REVIEW ARTICLE

Self–Other Relations in Social Development and Autism: Multiple Roles

for Mirror Neurons and Other Brain Bases
Justin H.G. Williams

Mirror neuron system dysfunction may underlie a self–other matching impairment, which has previously been suggested
to account for autism. Embodied Cognition Theory, which proposes that action provides a foundation for cognition has
lent further credence to these ideas. The hypotheses of a self–other matching deficit and impaired mirror neuron
function in autism have now been well supported by studies employing a range of methodologies. However, underlying
mechanisms require further exploration to explain how mirror neurons may be involved in attentional and mentalizing
processes. Impairments in self–other matching and mirror neuron function are not necessarily inextricably linked and it
seems possible that different sub-populations of mirror neurons, located in several regions, contribute differentially to
social cognitive functions. It is hypothesized that mirror neuron coding for action–direction may be required for
developing attentional sensitivity to self-directed actions, and consequently for person-oriented, stimulus-driven
attention. Mirror neuron networks may vary for different types of social learning such as ‘‘automatic’’ imitation and
imitation learning. Imitation learning may be more reliant on self–other comparison processes (based on mirror neurons)
that identify differences as well as similarities between actions. Differential connectivity with the amygdala–orbitofrontal
system may also be important. This could have implications for developing ‘‘theory of mind,’’ with intentional self–other
comparison being relevant to meta-representational abilities, and ‘‘automatic’’ imitation being more relevant to
empathy. While it seems clear that autism is associated with impaired development of embodied aspects of cognition, the
ways that mirror neurons contribute to these brain–behavior links are likely to be complex.

Keywords: autism; autistic disorder; Asperger’s syndrome; imitation; gaze; attention; motor control; perception; action;
mirror neurons; fMRI; parietal cortex; Broca’s area; pSTS; ‘theory of mind’ (TOM)

Introduction Consequent upon this, many of the issues raised by

Experimental neuroscience has burgeoned in the last decade
as a result of technologies that permit even more detailed
and direct measurement of brain function. Hypotheses that
explain psychopathology in terms of brain function can now
be tested directly. The ‘‘mirror neuron hypothesis of autism’’
is one example [Williams, Whiten, Suddendorf, & Perrett,
2001, discussed in detail below], advanced following the
discovery of mirror neurons in the F5 area [Gallese, Fadiga,
Fogassi, & Rizzolatti, 1996], and later in the inferior parietal
area [Fogassi et al., 2005], of the macaque monkey brain.
These neurons fire not only when an action toward an object
is executed but also when the same action is observed. The
role of these neurons in the evolution of human cognition
and social behavior has been subject to widespread specula-
tion [Rizzolatti & Craighero, 2004]. The last 7 years have seen
a great expansion in our knowledge both of mirror neurons
themselves, and the functions of the brain areas in which
they are located. The mirror neuron hypothesis of autism has
also received considerable attention [Iacoboni & Dapretto,
2006; Oberman & Ramachandran, 2007].
Williams et al. [2001] have been clarified and a review of
the hypothesis is timely. Before doing so, thought needs
to be given to an assertion made by Williams et al. [2001]
that mirror neuron dysfunction could be the single
primary deficit that explains the behavioral picture that
characterizes autism in all of its many presentations.
Arguing for this position (as to argue for any single
neurological primary deficit) risks being unproductive in
the longer term. Complex cognitive functions, such as
those that serve social interaction, depend upon net-
works of many component parts. To try and ascribe a
more central role to the mirror neuron system, than to,
for example, the amygdala, forces the debate to focus on
the question of whether one aspect of brain anatomy is
more important than another in the causation of autism.
If both are important and autism arises from deficits in
either one or other component or the connections
between them, such a contention would be unhelpful.
It may therefore be more fruitful to ask what contribution
(if any) a specific neurobiological process might make to the
development of those cognitive functions that are impaired

From the Department of Child Health, University of Aberdeen Medical School, Royal Aberdeen Children’s Hospital, Aberdeen, UK (J.H.G.W)
Received December 10, 2007; revised March 5, 2008; accepted 2 April 2008
Address for correspondence and reprints: Justin H.G. Williams, Department of Child Health, University of Aberdeen Medical School, Royal Aberdeen
Children’s Hospital, Aberdeen AB25 2ZG, UK. E-mail: justin.williams@abdn.ac.uk
Grant Sponsor: Northwood Charitable Trust.
Published online in Wiley InterScience (www. interscience.wiley.com)
DOI: 10.1002/aur.15
& 2008 International Society for Autism Research, Wiley Periodicals, Inc.

INSAR Autism Research 1: 73–90 2008 73

in autism. This requires the combination and interaction of
top-down and bottom-up approaches. From the top-down
position we can look at the behavioral picture of autism
and try to understand the cognitive functions that are
affected. Then, from the bottom-up position, we can ask
how a specific neurobiological process (in this case the
mirror neuron system) contributes to those cognitive
functions, and whether the specific neurobiological process
is disrupted in autism.
Taking this approach, the mirror neuron/self–other
matching theory of autism generates many testable
hypotheses that can be grouped into two separate levels:
the cognitive (or general) level and the neurobiological (or
specific) level. The form at the cognitive level was largely set
out by Rogers and Pennington [1991], based on a self–other
matching deficit. Although they suggest that a deficit in
praxis may underlie the self–other matching deficit,
validation of their theory is not dependent upon the
involvement of a specific neural substrate. The hypothesis
at the neurobiological level [Williams et al., 2001] requires
both that mirror neuron function in itself is disrupted in
autism, and also that this results in impairment of
self–other matching. These two levels of hypotheses are
linked but not inextricably so. It is possible that the mirror
neuron function can be impaired without it affecting
self–other matching, or that self–other matching can be
impaired without the mirror neuron function being
disrupted. As the evidence accumulates and is re-examined,
it is likely to be necessary to revise our understanding of the
systems involved, namely the cognitive function served by
self–other matching, what we understand to be the
contribution of the mirror neuron system to that cognitive
function and/or what we understand to be the contribution
of the mirror neuron system to other cognitive functions
that are impaired in autism. With constant re-examination
of the evidence, a program of research can evolve that may
contribute more fruitfully to our understanding of both
autism and social cognitive development more generally.
This article reviews the current evidence and is presented
in the following manner: Part I considers the background to
the cognitive and neurobiological hypotheses; Part II
examines tests of both cognitive and neurobiological
hypotheses; Part III is an evaluation of the evidence for
mirror neuron function in humans, particularly with
reference to their role in the cognitive functions impaired
in autism; Part IV discusses the consequent cognitive
hypothesis; finally Part V presents a summary and revised
perspective of how mirror neurons and self–other matching
may contribute to the deficits observed in autism.
Part I: Background
What are Mirror Neurons?
Mirror neurons are defined by their function: firing when
an action is observed but also when that same action is
74 Williams/Mirror neurons in autism
executed. On its own, the notion that self–other match-
ing is served by mirror neurons carries a degree of
tautology; it carries a risk of trying to explain a function
in terms of itself. The ‘‘action’’ aspect of the definition is
therefore a crucial component. ‘‘Mirror neurons’’ are
those neurons in premotor and parietal association
cortex (intraparietal sulcus—IPS), which converging
evidence points to as having mirror properties for the
observation and execution of action. This is the ‘‘core’’
mirror neuron system [Oztop & Arbib, 2002]. The
posterior superior temporal sulcus provides visual input
into the mirror neurons via the temporo-parietal junc-
tion (TPJ) and so these areas form an important part of
the ‘‘mirror neuron system’’ as a whole.
The Neurobiological (Mirror Neuron) Hypothesis of Autism
The discovery of mirror neurons led Williams et al. [2001]
to propose a revision of Rogers and Pennington’s [1991]
self–other translation model (discussed below). Their
argument at that time consisted of several points, which
are summarized here:
1 Autism is characterized by developmental
impairments in imitation, joint attention and
mental state representation. It is associated
with developmental coordination disorder
and language delay.
2 The ‘‘theory of mind’’ (ToM) deficit in autism
cannot be explained as resulting from a
deficit in false-belief understanding because it
develops before false-belief understanding
develops. An earlier developmental process
that underpins development of false-belief
understanding is more likely to be important.
3 A simulation ‘‘ToM’’ (representing another’s
mental state by imagining one’s self ‘‘in
another’s shoes’’) may develop on the basis
of an intact self–other matching function.
Understanding another’s intentions in the
context of memory allows for ‘‘retrodiction’’
of associated thoughts and memories.
4 Mirror neurons can serve a self–other match-
ing function for action coding. They also code
for the relationship between a goal and an
object, allowing for formation of intentional
representations.
5 Dysfunction of mirror neuron modulation
(perhaps disinhibition) could explain both
overactive copying in the case of echolalia
and also failure to generate covert or ‘‘off-
line’’ imitation. This latter function may be
necessary to develop ‘‘ToM.’’
INSAR
 6 Autism does not necessarily involve language aspects of action [Perra et al., 2008; Smith & Bryson,
impairment, suggesting that impairment of 2007], although not all agree [Hamilton, Brindley, &
‘‘mirroring’’ function in one domain (e.g. Frith, 2007; Vanvuchelen, Roeyers, & De Weerdt, 2007].
social reciprocity) does not necessarily require
impairment in another (e.g. language). Sepa- Embodied Cognition
rate ‘‘mirror neuron’’ networks may serve
The hypothesis that autism stems from a deficit in a
gaze and language.
mechanism that serves to match codings for action
7 There may also be separate mirror neurons between motor and perception domains is based on a
for other functions, most particularly joint more general principle that certain aspects of cognition
attention. There might also be neurons with are founded upon action, encapsulated by theories of
‘‘mirror’’ properties in the region of the ‘‘embodied cognition.’’ Embodied theories of cognition
superior temporal sulcus. [Niedenthal, Barsalou, Winkielman, Krauth-Gruber, &
Ric, 2005] view the processes of knowledge use and
The Self–Other Matching (Cognitive) Hypothesis acquisition as fundamentally grounded in their physical
context and the brain’s modality-specific systems. This
The origins of the self–other matching hypothesis of
means that those cognitive operations that are heavily
autism may be traced back to the first paper published on
influenced by both action plans and emotional states
the imitation impairment [Ritvo & Provence, 1953], just
come to function within the biological environment of
10 years after Kanner [1943] had published his seminal
the brain that serves action plans and emotional states.
paper on autism. Over the following decades this was
An example of embodied cognition would be found in a
followed by many now well-reviewed studies showing
model of empathy. When we observe emotions being
that children with autism did not imitate [Rogers, 1999;
expressed by others we may not only feel them ourselves
Rogers & Williams, 2006; Smith & Bryson, 1994;
but also express them in our actions by making subtle
Williams, Whiten, & Singh, 2004]. Rogers and Penning-
facial movements that can be detected using electromyo-
ton [1991] conducted an influential review that found
graphy [Hietanen, Surakka, & Linnankoski, 1998; Surakka
strong evidence for the existence of a deficit affecting
& Hietanen, 1998]. Empathy cannot be separated from
imitation of simple body movements as well as symbolic
the action-based systems that serve the experience and
imitation. Using Stern’s [1985] model of interpersonal
expression of emotion.
development, Rogers and Pennington suggested that a
Klin, Jones, Schultz, and Volkmar [2003] have ad-
biological impairment in autism restricted the capacity of
vanced an embodied cognitive model of autism, termed
the infant to ‘‘form and co-ordinate social representa-
the ‘‘enactive mind’’ (EM) approach. This construes the
tions of self and other at increasingly complex levels via
mind as an active entity that shapes itself as a result of
amodal or cross-modal representational processes.’’ They
solving problems experienced in the environment. The
hypothesized that a primary deficit in such a capacity
developing child’s actions are guided by perceptions,
would lead to a cascade of effects including impaired
which in turn are driven by attentional demands related
imitation, social, communicative and affective skills and
to social needs. The emphasis of their EM approach is on
that a deficit of praxis involving the prefrontal–limbic
perception and visual attention. In contrast, self–other
neural system could form the basis for this impairment.
matching theory considers cognitive development to be
Smith and Bryson’s [1994] review of 15 studies
grounded in systems that serve action. However, there is
hypothesized that the imitative deficit associated with
clearly cross-over, as both theories consider the develop-
autism could be due in part to impairment in the
ment of attentional control to be grounded in visuo-
perceptual organization of movements, manifesting in
motor systems that require cross-modal influences. A
an abnormal representation of actions. Increasingly
further essential component of the ‘‘self–other match-
sophisticated studies over the following decade demon-
ing’’ model of autism is its focus on detection of
strated imitation impairment in very young children
similarities and differences between self and other
with autism [Charman et al., 1997] and those with milder
[Pennington, Rogers, & Williams, 2006].
degrees of autism [Rogers, Bennetto, McEvoy, & Penning-
ton, 1996]. The impairment appeared to affect gesture
particularly [Roeyers, Van Oost, & Bothuyne, 1998] and
Part II: Tests of the Mirror Neuron Hypothesis of
interestingly, also, imitation of action ‘‘style’’ [Hobson &
Autism
Lee, 1999], though differences in controlling for task Tests of the Neurobiological Hypothesis
difficulty between gesture and action-on-object make it
difficult to judge whether specific aspects of imitation are Several studies using different methodologies have now
affected. The most recent studies support the hypothesis tested the mirror neuron hypothesis of autism. Nishitani,
that the imitation deficit concerns representational Avikainen, and Hari [2004] studied a mixed sex group of

INSAR Williams/Mirror neurons in autism 75

adults with Asperger’s syndrome. Subjects imitated still
images of orofacial gestures that were projected onto a
screen, while brain activity and lip movements were
recorded using magnetoencephalography and electro-
myograms (EMG). There was no difference in the delay
before which mouth movement started in each group,
but curiously EMGs lasted almost twice as long for the
autism spectrum disorder (ASD) group. In the control
group imitation was associated with activation in
occipital, inferior parietal, superior temporal and Broca’s
areas bilaterally. In the ASD group, several individuals
failed to activate Broca’s area on one or both sides. The
results of this study are consistent with those of Dapretto
et al. [2006]). They used functional magnetic resonance
imaging (fMRI) to examine differences in brain activity
between 10 children with autism and 10 controls (aged
about 12 yrs, normal IQ) imitating facial expressions
while in the scanner. They found no difference in
imitation abilities outside of the scanner but reduced
activity in Broca’s area inside the scanner. Most striking,
activity in Broca’s area correlated with the severity of
autism as measured on the social subscales of the ADI-R
[Lord, Rutter, & Lecouteur, 1994] and ADOS-G [Lord
et al., 2000].
The next question, for both studies, is whether group
differences were mediated by specific problems with
self–other matching (imitation). A possibility not yet
excluded is that group-wise effects reflect other differ-
ences between conditions, such as those that relate to the
attention or the direction of action. Unfortunately,
neither study benefited from having control tasks, which
might have shown that the group difference was
confined to the copying element of the task.
An effect of direction is suggested in a further study of
mirror neuron function in autism by Theoret et al.
[2005]. They also found impaired Broca’s area function
during action observation but suggest that the effect is
specific to the directional context in which the action is
performed. Theoret et al. drew on the methodology
originally used by Fadiga et al. [1999] that provided some
of the most compelling evidence for ‘‘mirror neurons’’ in
humans. Transcranial magnetic resonance stimulation
evokes activity within premotor cortex, which can then
be detected through its effects on myoelectrical activity
in the hand. Fadiga et al. showed that observation of an
action supplemented this activity but, importantly,
activity was only supplemented in the muscles involved
in the action being observed. Theoret et al. repeated the
technique in individuals with autism and controls. They
found expected patterns in controls; action observation
increased the motor-evoked potentials (MEP). In the 10
adult participants with Asperger’s syndrome, some action
observation supplemented the MEP but whether it did so
depended upon the direction of the action. Only actions
performed toward the observer were supplemented.
76 Williams/Mirror neurons in autism
One other fMRI study has examined imitation in
autism. Williams et al. [2006] used the protocol published
by Iacoboni et al. [1999] to examine neural correlates of
imitation in a group of normal IQ adolescent males with
autism. They found differences in the parietal lobe but
not in Broca’s area. The group differences were less
dramatic than those described by Dapretto et al. [2006],
perhaps because of the very simple and less social nature
of the imitation task. Engagement of parietal rather than
ventral premotor cortex may have occurred because the
task involved hand rather than facial imitation. This
study also highlighted other group differences that could
shed light on the imitation impairment in autism,
including differential activity in the amygdala across
several conditions, and also in a location within the
posterior aspect of the superior temporal sulcus (pSTS)
region, in the imitation vs. observation contrast. In
controls, the pSTS region was clearly active during
imitation but hardly active during observation. The
reverse was the case for the autism group. As pSTS
provides visual input into the mirror neuron system, this
study suggested that imitation in autism is associated
with greater dysfunction of other structures supporting
the core mirror neuron system, than of the core
components themselves.
Mu-wave suppression. Electroencephalography is
another useful tool in the investigation of the ‘‘mirror
neuron’’ impairment in autism. The mu rhythm is
detected over the premotor cortex and decreases during
preparation of motor actions. It is thought to reflect
down-stream modulation of motor neuron cells by the
premotor cortex [Pineda, 2005]. A link between the mu
rhythm and ‘‘mirror neurons’’ was first suggested by
Altschuler, Vankov, Wang, Ramachandran, and
Pineda, [1997]. Oberman et al. [2005] demonstrated
reduced mu-wave suppression during autism
when actions are observed, but not during action
following instruction. Again, or whether the effect was
specific to self–other matching was not demonstrated.
However, this finding has been replicated by Bernier,
Dawson, Webb, and Murias [2007], who found that
impairment correlated with degree of impaired
imitation ability. These results are consistent with those
mentioned previously, which showed decreased activity
in the ventral premotor cortex during imitation. These
data thus support the hypothesis that mirror neuron
function is impaired in autism, in a manner that relates
closely to imitation ability.
Structural neuroimaging. The mirror neuron
regions do not have a specific cytoarchitecture or
predefined area, so it has been difficult for structural
neuroimaging studies to look at whether they show
altered volume in autism. Nevertheless, decreased
cortical thickness in the mirror neuron regions in
both the parietal and ventral premotor cortex in autism
has been demonstrated [Hadjikhani, Joseph, Snyder, &
INSAR
Tager-Flusberg, 2006]. Furthermore, in a later study,
Hadjikhani, Joseph, Snyder, & Tager-Flusberg [2007]
found that decreased thickness of the inferior frontal
gyrus in autism was associated with decreased BOLD
signal in this area during face processing. Less directly,
several studies have shown decreased white matter
connectivity in autism [Barnea-Goraly et al., 2004;
Keller, Kana, & Just, 2007; McAlonan et al., 2005;
Waiter et al., 2005], raising the possibility that impaired
mirror neuron function in autism could be explained by
deficits in connectivity between elements of the network
[Minshew & Williams, 2007].
Functional imaging of ToM. If mirror neurons
are important for ToM, it might be that an appropriate
test of the mirror neuron hypothesis of autism would
be to measure mirror neuron activity in ToM studies.
At present there is little evidence for specifically reduced
mirror neuron activity in ToM in autism. The neural
substrate for ToM and other mental state attribution,
such as empathy, has now been well investigated
and reviewed [Amodio & Frith, 2006; Frith & Frith,
2003]. ToM is served by three brain areas: the medial
prefrontal cortex, posterior STS and the temporal pole.
Studies of empathy have highlighted roles of anterior
cingulate, temporal pole and insula [Singer et al., 2004;
de Vignemont & Singer, 2006; Vollm et al., 2006; Wicker
et al., 2003].
Gallese, Keysers, and Rizzolatti [2004] have argued
that the insula is part of the mirror neuron system
as it may also serve to match for actions, and therefore
mirror neurons are important for empathy. There is
perhaps a stronger case for a more general role of
mirror neurons in ToM. ToM is considered by some to
be served by cognitive function that is specific to it
(‘‘domain-specific’’ function), which requires separation
from other ‘‘domain-general’’ functions, which may also
include memory and executive function, but which
may nevertheless be vital to ToM development [Perner,
Aichhorn, Kronbichler, Staffen, & Ladurner, 2006;
Saxe & Baron-Cohen, 2006; Saxe, Schulz, & Jiang,
2006]. Therefore, as will be discussed later, mirror
neurons may be very important for ToM, but by serving
a domain-general function. In support of this position,
fMRI studies of ToM in autism have found differences in
activity in STS and Broca’s area [Baron-Cohen et al., 1999;
Castelli, Frith, Happe, & Frith, 2002] suggesting that the
mirror neuron system may be underactive during ToM
function in autism. Baron-Cohen et al. [2006] reported
(as a preliminary finding) that Broca’s area showed
reduced activity during an empathic task in parents of
children with autism compared to control parents, and
also that this area was less active in male controls
compared to female controls. Thus, they suggest that
this area could be hypermasculinized in autism. Most
recently, Pfeifer, Iacoboni, Mazziotta, & Dapretto [2008]
have also shown a close relationship between activity in
Broca’s area during observation and imitation of
INSAR Williams/Mirror neurons in autism
emotional expression, and measures of empathic ability
in children.
Recent Tests of the Cognitive (Self–Other Matching)
Hypothesis
This section reviews some of the ways that the self–other
matching hypothesis has been tested in autism besides
tests for imitation impairment, which have been recently
reviewed elsewhere [see above and Rogers & Williams,
2006; Williams et al., 2004].
Emotional contagion. A number of recent studies
have explored the role of facial mimicry in autism. In an
early study, Platek, Critton, Myers, & Gallup [2003] found
reduced contagious yawning in a group of individuals
with ‘‘schizoid personality traits.’’ It is possible that a
proportion of these participants had ASD. More recently,
Senju et al. [2007] found that children with autism were
less prone to contagious yawning than controls.
McIntosh, Reichmann-Decker, Winkielman, and
Wilbarger [2006] found that people with autism showed
a reduced electromyographic response in their facial
muscles when observing facial expressions but no
decrease in activity during intentional expressions.
These studies demonstrate that perceived facial
expression has a reduced power to evoke spontaneous
facial expression in autism. However, a lack of
spontaneous facial muscular activity in autism is well
known, perhaps resulting from an impairment at the
level of the brainstem [Rodier, 2002]. It therefore remains
unclear whether reduced emotional contagion effects are
the result of a self–other matching deficit or
nonspecifically reduced levels of tonic stimulation to
facial musculature.
Automatic imitation. Recently, a very interesting
study by Cattaneo et al. [2007] used similar methods to
McIntosh et al. [2006] by measuring electromyographic
activity during observation of an action, in muscles that
would be used were the action being imitated. However,
they looked at muscle activity that would be expected to
occur as a natural consequence of the action being
observed. Typical children, but not children with autism,
activated their jaw-opening muscles as they observed a
piece of food being grasped. The authors argue that
children with autism do not perceive intention. This may
be the case, but alternatively, children with autism may
simply not learn the same associations between actions
that are typically contingent upon one another.
Cross-modal influences. The ‘‘mirror neuron’’
hypothesis of autism predicted that there would be a
reduced McGurk effect [McGurk & MacDonald, 1976].
The McGurk effect constitutes an influence of observed
mouth movements on heard speech, so that the
perceived speech is a fusion of auditory and visual
stimuli. Williams et al. [2001] drew from Liberman’s
theory of speech perception [Liberman, Cooper,
Shankweiler, & Studdert-Kennedy, 1967; Liberman &
77
Whalen, 2000], which suggests that we hear the sounds
according to how we produce them. More recently,
mirror neurons have been shown to respond to the
sound of actions as well as the sight of them when those
actions have a characteristic sound [Gazzola, Aziz-Zadeh,
& Keysers, 2006; Kohler et al., 2002].
McGurk effect was not reduced in autism in one study
[Williams et al., 2004] but effect sizes were small and
perhaps confounded by effects in the monomodal
conditions. However, Smith and Bennetto [2007] found
reduced effect of visual speech on auditory perception in
autism. Bebko, Weiss, Demark, & Gomez, [2006]
demonstrated reduced sensitivity to temporal
asynchrony between auditory and visual linguistic
stimuli but not nonlinguistic stimuli.
Visual sensitivity to action. The pSTS (see a more
detailed discussion below) provides the visual input to
the mirror neuron system [Arbib, 2005; Iacoboni &
Dapretto, 2006; Iacoboni et al., 2001; Keysers & Perrett,
2004]. Furthermore, the pSTS is important for controlling
attention to visual stimuli and may be sensitive to input
from motor areas, which affects sensitivity to action
perception [Astafiev, Stanley, Shulman, & Corbetta, 2004;
Neri, Luu, & Levi, 2006]. Therefore, deficits in this area
may reflect dysfunction of the mirror neuron system as a
whole. Visual sensitivity to action is studied using films
displaying actions as moving light points, measuring the
ability to distinguish between genuine actions and
randomly moving light points. Moore, Hobson, and Lee
[1997] found that children with autism were as equally
sensitive to behavioral actions as controls but were less
sensitive to actions that conveyed emotions. Similarly,
Hubert et al. [2007] found that people with autism were
equally as able to label biological action content but were
less able to label emotional displays. Yet when a measure
of sensitivity not requiring discrimination between
action types was used, Blake, Turner, Smoski, Pozdol,
and Stone [2003] found that people with autism were less
sensitive to all biological motion. In this study,
impairment also correlated with autism severity. Others
[Klin, 2000; Rutherford, Pennington, & Rogers, 2006]
have detected a reduced sensitivity to animations in
autism, where two geometric objects move as apparently
autonomous agents. This has also been shown to be
associated with decreased activity in the area of the pSTS
and medial frontal cortex in autism [Castelli et al., 2002].
Joint attention in autism. Joint-attention abilities,
and particularly behaviors that concern initiation of joint
attention perhaps provide the strongest diagnostic
indicators of an autistic spectrum disorder [Mundy &
Newell, 2007]. To my knowledge there have been no
direct assessments of mirror neuron function in joint
attention in autism. However, Williams, Waiter, Perra,
Perrett, & Whiten [2005] conducted a relevant study of
‘‘joint-attention experience’’ in a group of normal
controls. They showed participants a video clip of a
moving spot and asked them to watch it. There was also a
person in the video who either watched the spot as well
78 Williams/Mirror neurons in autism
or looked elsewhere. Both conditions were associated
with activity in the region of the IPS (though not BA44),
but only watching with someone else created a joint-
attention experience. This was associated with greater
activity in the left frontal pole and the right ventromedial
frontal cortex. These findings have recently been
replicated by Bristow, Rees, and Frith [2007]. The left
frontal pole cluster was in the same location as an area of
structural difference in autism the same group [Waiter
et al., 2004] had detected previously using voxel-based
morphometry. The area is thought to serve an
‘‘information integration’’ function and has a
particularly low gray matter density [Ramnani & Owen,
2004]. Early findings therefore support the hypothesis
that the mirror neuron system is involved in joint
attention and also that the joint-attention problem in
autism stems from a self–other matching deficit.
However, as with ToM studies of empathy, areas outside
the mirror neuron system are emphasized in serving the
cognitive function most specific to joint- attention
impairment in autism.
Part III: Mirror Neurons: Contributions to Cognitive
Function
General Functional Neuroanatomy
Direct recordings of mirror neuron activity demonstrate
their presence in the monkey prefrontal cortex [area F5;
Gallese et al., 1996] and the parietal area known as ‘‘PF’’
[Fogassi et al., 2005]. Which exact areas of human brain
are homologous to these areas, is still a matter of some
debate, as the same techniques cannot be used to
demonstrate mirror neurons in humans. Neurophysiolo-
gical experiments [e.g. Fadiga et al., 1999; Hari et al.,
1998] provide experimental support in humans for effects
that could result from mirror neuron activity, but do not
provide high-resolution spatial information. fMRI has
been particularly useful (discussed below) but such
studies cannot show whether individual neurons have
specificity for particular actions or action types. Also,
since mirror neurons could have underpinned evolution
of human cognitive abilities [Whiten, 2006], new areas,
not serving a mirror function in monkeys, could have
evolved to serve this function in humans. Notwithstand-
ing these reservations, the mirror neuron system is
currently considered to be made up of neurons located
in two main areas: the ventral premotor cortex and the
inferior parietal cortex. The posterior temporal cortex is
considered integral as it provides the visual input to the
system [Iacoboni & Dapretto, 2006]. Another important
area is the superior parietal cortex [Arbib, 2008; Oztop
and Arbib, 2002].
Parietal cortex. There are several reasons why parietal
cortex may have ‘‘mirror neurons’’ that are important for
social cognition. Firstly, there is some evidence that the
human parietal cortex has expanded preferentially in
INSAR
recent evolution compared to other cortex [Astafiev
et al., 2003], suggesting that it could be important for
recently evolved social cognitive functions such as
imitation [Whiten & Byrne, 1997]. Secondly, it is
polymodal association cortex that receives and
integrates input from visual, motor and somatosensory
areas, used to plan bodily movements and to direct
attention [Grefkes & Fink, 2005; Rozzi et al., 2006].
Thirdly, lesions of the parietal cortex result in imitative
apraxia [Goldenberg, 1996]. Fourthly, Fogassi et al. [2005]
identified a population of mirror neurons in the inferior
parietal cortex of the monkey that fired differentially
whether an object was picked up to eat it or picked up to
place it elsewhere. Fogassi et al. conclude that ‘‘mirror
neurons’’ in the inferior parietal region code for
commonly observed and executed intention as well as
action itself and may serve intention representation in
the parietal lobe by matching contextual aspects of
action.
Iacoboni et al. [2005] tested a similar hypothesis in
humans, asking participants to observe video clips
showing a cup being grasped in isolation, or
in a context. The context showed whether the cup
was being grasped to be drunk from, or for cleaning up.
Additional effects of context on observing the
action were evident in inferior frontal gyrus but
not in inferior parietal cortex. Hamilton and Grafton
[2006] identified parietal activity that coded intention
by representing goals of actions. These studies highlight
differences in the relationships between actions and
goals, and actions and contexts. In Iacoboni et al. an
action’s context was used to predict its goal and
consequently its intention. In the study by Hamilton
and Grafton, the goal was determined by the position of
the object in relation to the direction of action.
Therefore, the object’s physical properties (in this case
its position in space relative to the action) or
‘‘affordances’’ [Arbib, 2005] imply the goal. It follows
that different mirror neurons may code for the
action–goal and action–context relationships.
Parietal cortex is extensive and its many functions have
been mapped most accurately in monkeys. It is divided
into inferior and superior parietal lobes by the IPS
[Grefkes and Fink, 2005]. Anterior IPS and the anterior
intraparietal area are closest to somatosensory cortex and
are active during grasping and object manipulation.
Lateral IPS serves shifts of visual attention, while medial
IPS serves planning and monitoring of reaching
movements. The ventral aspect of IPS integrates motion
processing in different sensory modalities. More caudal
aspects closer to visual cortex may process 3D object
characteristics [Shikata et al., 2003]. The function of an
area is not necessarily specific to effector, as common
areas of IPS serve looking, pointing and covert attention
[Astafiev et al., 2003]. Reciprocal connectivity with
frontal areas that include the frontal eye fields and
premotor cortex contributes to these functions. The
Oztop and Arbib [2002] model places most of the
parietal cortex outside of the mirror neuron system.
INSAR Williams/Mirror neurons in autism
More recently, Dinstein, Hasson, Rubin, & Heeger [2007]
suggest that more areas of parietal cortex serve neuron
functions in humans.
Broca’s area. The hypothesis that neurons in Broca’s
area could be important for imitation has received
support from several studies. Activity in Broca’s area is
greater during imitation than during observation or other
nonimitative action–execution conditions [Iacoboni
et al., 1999; Jackson, Meltzoff, & Decety, 2006]. Heiser
et al. [2003] found that applying transcranial magnetic
stimulation (TMS) over Broca’s area impaired reaction
times on an imitation task, but spared the control task.
Koski et al. [2002] found that imitation of a goal-directed
action was particularly associated with activation of
Broca’s area and Buccino et al. [2004] demonstrated
involvement of Broca’s area in sequential imitation.
Buccino et al. [2001] found that action observation
activated dorsal premotor cortex as well as Broca’s area.
A number of studies have questioned the role of Broca’s
area in imitation compared to other action–execution
conditions [Chaminade, Meltzoff, & Decety, 2005;
Grezes, Armony, Rowe, & Passingham, 2003; Makuuchi,
2005; Williams et al., 2006, 2007a,b]. Grezes et al. [2003]
suggested that this area may serve a less specific
action–execution function such as selecting a response
to a visual instruction. There may be several other
explanations for these conflicting results. The activity
when executed and observed actions match may not be
that much greater than when they are executed or
observed alone. Repetitive responses or stimulus
presentation may also be associated with reduced
activity. Also, Broca’s area mirror neurons may have an
important role in orienting attention to actions (see
further discussion below), resulting in greater activity
during nonimitation conditions as well as during
imitation. These confounding factors could mean that
the additional effect of self–other matching on Broca’s
area through imitation is relatively small and is only
detected by more powerful 3 T scanners.
The posterior STS. A number of features of the pSTS
make it a promising focus for research into mirror neuron
system functioning in autism. As well as being active
during imitation [Decety, Chaminade, Grezes, &
Meltzoff, 2002; Iacoboni et al., 2001], it is a
convergence point for two streams of visual processing,
deriving input from the motion-processing ‘‘MT’’ area of
visual cortex and the content-characterizing pathway of
the ventral stream [Puce & Perrett, 2003]. It also has close
connectivity with the orbitofrontal cortex (OFC) and
amygdala making it an integral part of Brothers’ social
brain [Brothers, 1990; Emory & Perrett, 2000]. Cells in the
Macaque STS respond to the sight of intentional actions
such as directed gaze and head or eye movements
[Jellema, Oram, Baker, & Perrett 2002; Jellema, Baker,
Wicker, & Perrett, 2000; Perrett et al., 1989]. In humans,
this area is active while viewing faces, mouths and eyes
[Puce, Allison, Bentin, Gore, & McCarthy, 1998] and also
during mental state representation, both intentional
79
attribution [Castelli, Happe, Frith, & Frith, 2000; Allison,
Puce, & McCarthy, 2000; Saxe & Kanwisher, 2003; Saxe
et al., 2004] and more complex meta-representation
[Gallagher et al., 2000; Vollm et al., 2006]. Roles in
action planning and visual attention are discussed below.
Social orienting and attentional control
It is possible that when attentional functions involve
social stimuli such as faces and gestures, they act
differently to when they serve other objects. Such social
attention processes include joint attention, which is
fundamental to the clinical picture of autism [Dawson
et al., 2004; Mundy & Newell, 2007]. Attention to social
stimuli is also a key component of imitation, and of the
tests of mirror neuron function reported above, which
require the participant’s attention to be drawn to a facial
expression or a gesture. This facial expression or gesture,
may, at the same time, be directed to the participant. Two
possibilities will be discussed. Firstly, that Broca’s area is
key to differentiating between social and nonsocial
attentional function, meaning that differential activity
in Broca’s area in autism, which has been reported as
evidence for mirror neuron dysfunction, could actually
be reflecting attentional rather than self–other matching
differences. However, a second possibility is that a
self–other matching function served by mirror neurons
in Broca’s area is necessary for developing this social
attentional function, which in turn has major develop-
mental implications for the way that we relate to others.
Broca’s area and visual attention. A widely
accepted model for visual attention [Corbetta &
Shulman, 2002] divides it into two processes: goal-
directed and stimulus-driven attention. Goal-directed
(or endogenous) attention is driven by ‘‘top-down’’
executive function processes and is required during
search tasks when attention is to be directed to a
previously identified object. Such attention is largely
under the control of a dorsal fronto-parietal network
(DFPN) that includes the dorsal frontal cortex (frontal eye
fields), the superior parietal lobe, the IPS and the dorsal
parietal cortex.
Stimulus-driven (exogenous) attention occurs in
response to an external stimulus, which demands
attention. An example would be a flash at the edge of a
visual field that will draw attention toward it. This
process is under the control of a right ventral fronto-
parietal network (RVPN). This involves involving inferior
and middle frontal gyrus that includes Broca’s area
[Downar, 2000, 2001] and TPJ.
The endogenous and exogenous attentional networks
are not completely independent. Activity within TPJ
(which is close to the pSTS) is modulated by the relevance
of the exogenous stimulus to the task; the sensitivity of
80 Williams/Mirror neurons in autism
the dorsal system is modulated by stimulus features and
task contingency.
Mirror neurons and social attention. Mirror
neurons in Broca’s area are not just sensitive to the
shape of an action, but are also sensitive to the direction
in which an action is performed relative to the observer.
Gallese et al. [1996] reported that 30 out of 47 mirror
neurons tested showed directional preference. It
therefore seems very possible that there will be mirror
neurons in Broca’s area that fire when actions are
observed as self-directed, and when they are executed
toward another person (i.e. they code for the
interpersonal direction of intention).
An important aspect of autism concerns the difficulties
that others may have in attracting the child’s attention. A
child with autism may not look up when his or her
parent enters the room, or may not follow a gaze or a
point. This seems to reflect a lack of sensitivity of the
exogenous attentional network to a familiar action
directed toward the individual. As mirror neurons
located in Broca’s area are sensitive to familiar actions
and action–direction, this makes the case for
hypothesizing a central role for mirror neurons in the
social attention problems characteristic of autism.
Furthermore, if cognition is founded upon action,
embodied cognitive theory would predict that this
deficit in orienting to self-directed action, would be
extended in development to have broader effects on
attentional control.
Action–direction includes the direction of a facial
expression. Williams, Perrett, Waiter, & Pechey [2007a]
found activity within Broca’s area (as well as brain areas
serving mentalizing) to be much greater when a face was
observed from the front compared to the side. This
greater activity was dependent upon intact serotonin
function, which may be impaired in autism [e.g. Devlin
et al., 2005]. The hypothesis that mirror neurons in
Broca’s area are important for social attention has several
implications as follows:
Social salience and orienting. In linking neural codings for
the perceptions of self-directed actions to codings for
actions that serve orienting behaviors toward others, the
mirror neuron system could play an essential role in
promoting the salience of exogenous, socially relevant
stimuli, which are directed toward the individual.
Consequently, when an action is perceived to be
directed toward a person, the mirror neuron system is
important in promoting a reciprocal action directed
toward the actor. Similarly, when an action is perceived
to be directed toward an object, this favors the execution
of an action being executed by the observer, toward the
same object.
In the imitation studies described above, mirror
neurons may be important for contributing to premotor
activity by fostering orienting actions-to-others in
response to observation of self-directed action. Dapretto
et al. [2006] suggested that the lack of behavioral
differences in their study could be accounted for by the
INSAR
increased visual attention to the images by the children
with autism, as evidenced by greater activity in visual and
parietal cortices. This could be further explained as
resulting from the absence of the mirror neuron
contribution to ‘‘bottom-up’’ stimulus-driven visual
attention, resulting in greater ‘‘top-down’’ attentional
influences in its absence. Social salience mediated by
Broca’s area may also be important for faster reaction
times when responses to observed stimuli are imitative,
because familiar actions activate mirror neurons and so
achieve greater visual salience (see further discussion
below).
Preventing fixed patterns of attention. Corbetta and
Shulman [2002] propose that the RVPN functions as a
‘‘circuit breaker.’’ Attention is maintained in a ‘‘top-
down’’ task by a circuit from visual cortex back to the
frontal eye fields. This can be interrupted by the RVPN,
which would appear to be well suited to serve this
function. For example, if you are looking at me when my
attention is directed toward another task, such as reading
a book, my attention toward that task will be interrupted
to look at you. In autism absence of ‘‘circuit breaking,’’
due to impaired mirror neuron function in Broca’s area, is
likely to enhance ‘‘top-down’’ attentional control by the
DFPN, perhaps resulting in fixed patterns of attention to
nonsocial stimuli [Landry & Bryson, 2004; Ozonoff et al.,
2004] as well as enhanced search abilities [O’Riordan,
Plaisted, Driver, & Baron-Cohen, 2001].
Development of egocentrism and allocentrism. It has often
been suggested that people with Asperger’s syndrome are
extremely ‘‘egocentric’’ [Asperger, 1944; Frith & de
Vignemont, 2005; Gillberg & Gillberg, 1989]. Williams
[2007] has recently challenged this view, arguing that
people with autism are in fact the exact opposite—
extreme allocentrists. In his early writing, Piaget
described ‘‘autistic’’ intelligence [Piaget & Warden,
1926]. The term ‘‘autism’’ had been introduced by
Bleuler and Piaget used it to describe ‘‘undirected
intelligence’’ as autistic. Undirected intelligence reflects
a lack of ‘‘egocentricity,’’ the latter being characterized by
framing experience in terms of the way it relates to the
self. Even though the condition of autism had not yet
been described, use of the term ‘‘autistic’’ was curiously
apposite for what we know about autism today, which
could be said to be characterized by failure to encode
experience in terms of its personal relevance [Williams,
2007]. Developmentally, a deficit in mirror neuron
function in autism could result in a failure to
discriminate (in terms of learning different patterns of
responses) between self-directed and other actions,
resulting in a tendency to treat all behavioral
observations similarly, regardless of whether they are
directed at one’s self or not. This may give rise to an
apparent lack of interest in other people’s behavior and
INSAR Williams/Mirror neurons in autism
attitudes. Consequently, extreme allocentricity may be
misconstrued as egocentricity.
Part IV. Further Development of the Cognitive
Hypothesis
Mirror Neurons and Mental State Representation
An important aspect of the self–other matching hypoth-
esis of autism has been the suggestion that the mirror
neuron system could play a role in attributing mental
states to others (‘‘mentalizing’’) through a ‘‘simulation’’
process. The original model [Gallese & Goldman, 1998]
has recently been expanded upon by Hurley [2008]. Both
these accounts draw upon earlier models of mentalizing
[Gordon, 1996; Meltzoff & Gopnik, 1993] arguing that
individuals develop models of others’ thoughts by
imagining themselves in the other’s position. Gallese
and Goldman [1998] suggest that mirroring processes
allow others’ perceived behavior to be matched to the
neural codings, which represent corresponding memories
of the same experience. The mental state that gave rise to
that action is then ‘‘retrodicted.’’ Such ‘‘off-line’’ simula-
tion requires that observation of an action ‘‘automati-
cally’’ activates the motor program for this same
behavior, but that it is then inhibited for processing
‘‘off-line.’’
Intentional and Automatic Imitation
The Gallese and Goldman [1998] model is therefore
predicated on the notion of ‘‘automatic’’ imitation. This
idea was originally espoused by William James who stated
that ‘‘every representation of a movement awakens in
some degree the actual movement which is its object; and
awakens it to a maximum degree whenever it is not kept
from doing so by an antagonistic representation present
simultaneously in the mind’’ [James, 1890; p 1134].
Automatic imitation can be observed in daily encounters,
whether through the unintentional copying of another’s
body posture or the adoption of others’ accents in
speech. Experimental evidence for this sort of imitation
is also plentiful [e.g. Chartrand & Bargh, 1999]. More
recently this has been referred to as the ‘‘Ideo-Motor
theory’’ [Brass & Heyes, 2005] and ‘‘automatic imitation’’
has been demonstrated in several experiments [Brass,
Bekkering, Wohlschlager, & Prinz, 2000; Kilner, Pau-
lignan, & Blakemore, 2003; Press, Bird, Flach, & Heyes,
2005] showing quicker or smoother responses to cues
when they are imitative compared to when they are
nonimitative [though nonspecific problems with cue-
salience and stimulus–response compatibility effects may
present problems with these studies; Aicken, Wilson,
Williams, & Mon-Williams, 2007; Jansson, Wilson,
Williams, & Mon-Williams, 2007]. With respect to facial
expression, experiments have shown that observation of
81
facial emotion results in unintentional activation of the
corresponding muscle groups in the observer [Hietanen
et al., 1998; McIntosh et al., 2006].
Not all imitation is automatic, and it is often inten-
tional and effortful [Grezes, Costes, & Decety, 1999]. If
cognitions are founded upon action [Niedenthal et al.,
2005], the boundary between automatic and effortful
imitation may determine that between empathy and
simulation ‘‘ToM.’’ Different types of social learning have
been classified according to the cognitive processes upon
which they are dependent [Whiten, 2006; Whiten and
Ham, 1992]. Imitation that involves learning a novel
action by watching someone else perform it appears to be
distinct from the imitation that occurs when an action
already exists in the motor repertoire, and is evoked by
observing another perform it. One test of whether or not
imitation is ‘‘automatic’’ is whether action observation
without execution necessarily requires inhibition of the
motor or premotor cortex. Using fMRI, Brass, Zysset, and
von Cramon [2001], and Brass, Derrfuss, and von
Cramon [2005] sought evidence for motor inhibition
when participants executed a similar but different action
to the one observed (they lifted an alternative finger to
the one they observed being lifted). They found greater
activity relating to self–other discrimination, but not
motor inhibition. Williams et al. [2007b] also found no
evidence of motor inhibition during a similar task.
In conclusion, imitation learning does not appear to be
automatic, and most imitation that falls into the category
of ‘‘automatic’’ concerns pre-learnt and salient actions,
perhaps achieving salience by being emotionally laden
and directed to the observer. As these qualities apply to
facial expressions of emotion, it follows that empathy is
automatic. Clinicians observe that echolalic content
tends to be dominated by emotionally salient aspects of
speech. Thus, swear words are not an uncommon form of
echolalic content. However, understanding another
person’s novel thoughts by imagining ones’ self in his or
her position is unlikely to be automatic and will be more
effortful. It may depend on additional cognitive function
that serves imitation learning.
Imitation learning. Imitation learning is the means
by which skilled movements are learned through the
observation of others [Whiten, 2006]. Imitation is
informed by the principles of motor learning involving
‘‘inverse models,’’ which describe the development of
motor skills as being practice-dependent [Wolpert, Doya,
& Kawato, 2003; Wolpert, Ghahramani, & Flanagan,
2001]. Attempts to achieve desired actions are made that
result in error feedback. This is utilized in order to modify
programs until the actions achieve their desired
trajectories. Error feedback is obtained from sensory
functions, which require cross-modal translation before
it can influence the motor-programing function. During
imitation, observation of another individual’s behavior
82 Williams/Mirror neurons in autism
may serve as the sensory input against which to compare
one’s own motor plans. Motor learning and imitation are
therefore intentional and incremental learning processes.
Oztop, Wolpert, and Kawato [2006] have developed
sophisticated computational models that show how
mirror neurons may serve imitation.
Williams, Whiten, Waiter, Pechey, & Perrett [2007b]
investigated this process in an fMRI study of imitation.
Brain activity was compared between imitation and a
condition where an alternative learnt action was enacted.
Differences in parietal and dorsal premotor cortex
reflected mirror neuron function. There were also
differences in lateral OFC and caudal anterior cingulate
cortex (cACC). The OFC is closely tied to emotional
learning and lateral OFC is thought to serve behavioral
change in response to error feedback. Error detection also
resulted in conflict-related activity in cACC.
Williams, Whiten, Waiter et al. [2007b] conceive of
imitation as a tracking function that continuously
compares and contrasts one’s self with others,
recognizing differences as well as similarities between
self and other. This is illustrated by an fMRI study [Calvo-
Merino, Glaser, Grezes, Passingham, & Haggard, 2005]
that looked at expert dancers’ brain activity as they
observed other dancers. The dancers being observed
exhibited a common expertise with the observer or an
expertise in a different form of dance (ballet or capoeira).
Calvo-Merino et al. concluded that the experiment
identified the brain areas serving action recognition.
Williams et al. [2007b] suggested that it also identified
brain areas serving self–other comparison. Observers ask
how they differ to others as well as how they are similar,
perhaps asking whether they are better or worse at
performing the skill. Comparing (as opposed to
‘‘matching’’ or ‘‘identifying’’) ourselves with others is a
fundamental aspect of social processes that is closely
related to imitation. Furthermore, the close relationship
between imitation and the OFC underlines the
importance of emotional learning in imitation and the
typical presence of a strong drive to be like others or
better than them.
One implication of this is that motor skills should not
only be measured in terms of dexterity, accuracy or speed,
but also their capacity for encapsulating and
communicating mental states such as emotions. This is
an important dimension of motor development that is
deeply relevant to autism. Consistent with this, Perra
et al. [2007] found that imitation impairments in people
with autism cluster with performance measures on ToM
tasks to discriminate between children with and without
autism. A strong theoretical case has been made for
abnormality of the amygdala–OFC circuit in autism
[e.g. Bachevalier & Loveland, 2006; Baron-Cohen et al.,
2000a; Dawson, Meltzoff, Osterling, & Rinaldi, 1998;
Schultz, 2005]. Reduced influence of the amygdala–
orbitofrontal circuit upon the mirror neuron system
could be important in influencing the socialization of
action–learning in autism. This could be an important
developmental influence and offers a feasible mechanism
INSAR
for developmental dysfunction of the mirror neuron
system in autism.
Imitation Learning and ‘‘ToM’’
The following paragraphs outline an alternative model
that could explain how self–other comparison is required
for ToM development. It may be comparable to recent
computational models [Oztop, Kawato, & Arbib, 2005;
Wolpert et al., 2003] that also considers how we can
estimate others’ mental states by comparison of predicted
and actual sensory feedback.
Perner [1991] classified mental state representation
abilities into a hierarchy that included secondary repre-
sentations. These sit between primary representations
(that reflect relatively well-grounded models of reality,
e.g. perceptions) and meta-representations (mental states
that represent mental states such as belief attributions).
Secondary representations consist of models of reality.
They are decoupled from the real world in some way but
help to predict or understand its behavior [Suddendorf &
Whiten, 2001]. Secondary representations are necessary
for processes such as causal understanding, object
permanence and symbolic reasoning.
Action may also be represented at a secondary level
within motor control structures. The ‘‘meaning’’ of an
action may be constituted by a learnt understanding of
how the character of a generic form of an action is
affected by differing contextual and emotional factors.
For example, a wave-good-bye has a generic form in the
sense of it being a hand moved in a rhythmic fashion as
the palm is held up, facing out. The manner of a wave
then varies according to a wide variety of situational,
emotional and cultural contextual influences in which it
takes place. These might include such diverse influences
such as whether the relationship is intimate, whether the
separation is to be brief or prolonged, whether the
departure is amicable, the age of recipient, the distance
between participants and the local cultural norms.
Imitation of a model by an observer allows the observer
to form the same associations between action plans and
memories in the observer as those that control the
model’s actions. Thus, through imitation, the observer
identifies differences as well as similarities between
different forms of an action (such as waving) and relates
these to emotional and contextual differences through
experience. Consequently, imitation results in an ob-
server developing an understanding of how emotion and
contextual memory impact upon the basic form of
action.
Imitation may therefore serve to develop a representa-
tional knowledge by a continuous process of self–other
comparison. In this way mentalizing is not just about
simulation, but also about understanding why indivi-
duals differ from one another, and how differences
INSAR Williams/Mirror neurons in autism
between other people’s behavior stem from different
motives. Tomasello, Carpenter, Call, Behne, and Moll
[2005] have discussed how the experience of sharing
intentions and goals forms a basis for the development of
social cognition. The suggestion here is that the notion of
shared experience should be broadened to include all
secondary representations of action, and also that mirror
neurons may play an important role in relating differ-
ences as well as similarities in experience, to differences
and similarities between observed and experienced
actions.
If secondary representational models of action are
developed through forming memories of an action’s
motor codings and its emotional and contextual associa-
tions, we would perhaps expect their neural basis to
depend upon connectivity between premotor, limbic and
orbitofrontal systems. Indeed, these systems meet each
other in medial prefrontal cortex, and this is also the
primary location in the brain for ToM function [Frith &
Frith, 2000; Amodio & Frith, 2006].
Within this alternative model, therefore, the contribu-
tion made by mirror neurons to ToM development occurs
through imitation learning but not just by ‘simulation.’’
Self–other differences are also important. Furthermore,
mirror neurons are indirectly involved by serving imita-
tion, which then facilitates development of ToM by
fostering connectivity between motor, limbic and OFC,
particularly in the medial prefrontal cortex.
Secondary Representation of Action and Autism
In autism, secondary representation that is embodied in
action seems to be particularly affected, whereas cogni-
tion that is disembodied from action such as that
involved in recognizing oneself in a mirror and object
permanence may be spared. Language and symbolic
understanding are relatively unaffected in Asperger’s
syndrome. The most diagnostically discriminative fea-
tures of autism, identified by the Autism Diagnostic
Interview-Revised (ADI-R) [Lord et al., 1994] and Autism
Diagnostic Observation Schedule-Generic (ADOS-G)
[Lord et al., 2000] concern secondary representation of
action and include gesture, imitation, following and
directing attention and imaginative play. Imperative
pointing (pointing to things to ask for them) is less
discriminative than declarative pointing (pointing to
direct attention).
Moreover, it appears that when secondary representa-
tions of action require intentional execution, this is
particularly diagnostic of autism. Therefore, expression of
emotion in facial expression is discriminative, but
whether such emotion is directed toward another
individual is more so. During joint-attention activities,
following another’s attention discriminates children with
autism less than whether they initiate joint attention
83
[Mundy & Newell, 2007]. Gesture recognition is impaired
[Smith & Bryson, 2007] but gesture production more so.
Imitation of gesture is performed less accurately than
imitation of actions on objects [Williams, Whiten, &
Singh, 2004]. Action planning is impaired [Ozonoff et al.,
2004], but intentional understanding is spared [Aldridge,
Stone, Sweeney, & Bower, 2000; Carpenter, Pennington,
& Rogers, 2001; Hamilton & Frith, 2007].
Part V: Conclusions and Synthesis
Across the spectrum of autism-related disorders, it
appears to be the cognitive functions that are embodied
by action that are most affected. While communication
skills based on gesture, facial expressions and eye move-
ments are diagnostic, those abilities that are less depen-
dent upon integration with action, such as certain
sensory, mathematical and mnemonic abilities may be
enhanced. It follows that the mechanisms that underpin
imitation and self–other matching are fundamental to
our understanding of autism. In this article, the relation-
ships between mirror neurons and self–other matching
functions in autism have been considered at neurobiolo-
gical and cognitive levels. Two important issues emerge.
One is that different features of actions may be coded for
by different groups of mirror neurons. A second is that
different social cognitive functions may be differentially
served by these different groups. These two issues will be
considered in turn.
Action Features
A traditional model conceives of mirror neurons as
homogeneous groups of neurons that fire in response to
specific actions, either when they are observed or when
they are executed. The more the character of an action
matches a mirror neurons’ prespecified character, the
stronger it will fire. Primate mirror neuron studies have
examined action character with respect to features such
as grasp type. However, actions also vary for other
features that include their speed, force, direction relative
to observer, emotional content and relationship to goal
and context. As different features of actions are coded for
by different brain areas, whether in the parietal or the
motor cortex, it follows that self–other matching of these
different features is also likely to be served by different
groups of cells, either in the classic mirror neuron areas or
outside. Therefore, a second model for mirror neuron
function, suggested by the work of Dinstein et al. [2007],
is that different populations of cells with mirror proper-
ties, each serve self–other matching for separate action
features. A simple extension of this model is that there
are also other groups of cells serving aspects of self–other
matching functions that are more independent of action
and lie beyond the mirror neuron system, in areas such as
84 Williams/Mirror neurons in autism
the superior frontal gyrus for joint attention, and
temporal pole, anterior cingulate and insula for aspects
of emotions [Gallese et al., 2004].
Social Cognitive Functions
A further issue that follows from this more complex
model of mirror neuron function is that the different cell
groups with mirroring functions are likely to be differ-
entially engaged in the various social cognitive functions
of relevance to autism. The role of mirror neurons in four
main elements of social cognitive development has been
discussed. Firstly, mirror neurons are likely to be involved
in empathy, emotional contagion and ‘‘automatic imita-
tion,’’ where pre-existing motor knowledge is ‘‘released’’
by observation of others’ actions. Secondly, mirror
neurons may be important for mediating influences of
observed actions on attentional systems. This could occur
by engaging mirror neurons that code the direction of
action relative to the self. Influences of the mirror neuron
system on attentional systems may be important for
development of joint-attention skills and fostering the
development of attentional salience for personally rele-
vant actions. Thirdly, mirror neurons may be important
for imitation learning, whereby the motor repertoire is
developed through experience of self–other comparison.
Fourthly, mirror neurons may be involved in a ToM
process that differs from empathy by drawing upon an
accumulated knowledge of action obtained through
self–other comparison.
Prediction and Tests
Mirror neurons may therefore serve a range of self–other
comparison functions, with the result that self–other
comparison can show variable profiles of impairment in
different individuals in autism. Both of two novel ideas
contained herein are readily testable. The first is that
autism can be associated with a specifically reduced
tendency to discriminate between self-directed and other
action, and that this is mediated by a reduced function of
Broca’s area, perhaps by reduced connectivity with the
orbitofrontal–amygdala circuit. The second is that meta-
representational ToM and empathy develop through
different mechanisms, though both involve the mirror
neuron system. Empathic impairment in autism will be
predicted by reduced tendency toward automatic imita-
tion. Meta-representational impairment will be asso-
ciated with impairment on aspects of motor learning
and imitation. Further separation seems unlikely as both
meta-representational and empathic development will be
affected by social attentional impairment. A key issue
that remains to be addressed concerns whether there are
specific features of action for which imitation is more
specifically impaired. A prediction that follows from the
model of learning described here will be that people with
INSAR
autism may particularly struggle to capture differences
between generic and context-specific forms of action
during imitation. For example, imitating a gesture such
as ‘‘thumbs-up’’ for ‘‘okay’’ may not be such a problem
for people with autism, as is learning to imitate ‘‘thumbs-
up’’ with the nuances that convey just how ‘‘okay’’ things
are. Developing experimental methods that can capture
these more subtle effects presents a challenge, though the
‘‘emphatic gesture’’ component of module 4 of the
ADOS-G [Lord et al., 2000] has already demonstrated
some success.
This self–other comparison/mirror neuron model of
autism does not make any assumptions about causes of
dysfunction. Important potential causes include impair-
ment of the orbitofrontal–amygdala circuit [Bachevalier
& Loveland, 2006] memory [Minshew & Goldstein,
2001], differential development of white matter path-
ways or variable lateralization of function. Serotonin may
be important in modulating differential responses to self-
directed and other action [Williams et al., 2007a], and the
suggestion has been made that Broca’s area could be
hypermasculinized in autism [Baron-Cohen et al., 2006].
In summary, this model offers several avenues to be
explored, both in testing the model and developing
strategies to diminish autism-related disability. For
example, it is possible that the influence of stimulus-
driven attention could be enhanced pharmacologically
[Corbetta & Shulman, 2002]. Aspects of social skill
training that may be worthy of development include
training motor skills to express emotion and developing
motor awareness. Further research into the self–other
matching function in autism promises to be a fruitful line
of research.
Acknowledgments
This research is supported by the Northwood Charitable
Trust. I am also grateful to Nina Williams, David Perrett,
Morven McWhirr, Michael Arbib, and Sally Rogers and to
two anonymous reviewers for helpful comments on
earlier drafts.
References
Aicken, M.D., Wilson, A.D., Williams, J.H., & Mon-Williams, M.
(2007). Methodological issues in measures of imitative
reaction times. Brain and Cognition, 63, 304–308.
Aldridge, M.A., Stone, K.R., Sweeney, M.H., & Bower, T.G.R.
(2000). Preverbal children with autism understand the
intentions of others. Developmental Science, 3, 294–301.
Allison, T., Puce, A., & McCarthy, G. (2000). Social perception
from visual cues: Role of the STS region. Trends in Cognitive
Sciences, 4, 267–278.
Altschuler, E.L., Vankov, V., Wang, V., Ramachandran, V.S., &
Pineda, J.A. (1997). Person see, person do: Human cortical
INSAR Williams/Mirror neurons in autism
electrophysiological correlates of monkey see, monkey do
cells. Poster presented at the 27th annual Meeting of the
Society of Neuroscience, New Orleans, LA.
Amodio, D.M., & Frith, C.D. (2006). Meeting of minds: The
medial frontal cortex and social cognition. Nature Reviews
Neuroscience, 7, 268–277.
Arbib, M.A. (2005). From monkey-like action recognition to
human language: An evolutionary framework for neurolin-
guistics. Behavioral and Brain Sciences, 28, 105–167.
Arbib, M.A. (2008). Autism—More than the mirror system.
Clinical Neuropsychiatry, in press: [doi://10.1016/j.casd.
2007.09.007].
Asperger, H. (1944). Die autistischen Psychopathen im Kinde-
salter. In: Frith, U. (Ed.), Autism and Asperger syndrome.
Cambridge: Cambridge University Press. Archiv für Psychia-
trie und Nervenkrankheiten 1991; 117, 76–136.1991.
Astafiev, S.V., Shulman, G.L., Stanley, C.M., Snyder, A.Z., Van
Essen, D.C., & Corbetta, M. (2003). Functional organization
of human intraparietal and frontal cortex for attending,
looking, and pointing. Journal of Neuroscience, 23,
4689–4699.
Astafiev, S.V., Stanley, C.M., Shulman, G.L., & Corbetta, M.
(2004). Extrastriate body area in human occipital cortex
responds to the performance of motor actions. Nature
Neuroscience, 7, 542–548.
Bachevalier, J., & Loveland, K.A. (2006). The orbitofrontal–a-
mygdala circuit and self-regulation of social–emotional
behavior in autism. Neuroscience and Biobehavioral Reviews,
30, 97–117.
Barnea-Goraly, N., Kwon, H., Menon, V., Eliez, S., Lotspeich, L.,
& Reiss, A.L. (2004). White matter structure in autism:
Preliminary evidence from diffusion tensor imaging. Biologi-
cal Psychiatry, 55, 323–326.
Baron-Cohen, S., Ring, H., Chitnis, X., Wheelwright, S., Gregory,
L., et al. (2006). fMRI of parents of children with Asperger
Syndrome: A pilot study. Brain and Cognition, 61, 122–130.
Baron-Cohen, S., Ring, H.A., Bullmore, E.T., Wheelwright, S.,
Ashwin, C., & Williams, S.C. (2000). The amygdala theory of
autism. Neuroscience and Biobehavioral Reviews, 24,
355–364.
Baron-Cohen, S., Ring, H.A., Wheelwright, S., Bullmore, E.T.,
Brammer, M.J., Simmons, A., et al. (1999). Social intelligence
in the normal and autistic brain: An fMRI study. The
European Journal of Neuroscience, 11, 1891–1898.
Bebko, J.M., Weiss, J.A., Demark, J.L., & Gomez, P. (2006).
Discrimination of temporal synchrony in intermodal events
by children with autism and children with developmental
disabilities without autism. Journal of Child Psychology and
Psychiatry, 47, 88–98.
Bernier, R., Dawson, G., Webb, S., & Murias, M. (2007). EEG mu
rhythm and imitation impairments in individuals with
autism spectrum disorder. Brain and Cognition, 64, 228–237.
Blake, R., Turner, L.M., Smoski, M.J., Pozdol, S.L., & Stone, W.L.
(2003). Visual recognition of biological motion is impaired in
children with autism. Psychological Science, 14, 151–157.
Brass, M., Bekkering, H., Wohlschlager, A., & Prinz, W. (2000).
Compatibility between observed and executed finger move-
ments: Comparing symbolic, spatial, and imitative cues.
Brain and Cognition, 44, 124–143.
85
Brass, M., Derrfuss, J., & von Cramon, D.Y. (2005). The inhibition
of imitative and overlearned responses: A functional double
dissociation. Neuropsychologia, 43, 89–98.
Brass, M., & Heyes, C. (2005). Imitation: Is cognitive neu-
roscience solving the correspondence problem? Trends in
Cognitive Sciences, 9, 489–495.
Brass, M., Zysset, S., & von Cramon, D.Y. (2001). The inhibition
of imitative response tendencies. NeuroImage, 14,
1416–1423.
Bristow, D., Rees, G., & Frith, C.D. (2007). Social interaction
modifies neural response to gaze shifts. Social Cognitive and
Affective Neuroscience, 2, 52–61.
Brothers, L. (1990). The social brain: A project for integrating
primate behavior and neurophysiology in a new domain.
Concepts in Neuroscience, 1, 27–51.
Buccino, G., Binkofski, F., Fink, G.R., Fadiga, L., Fogassi, L., et al.
(2001). Action observation activates premotor and parietal
areas in a somatotopic manner: An fMRI study. The European
Journal of Neuroscience, 13, 400–404.
Buccino, G., Vogt, S., Ritzl, A., Fink, G.R., Zilles, K., et al. (2004).
Neural circuits underlying imitation learning of hand actions:
An event-related fMRI study. Neuron, 42, 323–334.
Calvo-Merino, B., Glaser, D.E., Grezes, J., Passingham, R.E., &
Haggard, P. (2005). Action observation and acquired motor
skills: An FMRI study with expert dancers. Cerebral Cortex,
15, 1243–1249.
Carpenter, M., Pennington, B.F., & Rogers, S.J. (2001). Under-
standing of others’ intentions in children with autism.
Journal of Autism and Developmental Disorders, 31,
589–599.
Castelli, F., Frith, C., Happe, F., & Frith, U. (2002). Autism,
Asperger syndrome and brain mechanisms for the attribution
of mental states to animated shapes. Brain, 125, 1839–1849.
Castelli, F., Happe, F., Frith, U., & Frith, C. (2000). Movement
and mind: A functional imaging study of perception and
interpretation of complex intentional movement patterns.
NeuroImage, 12, 314–325.
Cattaneo, L., Fabbri-Destro, M., Boria, S., Pieraccini, C., Monti,
A., et al. (2007). Impairment of actions chains in autism and
its possible role in intention understanding. Proceedings of
the National Academy of Sciences of the United States of
America, 104, 17825–17830.
Chaminade, T., Meltzoff, A.N., & Decety, J. (2005). An fMRI
study of imitation: Action representation and body schema.
Neuropsychologia, 43, 115–127.
Charman, T., Swettenham, J., Baron-Cohen, S., Cox, A., Baird,
G., & Drew, A. (1997). Infants with autism: An investigation
of empathy, pretend play, joint attention, and imitation.
Developmental Psychology, 33, 781–789.
Chartrand, T.L., & Bargh, J.A. (1999). The chameleon effect: The
perception-behavior link and social interaction. Journal of
Personality and Social Psychology, 76, 893–910.
Corbetta, M., & Shulman, G.L. (2002). Control of goal-directed
and stimulus-driven attention in the brain. Nature Reviews
Neuroscience, 3, 201–215.
Dapretto, M., Davies, M.S., Pfeifer, J.H., Scott, A.A., Sigman, M.,
et al. (2006). Understanding emotions in others: Mirror
neuron dysfunction in children with autism spectrum
disorders. Nature Neuroscience, 9, 28–30.
86 Williams/Mirror neurons in autism
Dawson, G., Meltzoff, A.N., Osterling, J., & Rinaldi, J. (1998).
Neuropsychological correlates of early symptoms of autism.
Child Development, 69, 1276–1285.
Dawson, G., Toth, K., Abbott, R., Osterling, J., Munson, J., Estes,
A., et al. (2004). Early social attention impairments in autism:
Social orienting, joint attention, and attention to distress.
Developmental Psychology, 40, 271–283.
Decety, J., Chaminade, T., Grezes, J., & Meltzoff, A.N. (2002). A
PET exploration of the neural mechanisms involved in
reciprocal imitation. NeuroImage, 15, 265–272.
Devlin, B., Cook Jr. E.H., Coon, H., Dawson, G., Grigorenko, E.L.,
et al. (2005). Autism and the serotonin transporter: The long
and short of it. Molecular Psychiatry, 10(12), 1110–1116.
de Vignemont, F., & Singer, T. (2006). The empathic brain: How,
when and why? Trends in Cognitive Sciences, 10(10),
435–441.
Dinstein, I., Hasson, U., Rubin, N., & Heeger, D.J. (2007). Brain
areas selective for both observed and executed movements.
Journal of Neurophysiology, 98, 1415–1427.
Downar, J., Crawley, A.P., Mikulis, D.J., & Davis, K.D. (2000). A
multimodal cortical network for the detection of changes in
the sensory environment. Nature Neuroscience, 3, 277–283.
Downar, J., Crawley, A.P., Mikulis, D.J., & Davis, K.D. (2001). The
effect of task relevance on the cortical response to changes in
visual and auditory stimuli: An event-related fMRI study.
NeuroImage, 14, 1256–1267.
Emery, N.J., & Perrett, D.I. (2000). How can studies of monkey
brain help us to understand ‘theory of mind’ and autism in
humans? In: Baron-Cohen S., Tager-Flusberg H., & Cohen D.J.
(Eds.), Understanding other minds—perspectives from devel-
opmental cognitive neuroscience (pp 274–306). Oxford:
Oxford University Press.
Fadiga, L., Buccino, G., Craighero, L., Fogassi, L., Gallese, V., &
Pavesi, G. (1999). Corticospinal excitability is specifically
modulated by motor imagery: A magnetic stimulation study.
Neuropsychologia, 37, 147–158.
Fogassi, L., Ferrari, P.F., Gesierich, B., Rozzi, S., Chersi, F., &
Rizzolatti, G. (2005). Parietal lobe: From action organization
to intention understanding. Science, 308, 662–667.
Frith, C.D., & Frith, U. (2000). The physiological basis of theory
of mind: Functional neuroimaging studies. In: Baron-Cohen
S., Tager-Flusberg H., & Cohen D.J. (Eds.), Understanding
other minds—Perspectives from developmental cognitive
neuroscience. (2nd ed.). Oxford: Oxford University Press.
Frith, U., & de Vignemont, F. (2005b). Egocentrism, allocentrism,
and Asperger syndrome. Consciousness and Cognition, 14,
719–738.
Frith, U., & Frith, C.D. (2003). Development and neurophysiol-
ogy of mentalizing. Philosophical Transactions of the Royal
Society of London Series B—Biological Sciences, 358,
459–473.
Gallagher, H.L., Happe, F., Brunswick, N., Fletcher, P.C., Frith, U.,
& Frith, C.D. (2000). Reading the mind in cartoons and
stories: An fMRI study of ‘‘theory of mind’’ in verbal and
nonverbal tasks. Neuropsychologia, 38, 11–21.
Gallese, V., Fadiga, L., Fogassi, L., & Rizzolatti, G. (1996). Action
recognition in the premotor cortex. Brain, 119, 593–609.
INSAR
Gallese, V., & Goldman, A. (1998). Mirror neurons and the
simulation theory of mind-reading. Trends in Cognitive
Sciences, 2, 493–501.
Gallese, V., Keysers, C., & Rizzolatti, G. (2004). A unifying view of
the basis of social cognition. Trends in Cognitive Sciences, 8,
396–403.
Gazzola, V., Aziz-Zadeh, L., & Keysers, C. (2006). Empathy and
the somatotopic auditory mirror system in humans. Current
Biology, 16, 1824–1829.
Gillberg, I.C., & Gillberg, C. (1989). Asperger syndrome—Some
epidemiological considerations: A research note. Journal of
Child Psychology and Psychiatry, 30, 631–638.
Goldenberg, G. (1996). Defective imitation of gestures in
patients with damage in the left or right hemispheres.
Journal of Neurology Neurosurgery and Psychiatry, 61,
176–180.
Gordon, R.M. (1996). Radical simulationism. In: Carruthers P. &
Smith P.K. (Eds.), Theories of theories of mind (p. 11–21).
Cambridge: Cambridge University Press.
Grefkes, C., & Fink, G.R. (2005). The functional organization of
the intraparietal sulcus in humans and monkeys. Journal of
Anatomy, 207, 3–17.
Grezes, J., Armony, J.L., Rowe, J., & Passingham, R.E. (2003).
Activations related to ‘‘mirror’’ and ‘‘canonical’’ neurones in
the human brain: An fMRI study. NeuroImage, 18, 928–937.
Grezes, J., Costes, N., & Decety, J. (1999). The effects of learning
and intention on the neural network involved in the
perception of meaningless actions. Brain, 122, 1875–1887.
Hadjikhani, N., Joseph, R.M., Snyder, J., & Tager-Flusberg, H.
(2006). Anatomical differences in the mirror neuron system
and social cognition network in autism. Cerebral Cortex, 16,
1276–1282.
Hadjikhani, N., Joseph, R.M., Snyder, J., & Tager-Flusberg, H.
(2007). Abnormal activation of the social brain during face
perception in autism. Human Brain Mapping, 28, 441–449.
Hamilton, A.F., Brindley, R.M., & Frith, U. (2007). Imitation and
action understanding in autistic spectrum disorders: How
valid is the hypothesis of a deficit in the mirror neuron
system? Neuropsychologia, 45, 1859–1868.
Hamilton, A.F., & Grafton, S.T. (2006). Goal representation in
human anterior intraparietal sulcus. The Journal of Neu-
roscience, 26, 1133–1137.
Hari, R., Forss, N., Avikainen, S., Kirveskari, E., Salenius, S., &
Rizzolatti, G. (1998). Activation of human primary motor
cortex during action observation: A neuromagnetic study.
Proceedings of the National Academy of Sciences of the
United States of America, 95, 15061–15065.
Heiser, M., Iacobini, M., Maeda, F., Marcus, J., & Mazziotta, J.C.
(2003). The essential role of Broca’s area in imitation.
European Journal of Neuroscience, 17, 1123–1128.
Hietanen, J.K., Surakka, V., & Linnankoski, I. (1998). Facial
electromyographic responses to vocal affect expressions.
Psychophysiology, 35, 530–536.
Hobson, R.P., & Lee, A. (1999). Imitation and identification in
autism. Journal of Child Psychology and Psychiatry, 40,
649–659.
Hubert, B., Wicker, B., Moore, D.G., Monfardini, E., Duverger, H.,
et al. (2007). Brief report: Recognition of emotional and non-
emotional biological motion in individuals with autistic
INSAR Williams/Mirror neurons in autism
spectrum disorders. Journal of Autism and Developmental
Disorders, 37, 1386–1392.
Hurley, S. (2008). The shared circuits model: How control,
mirroring, and simulation can enable imitation, deliberation,
and mindreading. Behavioral and Brain Sciences, 31, 1–22.
Iacoboni, M., & Dapretto, M. (2006). The mirror neuron system
and the consequences of its dysfunction. Nature Reviews
Neuroscience, 7, 942–951.
Iacoboni, M., Koski, L.M., Brass, M., Bekkering, H., Woods, R.P.,
et al. (2001). Reafferent copies of imitated actions in the right
superior temporal cortex. Proceedings of the National
Academy of Sciences of the United States of America, 98,
13995–13999.
Iacoboni, M., Molnar-Szakacs, I., Gallese, V., Buccino, G.,
Mazziotta, J.C., & Rizzolatti, G. (2005). Grasping the inten-
tions of others with one’s own mirror neuron system. PLoS
Biology, 3, 529–535.
Iacoboni, M., Woods, R.P., Brass, M., Bekkering, H., Mazziotta,
J.C., & Rizzolatti, G. (1999). Cortical mechanisms of human
imitation. Science, 286, 2526–2528.
Jackson, P.L., Meltzoff, A.N., & Decety, J. (2006). Neural circuits
involved in imitation and perspective-taking. NeuroImage,
31, 429–439.
James, W. (1890). Principles of psychology. London: Macmillan.
Jansson, E., Wilson, A.D., Williams, J.H., & Mon-Williams, M.
(2007). Methodological problems undermine tests of the
ideo-motor conjecture. Experimental Brain Research, 182,
549–558.
Jellema, T., Baker, C.I., Wicker, B., & Perrett, D.I. (2000). Neural
representation for the perception of the intentionality of
actions. Brain and Cognition, 44, 280–302.
Jellema, T., Oram, M.W., Baker, C.I., & Perrett, D.I. (2002). Cell
population in the bank of the superior temporal sulcus of the
macaque and imitation. In: Meltzoff A. & Prinz W. (Eds.), The
imitative mind: Development, evolution and brain bases.
Cambridge: Cambridge University Press.
Kanner, L. (1943). Autistic disturbances of affective content.
Nervous Child 2, 217–250.
Keller, T.A., Kana, R.K., & Just, M.A. (2007). A developmental
study of the structural integrity of white matter in autism.
Neuroreport, 18, 23–27.
Keysers, C., & Perrett, D.I. (2004). Demystifying social cognition:
A Hebbian perspective. Trends in Cognitive Sciences, 8,
501–507.
Kilner, J.M., Paulignan, Y., & Blakemore, S.J. (2003). An
interference effect of observed biological movement on
action. Current Biology, 13, 522–525.
Klin, A. (2000). Attributing social meaning to ambiguous visual
stimuli in higher-functioning autism and Asperger syndrome:
The social attribution task. Journal of Child Psychology and
Psychiatry, 41, 831–846.
Klin, A., Jones, W., Schultz, R., & Volkmar, F. (2003). The
enactive mind, or from actions to cognition: Lessons from
autism. Philosophical Transactions of the Royal Society of
London Series B—Biological Sciences, 358, 345–360.
Kohler, E., Keysers, C., Umilta, M.A., Fogassi, L., Gallese, V., &
Rizzolatti, G. (2002). Hearing sounds, understanding actions:
Action representation in mirror neurons. Science, 297,
846–848.
87
Koski, L., Wohlschlager, A., Bekkering, H., Woods, R.P., Dubeau,
M.C., et al. (2002). Modulation of motor and premotor
activity during imitation of target-directed actions. Cerebral
Cortex, 12, 847–855.
Landry, R., & Bryson, S.E. (2004). Impaired disengagement of
attention in young children with autism. Journal of Child
Psychology and Psychiatry, 45, 1115–1122.
Liberman, A.M., Cooper, F.S., Shankweiler, D.P., & Studdert-
Kennedy, M. (1967). Perception of the speech code. Psycho-
logical Review, 74, 431–461.
Liberman, A.M., & Whalen, D.H. (2000). On the relation of
speech to language. Trends in Cognitive Sciences, 4, 187–196.
Lord, C., Risi, S., Lambrecht, L., Cook, Jr. E.H., Leventhal, B.L.,
et al. (2000). The autism diagnostic observation schedule-
generic: A standard measure of social and communication
deficits associated with the spectrum of autism. Journal of
Autism and Developmental Disorders, 30, 205–223.
Lord, C., Rutter, M., & Lecouteur, A. (1994). Autism Diagnostic
Interview-Revised—A revised version of a diagnostic inter-
view for caregivers of individuals with possible pervasive
developmental disorders. Journal of Autism and Develop-
mental Disorders, 24, 659–685.
Makuuchi, M. (2005). Is Broca’s area crucial for imitation?
Cerebral Cortex, 15, 563–570.
McAlonan, G.M., Cheung, V., Cheung, C., Suckling, J., Lam,
G.Y., et al. (2005). Mapping the brain in autism. A voxel-
based MRI study of volumetric differences and intercorrela-
tions in autism. Brain, 128, 268–276.
McGurk, H., & MacDonald, J. (1976). Hearing lips and seeing
voices. Nature, 264, 746–748.
McIntosh, D.N., Reichmann-Decker, A., Winkielman, P., &
Wilbarger, J.L. (2006). When the social mirror breaks: Deficits
in automatic, but not voluntary, mimicry of emotional facial
expressions in autism. Developmental Science, 9, 295–302.
Meltzoff, A.N., & Gopnik, A. (1993). The role of imitation in
understanding persons and developing a theory of mind. In:
Baron-Cohen S., Tager-Flusberg H., & Cohen D.J. (Eds.),
Understanding other minds, perspectives from autism.
Oxford: Oxford University Press.
Minshew, N.J., & Goldstein, G. (2001). The pattern of intact and
impaired memory functions in autism. Journal of Child
Psychology and Psychiatry, 42, 1095–1101.
Minshew, N.J., & Williams, D.L. (2007). The new neurobiology of
autism: Cortex, connectivity, and neuronal organization.
Archives of Neurology, 64, 945–950.
Moore, D.G., Hobson, R.P., & Lee, A. (1997). Components of
person perception: An investigation with autistic, non-
autistic retarded and typically developing children and
adolescents. British Journal of Developmental Psychology,
15, 401–423.
Mundy, P., & Newell, L. (2007). Attention, joint attention, and
social cognition. Current Directions in Psychological Science,
16, 269–274.
Neri, P., Luu, J.Y., & Levi, D.M. (2006). Meaningful interactions
can enhance visual discrimination of human agents. Nature
Neuroscience, 9, 1186–1192.
Niedenthal, P.M., Barsalou, L.W., Winkielman, P., Krauth-Gruber,
S., & Ric, F. (2005). Embodiment in attitudes, social percep-
88 Williams/Mirror neurons in autism
tion, and emotion. Personality and Social Psychology Review,
9, 184–211.
Nishitani, N., Avikainen, S., & Hari, R. (2004). Abnormal
imitation-related cortical activation sequences in Asperger’s
syndrome. Annals of Neurology, 55, 558–562.
O’Riordan, M.A., Plaisted, K.C., Driver, J., & Baron-Cohen, S.
(2001). Superior visual search in autism. Journal of Experi-
mental Psychology. Human Perception and Performance, 27,
719–730.
Oberman, L.M., Hubbard, E.M., McCleery, J.P., Altschuler, E.L.,
Ramachandran, V.S., & Pineda, J.A. (2005). EEG evidence for
mirror neuron dysfunction in autism spectrum disorders.
Cognitive Brain Research, 24, 190–198.
Oberman, L.M., & Ramachandran, V.S. (2007). The simulating
social mind: The role of the mirror neuron system and
simulation in the social and communicative deficits of
autism spectrum disorders. Psychological Bulletin, 133,
310–327.
Ozonoff, S., Cook, I., Coon, H., Dawson, G., Joseph, R.M., et al.
(2004). Performance on Cambridge Neuropsychological Test
Automated Battery subtests sensitive to frontal lobe function
in people with autistic disorder: Evidence from the Colla-
borative Programs of Excellence in Autism Network. Journal
of Autism and Developmental Disorders, 34, 139–150.
Oztop, E., Wolpert, D., Kawoto, M. (2005). Mental state inference
using visual control parameters. Cognitive Brain Research,
22, 129–151.
Oztop, E., Kawoto, M., & Arbib, M. (2006). Mirror neurons and
imitation: A computationally guided review. Neural Net-
works, 19, 254–271.
Oztop, E., & Arbib, M.A. (2002). Schema design and implemen-
tation of the grasp-related mirror neuron system. Biological
Cybernetics, 87, 116–140.
Pennington, B.F., Rogers, S.J., & Williams, J.H.G. (2006).
Conclusions. In: Imitation and the social mind: Autism and
typical development (pp. 431–453). New York: Guilford Press.
Perner, J. (1991). Understanding the representational mind.
Cambridge, MA: MIT Press.
Perner, J., Aichhorn, M., Kronbichler, M., Staffen, W., &
Ladurner, G. (2006). Thinking of mental and other represen-
tations: The roles of left and right temporo-parietal junction.
Social Neuroscience, 1, 245–258.
Perra, O., Williams, J.H.G., Whiten, A., Fraser, L., Benzie, H., &
Perrett, D.I. (2008). Imitation and ‘‘theory of mind’’ compe-
tencies in discrimination of autism from other neurodevelop-
mental disorders. Research in Autism Spectrum Disorders,
doi: 10.1016/j.rasd.2007.09.007.
Perrett, D.I., Harries, M.H., Bevan, R., Thomas, S., Benson, P.J.,
et al. (1989). Frameworks of analysis for the neural represen-
tation of animate objects and actions. The Journal of
Experimental Biology, 146, 87–113.
Pfeifer, J.H., Iacoboni, M., Mazziotta, J.C., & Dapretto, M. (2008).
Mirroring others’ emotions relates to empathy and inter-
personal competence in children. NeuroImage, 39,
2076–2085.
Piaget, J., & Warden, M. (1926). The language and thought of the
child. London: K. Paul, Trench, Trubner & Co. Ltd.
INSAR
Pineda, J.A. (2005). The functional significance of mu rhythms:
Translating ‘seeing’’ and ‘‘hearing’’ into ‘‘doing’’. Brain
Research Reviews, 50, 57–68.
Platek, S.M., Critton, S.R., Myers, T.E., & Gallup, G.G. (2003).
Contagious yawning: The role of self-awareness and mental
state attribution. Cognitive Brain Research, 17, 223–227.
Press, C., Bird, G., Flach, R., & Heyes, C. (2005). Robotic
movement elicits automatic imitation. Cognitive Brain
Research, 25, 632–640.
Puce, A., Allison, T., Bentin, S., Gore, J.C., & McCarthy, G.
(1998). Temporal cortex activation in humans viewing eye
and mouth movements. Journal of Neuroscience, 18,
2188–2199.
Puce, A., & Perrett, D. (2003). Electrophysiology and brain
imaging of biological motion. Philosophical Transactions of
the Royal Society of London Series B—Biological Sciences,
358, 435–445.
Ramnani, N., & Owen, A.M. (2004). Anterior prefrontal cortex:
Insights into function from anatomy and neuroimaging.
Nature Reviews Neuroscience, 5, 184–194.
Ritvo, S., & Provence, S. (1953). Form perception and imitation
in some autistic children: Diagnostic findings and their
contextual interpretation. The Psychoanalytical Study of the
Child, 8, 155–161.
Rizzolatti, G., & Craighero, L. (2004). The mirror-neuron system.
Annual Review of Neuroscience, 27, 169–192.
Rodier, P.M. (2002). Converging evidence for brain stem injury
in autism. Development and Psychopathology, 14, 537–557.
Roeyers, H., Van Oost, P., & Bothuyne, S. (1998). Immediate
imitation and joint attention in young children with autism.
Development and Psychopathology, 10, 441–450.
Rogers, S.J. (1999). An examination of the imitation deficit in
autism. In: Nadel J. & Butterworth G. (Eds.), Imitation in
infancy (pp. 254–283). Cambridge: Cambridge University
Press.
Rogers, S.J., Bennetto, L., McEvoy, R., & Pennington, B.F. (1996).
Imitation and pantomime in high-functioning adolescents
with autism spectrum disorders. Child Development, 67,
2060–2073.
Rogers, S.J., & Pennington, B.F. (1991). A theoretical approach to
the deficits in infantile autism. Development and Psycho-
pathology, 3, 137–162.
Rogers, S.J., & Williams, J.H.G. (2006). Imitation and the social
mind: Autism and typical development. New York: Guilford
Press.
Rozzi, S., Calzavara, R., Belmalih, A., Borra, E., Gregoriou, G.G.,
Matelli, M., & Luppino, G. (2006). Cortical connections of
the inferior parietal cortical convexity of the macaque
monkey. Cerebral Cortex, 16, 1389–1417.
Rutherford, M.D., Pennington, B.F., & Rogers, S.J. (2006). The
perception of animacy in young children with autism.
Journal of Autism and Developmental Disorders, 36,
983–992.
Saxe, R., & Baron-Cohen, S. (2006). Editorial: The neuroscience
of theory of mind. Social Neuroscience, 1, 1–9.
Saxe, R., & Kanwisher, N. (2003). People thinking about thinking
people—The role of the temporo-parietal junction in ‘‘theory
of mind’’. NeuroImage, 19, 1835–1842.
INSAR Williams/Mirror neurons in autism
Saxe, R., Schulz, L.E., & Jiang, Y.V. (2006). Reading minds versus
following rules: Dissociating theory of mind and executive
control in the brain. Social Neuroscience, 1, 284–298.
Saxe, R., Xiao, D.K., Kovacs, G., Perrett, D.I., & Kanwisher, N.
(2004). A region of right posterior superior temporal sulcus
responds to observed intentional actions. Neuropsychologia,
42, 1435–1446.
Senju, A., Maeda, M., Kikuchi, Y., Hasegawa, T., Tojo, Y., &
Osanai, H. (2007). Absence of contagious yawning in children
with autism spectrum disorder. Biology Letters, 3, 706–708.
Schultz, R.T. (2005). Developmental deficits in social perception
in autism: The role of the amygdala and fusiform face area.
International Journal of Developmental Neuroscience, 23,
125–141.
Singer, T., Seymour, B., O’Doherty, J., Kaube, H., Dolan, R.J., &
Frith, C.D. (2004). Empathy for pain involves the affective
but not sensory components of pain. Science, 303,
1157–1162.
Shikata, E., Hamzei, F., Glauche, V., Koch, M., Weiller, C.,
Binkofski, F., et al. (2003). Functional properties and interac-
tion of the anterior and posterior intraparietal areas in
humans. The European Journal of Neuroscience, 17,
1105–1110.
Smith, E.G., & Bennetto, L. (2007). Audiovisual speech integra-
tion and lipreading in autism. Journal of Child Psychology
and Psychiatry, 48, 813–821.
Smith, I.M., & Bryson, S.E. (1994). Imitation and action in
autism: A critical review. Psychological Bulletin, 116,
259–273.
Smith, I.M., & Bryson, S.E. (2007). Gesture imitation in autism.
II. Symbolic gestures and pantomimed object use. Cognitive
Neuropsychology, 24, 679–700.
Stern, D.N. (1985). The interpersonal world of the human infant.
New York: Basic Books.
Suddendorf, T., & Whiten, A. (2001). Mental evolution and
development: Evidence for secondary representation in
children, great ages, and other animals. Psychological
Bulletin, 127, 629–650.
Surakka, V., & Hietanen, J.K. (1998). Facial and emotional
reactions to Duchenne and non-Duchenne smiles. Interna-
tional Journal of Psychophysiology, 29, 23–33.
Theoret, H., Halligan, E., Kobayashi, M., Fregni, F., Tager-
Flusberg, H., & Pascual-Leone, A. (2005). Impaired motor
facilitation during action observation in individuals with
autism spectrum disorder. Current Biology, 15, R84–R85.
Tomasello, M., Carpenter, M., Call, J., Behne, T., & Moll, H.
(2005). Understanding and sharing intentions: The origins of
cultural cognition. The Behavioral and Brain Sciences, 28,
675–691.
Vanvuchelen, M., Roeyers, H., & De Weerdt, W. (2007). Nature of
motor imitation problems in school-aged boys with autism—
A motor or a cognitive problem? Autism, 11, 225–240.
Vollm, B.A., Taylor, A.N., Richardson, P., Corcoran, R., Stirling, J.,
et al. (2006). Neuronal correlates of theory of mind and
empathy: A functional magnetic resonance imaging study in
a nonverbal task. NeuroImage, 29, 90–98.
Waiter, G.D., Williams, J.H.G., Murray, A.D., Gilchrist, A.,
Perrett, D.I., & Whiten, A. (2004). A voxel-based investigation
89
 of brain structure in male adolescents with autistic spectrum
disorder. NeuroImage, 22, 619–625.
Waiter, G.D., Williams, J.H.G., Murray, A.D., Gilchrist, A.,
Perrett, D.I., & Whiten, A. (2005). Structural white matter
deficits in high-functioning individuals with autistic spec-
trum disorder: A voxel-based investigation. NeuroImage, 24,
455–461.
Whiten, A. (2006). The dissection of imitation and its cognitive
kin in comparative and developmental psychology. In: Rogers
S.J. & Williams J.H.G. (Eds.), Imitation and development of
the social mind: Lessons from autism and typical develop-
ment (pp. 227–250). New York: Guilford Press.
Whiten, A., & Ham, R. (1992). In: Slater P.J.B., Rosenblatt C., &
Milinski M. (Eds), On the nature and evolution of imitation
in the animal kingdom: Reappraisal of a century of research.
Whiten, A., & Byrne, R.W. (1997). Machiavellian intelligence. II:
Evaluations and extensions. Cambridge: Cambridge Univer-
sity Press.
Wicker, B., Keysers, C., Plailly, J., Royet, J.P., Gallese, V., &
Rizzolatti, G. (2003). Both of us disgusted in My Insula: The
common neural basis of seeing and feeling disgust. Neuron,
40, 655–664.
Williams, J.H., Massaro, D.W., Peel, N.J., Bosseler, A., &
Suddendorf, T. (2004). Visual-auditory integration during
speech imitation in autism. Research in Developmental
Disabilities, 25, 559–575.
Williams, J.H., Whiten, A., Suddendorf, T., & Perrett, D.I. (2001).
Imitation, mirror neurons and autism. Neuroscience and
Biobehavioral Reviews, 25, 287–295.
Williams, J.H.G. (2008). Imitation and the effort of learning.
Commentary on: The shared circuits model: How control,
mirroring, and simulation can enable imitation, deliberation,
90 Williams/Mirror neurons in autism
and mindreading by Susan Hurley. Behavioral and Brain
Sciences, 31, 60–71.
Williams, J.H.G. (2007). Directedness, egocentrism and
autism. In: McGregor E., Nunez M., Williams K., & Gomez
J.C. (Eds.), An integrated view of autism: Perspectives from
neurocognitive, clinical and intervention research. Oxford:
Blackwell.
Williams, J.H.G., Perrett, D.I., Waiter, G.D., & Pechey, S. (2007a).
Differential effects of tryptophan depletion on emotion
processing according to face direction. Social Cognitive and
Affective Neuroscience.
Williams, J.H.G., Whiten, A., Waiter, G.D., Pechey, S., & Perrett,
D.I. (2007b). Cortical and subcortical mechanisms at the core
of imitation. Social Neuroscience, 2, 66–78.
Williams, J.H.G., Waiter, G.D., Gilchrist, A., Perrett, D.I., Murray,
A.D., & Whiten, A. (2006). Neural mechanisms of imitation
and ‘‘mirror neuron’’ functioning in autistic spectrum
disorder. Neuropsychologia, 44, 608–619.
Williams, J.H.G., Waiter, G.D., Perra, O., Perrett, D.I., & Whiten,
A. (2005). An fMRI study of joint attention experience.
NeuroImage, 25, 133–140.
Williams, J.H.G., Whiten, A., & Singh, T. (2004). A systematic
review of action imitation in autistic spectrum disorder.
Journal of Autism and Developmental Disorders, 34,
285–299.
Wolpert, D.M., Doya, K., & Kawato, M. (2003). A unifying
computational framework for motor control and social
interaction. Philosophical Transactions of the Royal Society
of London Series B—Biological Sciences, 358, 593–602.
Wolpert, D.M., Ghahramani, Z., & Flanagan, J.R. (2001).
Perspectives and problems in motor learning. Trends in
Cognitive Sciences, 5, 487–494.
INSAR