dahlgren Sandberg A, Larsson M. 2010. Theory of mind in
children with severe speech and physical impairments. Res Dev Disabil
31:617–624.
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.
Dawson G, Jones EJ, Merkle K, Venema K, Lowy R, Faja S, Kamara D,
Murias M, Greenson J, Winter J, Smith M, Rogers SJ, Webb SJ. 2012. Early
behavioral intervention is associated with normalized brain activity in
young children with autism. J Am Acad Child Adolesc Psychiatry
51:1150–1159.
de Gelder B. 1987. On not having a theory of mind. Cognition 27:285–
290.
Depienne C, Moreno-De-Luca D, Heron D, Bouteiller D, Gennetier A,
Delorme R, Chaste P, Siffroi JP, Chantot-Bastaraud S, Benyahia B,
Trouillard O, Nygren G, Kopp S, Johansson M, Rastam M, Burglen L,
Leguern E, Verloes A, Leboyer M, Brice A, Gillberg C, Betancur C. 2009.
Screening for genomic rearrangements and methylation abnormalities of
the 15q11-q13 region in autism spectrum disorders. Biol Psychiatry
66:349–359.
Dyck MJ, Ferguson K, Shochet IM. 2001. Do autism spectrum disorders
differ from each other and from non-spectrum disorders on emotion
recognition tasks? Eur Child Adolesc Psychiatry 10:105–116.
Fadiga L, Craighero L. 2003. New insights on sensorimotor integration:
From hand action to speech perception. Brain Cogn 53:514–524.
Fein D, Pennington B, Markowitz P, Braverman M, Waterhouse L. 1986.
Toward a neuropsychological model of infantile autism: Are the social
deficits primary? J Am Acad Child Psychiatry 25:198–212.
Feng J, Schroer R, Yan J, Song W, Yang C, Bockholt A, Cook EH Jr, Skinner
C, Schwartz CE, Sommer SS. 2006. High frequency of neurexin 1beta
signal peptide structural variants in patients with autism. Neurosci Lett
409:10–13.
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
Fisch GS. 2007. Animal models and human neuropsychiatric disorders.
Behav Genet 37:1–10.
Fisch GS, Grossfeld P, Falk R, Battaglia A, Youngblom J, Simensen R. 2010.
Cognitive-behavioral features of Wolf–Hirschhorn syndrome and other
subtelomeric microdeletions. Am J Med Genet Part C 154C:417–426.
Flavell J. 1999. Cognitive development: Children’s knowledge about mind.
Annu Rev Psychol 50:21–45.
Fodor J. 1983. The modularity of mind. Cambridge, MA: MIT/Bradford
Books.
Fogassi L, Ferrari PF. 2007. Mirror neurons and the evolution of embodied
language. Curr Dir Psychol Sci 16:136–141.
Fogassi L, Ferrari PF, Gesierich B, Rozzi S, Chersi F, Rizzolatti G. Parietal
lobe: From action organization to intention understanding. Science 2005.
308:662–667.
Friedman E. 1969. The autistic syndrome and phenylketonuria. Schizo-
phrenia 10:249–261.
Frith U. 2012. The 38th Sir Frederick Bartlett Lecture: Why we need
cognitive explanations of autism. Q J Exp Psychol 65:2073–2092.
Gallagher S. 2004. Understanding interpersonal problems in autism:
Interaction theory as an alternative to Theory of Mind. Philos Psychiatry
Psychol 11:199–217.
Garfield JL, Peterson CC, Perry T. 2001. Social cognition, language
acquisition and the development of the theory of mind. Mind Lang
16:494–541.
Gernsbacher MA, Frymiare JL. 2005. Does the autistic brain lack core
modules? Division of Learning Disabilities Journal, 1:3–16.
Gesell A, Amatruda CS. 1941. Developmental diagnosis: normal and
abnormal child development. New York: Paul B. Hoeber, Inc. pp 3–25.
Goldstein MH, Schwade JA. 2008. Social feedback to infants’ babbling
facilitates rapid phonological learning. Psychol Sci 19:515–523.
Gopnik A, Astington JW. 1988. Children’s understanding of representa-
tional change and its relation to the understanding of false belief and the
appearance-reality distinction. Child Dev 59:26–37.
Gopnik A. 1993. How we know our minds: The illusion of first-person
knowledge of intentionality. Behav Brain Sci 16:29–113.
Grant CM, Grayson A, Boucher J. 2001. Using tests of false belief with
children with autism: How valid and reliable are they? Autism 5:135–145.
Grant CM, Boucher J, Riggs KJ, Grayson A. 2005. Moral understanding in
children with autism. Autism 9:317–331.
Grant CM, Apperly I, Oliver C. 2007. Is theory of mind understanding
impaired in males with fragile X syndrome? J Abnorm Child Psychol
35:17–28.
Grice HP. 1975. Logic and conversation. In: Cole R, Morgan J, editors.
Syntax and semantics: Speech acts. New York: Academic Press. pp 41–58.
Guajardo NR, Watson AC. 2002. Narrative discourse and theory of mind
development. J Genet Psychol 163:305–325.
Hala S, Chandler M, Fritz AS. 1991. Fledging theories of mind: Deception as
a marker of three-year olds’ understanding of false belief. Child Dev
62:83–97.
Hallerbäck MU, Lungnegård T, Hjärthag F, Gillberg C. 2009. The reading of
mind in the eyes test: Test-retest reliability in a Swedish population. Cogn
Neuropsychiatry 14:127–143.
Heyes CM. 1978. Theory of mind in nonhuman primates [with commen-
taries]. Behav Brain Sci 21:101–148.
Hobson RP. 1990. On acquiring knowledge about people and the capacity
to pretend: Response to Leslie (1987). Psychol Rev 97:114–121.
FISCH
Hogart A, Nagarajan RP, Patzel KA, Yasui DH, Lasalle JM. 2007. 15q11-13
GABAA receptor genes are normally biallelically expressed in brain yet are
subject to epigenetic dysregulation in autism-spectrum disorders. Hum
Mol Genet 16:691–703.
Iacoboni M, Molnar-Szakacs I, Gallese V, Buccino G, Mazziotta JC,
Rizzolatti G. 2005. Grasping the intentions of others with one’s own
mirror system. PLoS Biology 3:0529–0535.
Jamain S, Quach H, Betancur C, Råstam M, Colineaux C, Gillberg IC,
Soderstrom H, Giros B, Leboyer M, Gillberg C, Bourgeron T, Paris
Autism Research International Sibpair Study. 2003. Mutations of the X-
linked genes encoding neuroligins NLGN3 and NLGN4 are associated
with autism. Nat Genet 34:27–29.
Jarrold C, Smith P, Boucher J, Harris P. 1994. Comprehension of pretense
in children with autism. J Autism Dev Disord 24:433–455.
Jarrold C, Mansergh R, Whiting C. 2010. The representational status of
pretence: Evidence from typical development and autism. Br J Dev
Psychol 28:239–254.
Kaminski J, Call J, Tomasello M. 2008. Chimpanzees know what others
know, but not what they believe. Cognition 109:224–234.
Kanner L. 1943. Autistic disturbances of affect contact. Nervous Child
2:217–250.
Kanner L. 1949. Problems of nosology and psychodynamics of early
infantile autism. Am J Orthopsychiatry 19:416–426.
Klin A, Volkmar FR, Sparrow SS. 1992. Autistic social dysfunction: Some
limitations of the theory of mind hypothesis. J Child Psychol Psychiatry
33:861–876.
Kobayakawa M, Tsuruya N, Kawamura M. 2012. Theory of mind im-
pairment in adult-onset myotonic dystrophy type 1. Neurosci Res
72:341–346.
Kobayashi C, Glover GH, Temple E. 2007. Cultural and linguistic effects on
neural bases of ‘Theory of Mind’ in American and Japanese children.
Brain Res 1164:95–107.
Köhler W. 1925. The mentality of apes. London: Routledge and Kegan Paul.
Koochek M, Harvard C, Hildebrand MJ, Van Allen M, Wingert H,
Mickelson E, Holden JJ, Rajcan-Separovic E, Lewis ME. 2006. 15q
duplication associated with autism in a multiplex family with a familial
cryptic translocation t(14;15)(q11.2;q13.3) detected using array-CGH.
Clin Genet 69:124–134.
Laumonnier F, Bonnet-Brilhault F, Gomot M, Blanc R, David A, Moizard
MP, Raynaud M, Ronce N, Lemonnier E, Calvas P, Laudier B, Chelly J,
Fryns JP, Ropers HH, Hamel BC, Andres C, Barthélémy C, Moraine C,
Briault S. 2004. X-linked mental retardation and autism are associated
with a mutation in the NLGN4 gene, a member of the neuroligin family.
Am J Hum Genet 74:552–557.
Leekam SR, Perner J. 1991. Does the autistic child have a metarepresenta-
tional deficit? Cognition 40:203–218.
Leslie AM. 1987. Pretense and Representation: The origins of “Theory of
Mind. Psychological Review 94:412–426.
Leslie AM, Frith U. 1987. Metarepresentation and autism: How not to lose
one’s marbles. Cognition 27:291–294.
Leslie AM, Frith U. 1990. Prospects for a cognitive neuropsychology of
autism: Hobson’s choice. Psychol Rev 97:122–131.
Levy SE, Mandell DS, Schultz RT. 2009. Autism. Lancet 374:1627–1638.
Lewis V, Boucher J. 1988. Spontaneous, instructed and elicited play in
relatively able autistic children. Br J Dev Psychol 6:325–339.
Lillard AS. 1997. Other folks’ theories of mind and behavior. Psychol Sci
8:268–274.
2479
Lillard AS. 1998a. Ethnopsychologies: Cultural variations in theory of
mind. Psychol Bull 123:3–32.
Lillard A. 1998b. Theories behind theories of mind. Hum Dev 41:40–46.
Martı́n-Rodriguez JF, León-Carrión J. 2010. Theory of mind deficits in
patients with acquired brain injury. Neuropsychologia 48:1181–1191.
Mayes LC, Klin A, Tercyak KP Jr, Cicchetti DV, Cohen DJ. 1996. Test-retest
reliability for false-belief tasks. J Child Psychol Psychiatry 37:313–319.
McGraw MB. 1943. The neuromuscular maturation of the infant. New
York: Columbia University Press. pp 3–23.
Melis AP, Call J, Tomasello M. 2010. 36-month-olds conceal visual and
auditory information. Dev Sci 13:479–489.
Miller CA. 2001. False belief understanding in children with specific
language impairment. J Commun Disord 34:73–86.
Minshew NJ, Sung K, Jones B, Furman JM. 2004. Underdevelopment of the
postural control system in autism. Neurology 63:2056–2061.
Minshew NJ, Scherf KS, Behrmann M, Humphreys K. 2011. Autism as a
developmental neurobiological disorder: New insights from functional
imaging. In: Amaral DG, Dawson G, Geschwind DH, editors. Autism
spectrum disorders. Oxford: Oxford University Press. pp 632–650.
Minter M, Hobson RP, Bishop M. 1998. Congenital visual impairment and
‘theory of mind’. Br J Dev Psychol 16:183–196.
Muller F, Simion A, Reviriego E, Galera C, Mazaux J-M, Joseph P-A. 2010.
Exploring theory of mind after severe traumatic brain injury. Cortex
46:1088–1099.
Onishi KH, Baillargeon R. 2005. Do 15-month-old infants understand false
beliefs? Science 308:255–258.
Osterling J, Dawson G. 1994. Early recognition of children with autism: A
study of first birthday home videotapes. J Autism Dev Disord 24:247–257.
Ozonoff S, Pennington BF, Rogers SJ. 1991. Executive function deficits in
high-functioning autistic individuals: Relationship to theory of mind. J
Child Psychol Psychiatry 32:1081–1105.
Penn DC, Povinelli DJ. 2007. On the lack of evidence that non-human
animals possess anything remotely resembling a ‘theory of mind’. Philos
Trans R Soc B 362:731–744.
Perner J. 1991. Understanding the representational mind. Cambridge, MA:
MIT Press.
Perner J, Frith U, Leslie AM, Leekam SR. 1989. Exploration of the autistic
child’s theory of mind: Belief, and communication. Child Dev 60:689–
700.
Peterson CC, Siegal M. 1995. Deafness, conversation and theory of mind. J
Child Psychol Psychiatry 36:459–474.
Peterson CC, Siegal M. 1999. Representing inner worlds: Theory of mind in
autistic, deaf, and normal hearing children. Psychol Sci 10:126–129.
Peterson CC, Slaughter V. 2009. Theory of Mind (ToM) in children with
autism or typical development: Links between eye-reading and false-
belief understanding. Res Autism Spectr Disord 3:462–473.
Poletti M, Enrici I, Bonuccelli U, Adenzato M. 2011. Theory of mind in
Parkinson’s disease. Behav Brain Res 219:342–350.
Porter MA, Coltheart M, Langdon R. 2008. Theory of mind in Williams
syndrome assessed using a nonverbal task. J Autism Dev Disord 38:806–
814.
Povinelli DJ, Eddy TJ. 1996. What young chimpanzees know about seeing.
Monogr Soc Res Child Dev 61:1–152
Premack D, Woodruff G. 1978. Does the chimpanzee have a theory of
mind? Behav Brain Sci 4:515–526.
2480
Premack D, Woodruff G. 1979. Chimpanzee problem comprehension:
Insufficient evidence. Science 206:1201–1202.
Prior M, Dahlstrom B, Squires TL. 1990. Autistic children’s knowledge of
thinking and feeling states in other people. J Child Psychol Psychiatry
31:587–601.
Pylyshyn ZW. 1978. When is attribution of beliefs justified? Behav Brain Sci
1:592–593.
Reddy V, Morris P. 2004. Participants don’t need theories: Knowing minds
in engagement. Theory Psychol 14:647–665.
Repacholi BM, Gopnik A. 1997. Early reasoning about desires: Evidence
from 14- and 18-month-olds. Dev Psychol 33:12–21.
Rizzolatti G, Arbib MA. 1998. Language within our grasp. Trends in
Neurosciences 21:188–194.
Rizzolatti G, Fadiga L, Gallese V, Fogassi L. 1996. Premotor cortex and the
recognition of motor actions. Brain Res Cogn Brain Res 3:131–141.
Rizzolatti G, Fogassi L, Gallese V. 2001. Neurophysiological mechanisms
underlying the understanding and imitation of action. Nat Rev Neurosci
2:661–670.
Rogers S. 2009. What are infants teaching us about autism in infancy?
Autism Res 2:125–137.
Sato D, Lionel AC, Leblond CS, Prasad A, Pinto D, Walker S, O’Connor I,
Russell C, Drmic IE, Hamdan FF, Michaud JL, Endris V, Roeth R,
Delorme R, Huguet G, Leboyer M, Rastam M, Gillberg C, Lathrop M,
Stavropoulos DJ, Anagnostou E, Weksberg R, Fombonne E, Zwaigen-
baum L, Fernandez BA, Roberts W, Rappold GA, Marshall CR, Bour-
geron T, Szatmari P, Scherer SW. 2012a. SHANK1 deletions in males with
autism spectrum disorder. Am J Hum Genet 90:879–887.
Sato W, Toichi M, Uono S, Kochiyama T. 2012b. Impaired social brain
network for processing dynamic facial expressions in autism spectrum
disorders. BMC Neurosci 1313:99.
Savage-Rumbaugh ES, Rumbaugh D, Boysen S. 1978. SArah’ problems of
comprehension. Behav Brain Sci 4:555–557.
Searle JR. 1990. Consciousness, explanatory inversion, and cognitive
science [target article]. Behav Brain Sci 13:585–642.
Shahaeian A, Peterson CC, Slaughter V, Wellman HM. 2011. Culture and
the sequence of steps in theory of mind development. Dev Psychol
47:1239–1247.
Sharrock W, Coulter J. 2004. ToM A critical commentary. Theory Psychol
14:579–600.
Shrout PE. 1998. Measurement reliability and agreement in psychiatry. Stat
Meth Med Res 7:301–317.
Skafidas E, Testa R, Zantomio D, Chana G, Everall IP, Pantelis C. 2012.
Predicting the diagnosis of autism spectrum disorder using gene pathway
analysis. Mol Psychiatry Sep 11 [Epub ahead of print].
Smalley SL. 1991. Genetic influences in autism. Psychiatr Clin N Am
14:125–139.
AMERICAN JOURNAL OF MEDICAL GENETICS PART A
Sparrevohn R, Howie PM. 1995. Theory of mind in children with autistic
disorder: Evidence of developmental progression and the role of verbal
ability. J Child Psychol Psychiatry 36:249–263.
Stone VE, Gerrans P. 2006. What is domain-specific about theory of mind?
Soc Neurosci 1:309–319.
Surian L, Caldi S, Sperber D. 2007. Attribution of beliefs by 13-month-old
infants. Psychol Sci 18:580–586.
Tardif T, Wellman HM, Cheung KM. 2004. False belief understanding in
Cantonese-speaking children. J Child Lang 31:779–800.
Volkmar FR. 2011. Understanding the social brain in autism. Dev Psycho-
biol 53:428–434.
Vonèche J, Vidal F. 1985. Jean Piaget and the child psychologist. Synthese
65:121–138.
Voracek M, Dressler SG. 2006. Lack of correlation between digit ratio
(2D:4D) and Baron-Cohen’s “Reading the Mind in the Eyes” test,
empathy, systematizing, and autism-spectrum quotients in a general
population sample. Pers Individ Differ 41:1481–1491.
Vorstman JA, Ophoff RA. 2013. Genetic causes of developmental disorders.
Curr Opin Neurol 26:128–136.
Vorstman JA, Morcus ME, Duijff SN, Klaassen PW, Heineman-de Boer JA,
Beemer FA, Swaab H, Kahn RS, van Engeland H. 2006. The 22q11.2
deletion in children: High rate of autistic disorders and early onset
of psychotic symptoms. J Am Acad Child Adolesc Psychiatry 45:1104–
1113.
Wahi S, Johri R. 1994. Questioning a universal theory of mind: Mental-real
distinctions made by Indian children. J Genet Psychol 155:503–510.
Williams BT, Gray KM, Tonge BJ. 2012. Teaching emotion recognition
skills to young children with autism: A randomized controlled trial of
an emotion training programme. J Child Psychol Psychiatry 53:1268–
1276.
Wimmer H, Perner J. 1983. Beliefs about beliefs: Representation and
constraining function of wrong beliefs in young children’s understanding
of deception. Cognition 13:103–128.
Yanagi K, Kaname T, Wakui K, Hashimoto O, Fukushima Y, Naritomi K.
2012. Identification of four novel synonymous substitutions in the X-
linked genes neuroligin 3 and neuroligin 4X in Japanese patients with
autistic spectrum disorder. Autism Res Treat ID724072:1–5.
Yirmiya N, Erel O, Shaked M, Solomonica-Levi D. 1998. Meta-analyses
comparing theory of mind abilities of individuals with mental retarda-
tion, and normally developing individuals. Psychol Bull 124:283–307.
Zelazo PD, Burack JA, Benedetto E, Frye D. 1996. Theory of mind and rule
use in individuals with Down’s syndrome: A test of the uniqueness and
specificity claims. J Child Psychol Psychiatry 37:479–484.
Zielinski BA, Anderson JS, Froehlich AL, Prigge MB, Nielsen JA, Cooper-
rider JR, Cariello AN, Fletcher PT, Alexander AL, Lange N, Bigler ED,
Lainhart JE. 2012. scMRI reveals large-scale brain network abnormalities
in autism. PLoS ONE 7:e49172.
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