REVIEW ARTICLE

SelfOther 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 selfother 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 selfother 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 selfother 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 actiondirection 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 selfother comparison processes (based on mirror neurons)
that identify differences as well as similarities between actions. Differential connectivity with the amygdalaorbitofrontal
system may also be important. This could have implications for developing theory of mind, with intentional selfother
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 brainbehavior links are likely to be complex.
Keywords: autism; autistic disorder; Aspergers syndrome; imitation; gaze; attention; motor control; perception; action;
mirror neurons; fMRI; parietal cortex; Brocas area; pSTS; theory of mind (TOM)

Introduction
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 speculation [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].

Consequent upon this, many of the issues raised by

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 networks 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 Childrens 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
Childrens 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.

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Autism Research 1: 7390 2008

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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/selfother
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 selfother
matching deficit. Although they suggest that a deficit in
praxis may underlie the selfother 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
selfother 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
selfother matching, or that selfother 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
selfother 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 selfother 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

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executed. On its own, the notion that selfother matching 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 sulcusIPS), 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 junction (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 Penningtons [1991]
selfother translation model (discussed below). Their
argument at that time consisted of several points, which
are summarized here:

Autism is characterized by developmental

impairments in imitation, joint attention and
mental state representation. It is associated
with developmental coordination disorder
and language delay.

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.

A simulation ToM (representing anothers

mental state by imagining ones self in
anothers shoes) may develop on the basis
of an intact selfother matching function.
Understanding anothers intentions in the
context of memory allows for retrodiction
of associated thoughts and memories.

Mirror neurons can serve a selfother matching function for action coding. They also code
for the relationship between a goal and an
object, allowing for formation of intentional
representations.

Dysfunction of mirror neuron modulation

(perhaps disinhibition) could explain both
overactive copying in the case of echolalia
and also failure to generate covert or offline imitation. This latter function may be
necessary to develop ToM.

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Autism does not necessarily involve language

impairment, suggesting that impairment of
mirroring function in one domain (e.g.
social reciprocity) does not necessarily require
impairment in another (e.g. language). Separate mirror neuron networks may serve
gaze and language.
There may also be separate mirror neurons
for other functions, most particularly joint
attention. There might also be neurons with
mirror properties in the region of the
superior temporal sulcus.

The SelfOther Matching (Cognitive) Hypothesis

The origins of the selfother matching hypothesis of
autism may be traced back to the first paper published on
the imitation impairment [Ritvo & Provence, 1953], just
10 years after Kanner [1943] had published his seminal
paper on autism. Over the following decades this was
followed by many now well-reviewed studies showing
that children with autism did not imitate [Rogers, 1999;
Rogers & Williams, 2006; Smith & Bryson, 1994;
Williams, Whiten, & Singh, 2004]. Rogers and Pennington [1991] conducted an influential review that found
strong evidence for the existence of a deficit affecting
imitation of simple body movements as well as symbolic
imitation. Using Sterns [1985] model of interpersonal
development, Rogers and Pennington suggested that a
biological impairment in autism restricted the capacity of
the infant to form and co-ordinate social representations of self and other at increasingly complex levels via
amodal or cross-modal representational processes. They
hypothesized that a primary deficit in such a capacity
would lead to a cascade of effects including impaired
imitation, social, communicative and affective skills and
that a deficit of praxis involving the prefrontallimbic
neural system could form the basis for this impairment.
Smith and Brysons [1994] review of 15 studies
hypothesized that the imitative deficit associated with
autism could be due in part to impairment in the
perceptual organization of movements, manifesting in
an abnormal representation of actions. Increasingly
sophisticated studies over the following decade demonstrated imitation impairment in very young children
with autism [Charman et al., 1997] and those with milder
degrees of autism [Rogers, Bennetto, McEvoy, & Pennington, 1996]. The impairment appeared to affect gesture
particularly [Roeyers, Van Oost, & Bothuyne, 1998] and
interestingly, also, imitation of action style [Hobson &
Lee, 1999], though differences in controlling for task
difficulty between gesture and action-on-object make it
difficult to judge whether specific aspects of imitation are
affected. The most recent studies support the hypothesis
that the imitation deficit concerns representational

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aspects of action [Perra et al., 2008; Smith & Bryson,

2007], although not all agree [Hamilton, Brindley, &
Frith, 2007; Vanvuchelen, Roeyers, & De Weerdt, 2007].
Embodied Cognition
The hypothesis that autism stems from a deficit in a
mechanism that serves to match codings for action
between motor and perception domains is based on a
more general principle that certain aspects of cognition
are founded upon action, encapsulated by theories of
embodied cognition. Embodied theories of cognition
[Niedenthal, Barsalou, Winkielman, Krauth-Gruber, &
Ric, 2005] view the processes of knowledge use and
acquisition as fundamentally grounded in their physical
context and the brains modality-specific systems. This
means that those cognitive operations that are heavily
influenced by both action plans and emotional states
come to function within the biological environment of
the brain that serves action plans and emotional states.
An example of embodied cognition would be found in a
model of empathy. When we observe emotions being
expressed by others we may not only feel them ourselves
but also express them in our actions by making subtle
facial movements that can be detected using electromyography [Hietanen, Surakka, & Linnankoski, 1998; Surakka
& Hietanen, 1998]. Empathy cannot be separated from
the action-based systems that serve the experience and
expression of emotion.
Klin, Jones, Schultz, and Volkmar [2003] have advanced an embodied cognitive model of autism, termed
the enactive mind (EM) approach. This construes the
mind as an active entity that shapes itself as a result of
solving problems experienced in the environment. The
developing childs actions are guided by perceptions,
which in turn are driven by attentional demands related
to social needs. The emphasis of their EM approach is on
perception and visual attention. In contrast, selfother
matching theory considers cognitive development to be
grounded in systems that serve action. However, there is
clearly cross-over, as both theories consider the development of attentional control to be grounded in visuomotor systems that require cross-modal influences. A
further essential component of the selfother matching model of autism is its focus on detection of
similarities and differences between self and other
[Pennington, Rogers, & Williams, 2006].

Part II: Tests of the Mirror Neuron Hypothesis of

Autism
Tests of the Neurobiological Hypothesis
Several studies using different methodologies have now
tested the mirror neuron hypothesis of autism. Nishitani,
Avikainen, and Hari [2004] studied a mixed sex group of

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adults with Aspergers 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 electromyograms (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 Brocas
areas bilaterally. In the ASD group, several individuals
failed to activate Brocas 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 Brocas area inside the scanner. Most striking,
activity in Brocas 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
selfother matching (imitation). A possibility not yet
excluded is that group-wise effects reflect other differences 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 Brocas 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 Aspergers 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.

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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 Brocas 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 selfother 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, &

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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 Brocas 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 Brocas 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
Brocas area during observation and imitation of

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emotional expression, and measures of empathic ability

in children.
Recent Tests of the Cognitive (SelfOther Matching)
Hypothesis
This section reviews some of the ways that the selfother
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 selfother 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 Libermans
theory of speech perception [Liberman, Cooper,
Shankweiler, & Studdert-Kennedy, 1967; Liberman &

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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

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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 jointattention 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 selfother 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. Neurophysiological 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. Notwithstanding 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

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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
actions 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 objects 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
actiongoal and actioncontext 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.

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More recently, Dinstein, Hasson, Rubin, & Heeger [2007]

suggest that more areas of parietal cortex serve neuron
functions in humans.
Brocas area. The hypothesis that neurons in Brocas
area could be important for imitation has received
support from several studies. Activity in Brocas area is
greater during imitation than during observation or other
nonimitative actionexecution conditions [Iacoboni
et al., 1999; Jackson, Meltzoff, & Decety, 2006]. Heiser
et al. [2003] found that applying transcranial magnetic
stimulation (TMS) over Brocas 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
Brocas area and Buccino et al. [2004] demonstrated
involvement of Brocas area in sequential imitation.
Buccino et al. [2001] found that action observation
activated dorsal premotor cortex as well as Brocas area.
A number of studies have questioned the role of Brocas
area in imitation compared to other actionexecution
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
actionexecution 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, Brocas 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 selfother matching on Brocas
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

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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 participants 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 Brocas area is
key to differentiating between social and nonsocial
attentional function, meaning that differential activity
in Brocas area in autism, which has been reported as
evidence for mirror neuron dysfunction, could actually
be reflecting attentional rather than selfother matching
differences. However, a second possibility is that a
selfother matching function served by mirror neurons
in Brocas area is necessary for developing this social
attentional function, which in turn has major developmental implications for the way that we relate to others.

Brocas area and visual attention. A widely

accepted model for visual attention [Corbetta &
Shulman, 2002] divides it into two processes: goaldirected 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 frontoparietal network (RVPN). This involves involving inferior
and middle frontal gyrus that includes Brocas 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

the dorsal system is modulated by stimulus features and

task contingency.
Mirror neurons and social attention. Mirror
neurons in Brocas 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 Brocas 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 childs 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 Brocas area are sensitive to familiar actions
and actiondirection, 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.
Actiondirection includes the direction of a facial
expression. Williams, Perrett, Waiter, & Pechey [2007a]
found activity within Brocas 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
Brocas 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

Williams/Mirror neurons in autism

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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
Brocas 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 topdown 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 Brocas 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 [ORiordan,
Plaisted, Driver, & Baron-Cohen, 2001].

Development of egocentrism and allocentrism. It has often

been suggested that people with Aspergers 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 ones self or not. This may give rise to an
apparent lack of interest in other peoples behavior and

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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 selfother matching hypothesis 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 others 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 simulation requires that observation of an action automatically 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 anothers
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, Paulignan, & 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 cuesalience and stimulusresponse 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

Williams/Mirror neurons in autism

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 intentional 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 selfother 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
persons 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 individuals behavior

82

may serve as the sensory input against which to compare

ones 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 ones self with others,
recognizing differences as well as similarities between
self and other. This is illustrated by an fMRI study [CalvoMerino, 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 selfother 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 amygdalaOFC 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
actionlearning in autism. This could be an important
developmental influence and offers a feasible mechanism

Williams/Mirror neurons in autism

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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 selfother 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 representations. 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
models 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 observer developing an understanding of how emotion and
contextual memory impact upon the basic form of
action.
Imitation may therefore serve to develop a representational knowledge by a continuous process of selfother
comparison. In this way mentalizing is not just about
simulation, but also about understanding why individuals differ from one another, and how differences

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between other peoples 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 differences 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 actions
motor codings and its emotional and contextual associations, 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 contribution made by mirror neurons to ToM development occurs
through imitation learning but not just by simulation.
Selfother differences are also important. Furthermore,
mirror neurons are indirectly involved by serving imitation, 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 cognition 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 Aspergers
syndrome. The most diagnostically discriminative features 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 representations 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 anothers attention discriminates children with
autism less than whether they initiate joint attention

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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].

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

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 movements are diagnostic, those abilities that are less dependent upon integration with action, such as certain
sensory, mathematical and mnemonic abilities may be
enhanced. It follows that the mechanisms that underpin
imitation and selfother matching are fundamental to
our understanding of autism. In this article, the relationships between mirror neurons and selfother matching
functions in autism have been considered at neurobiological 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.

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 differentially 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 imitation, 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 relevant actions. Thirdly, mirror neurons may be important
for imitation learning, whereby the motor repertoire is
developed through experience of selfother 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
selfother comparison.

Action Features

Prediction and Tests

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 selfother 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 properties, each serve selfother matching for separate action
features. A simple extension of this model is that there
are also other groups of cells serving aspects of selfother
matching functions that are more independent of action
and lie beyond the mirror neuron system, in areas such as

Mirror neurons may therefore serve a range of selfother

comparison functions, with the result that selfother
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
Brocas area, perhaps by reduced connectivity with the
orbitofrontalamygdala circuit. The second is that metarepresentational 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 imitation. Meta-representational impairment will be associated 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

Part V: Conclusions and Synthesis

84

Williams/Mirror neurons in autism

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 thumbsup 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 selfother comparison/mirror neuron model of
autism does not make any assumptions about causes of
dysfunction. Important potential causes include impairment of the orbitofrontalamygdala circuit [Bachevalier
& Loveland, 2006] memory [Minshew & Goldstein,
2001], differential development of white matter pathways or variable lateralization of function. Serotonin may
be important in modulating differential responses to selfdirected and other action [Williams et al., 2007a], and the
suggestion has been made that Brocas 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 stimulusdriven 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 selfother
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.

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