Mirror Neuron Activity Associated with Social
Impairments but not Age in Autism Spectrum Disorder
Peter G. Enticott, Hayley A. Kennedy, Nicole J. Rinehart, Bruce J. Tonge, John L. Bradshaw, John R. Taffe,
Zafiris J. Daskalakis, and Paul B. Fitzgerald
Background: The neurobiology of autism spectrum disorder (ASD) is not particularly well understood, and biomedical treatment ap-
tion within the mirror neuron system, while a recent neuroimaging study suggests that these impairments in ASD might reduce with age.
Methods: Participants with autism spectrum disorder (i.e., DSM-IV autistic disorder or Asperger’s disorder) (n ? 34) and matched control
tion of hand gestures.
Results: Regression analyses revealed that the ASD group presented with significantly reduced corticospinal excitability during the
putative mirror neuron activity and self-reported social-relating impairments, but there was no indication that mirror neuron impairments
in ASD decrease with age.
Conclusions: These data provide general support for the mirror neuron hypothesis of autism; researchers now must clarify the precise
should be used as targets for the treatment of ASD.
neuron system, primary motor cortex, transcranial magnetic
cent account suggests that dysfunction of mirror neurons might
underlie aspects of ASD, particularly with respect to social relating
(1). Originally discovered via depth electrode recordings in ma-
caque monkeys (2), mirror neurons are brain cells that become
active not only when a behavior is performed but also when that
of modalities (e.g., behavior, sensation, pain, emotion) (3,4). Theo-
simulation that not only allows an understanding of the actions of
others but also facilitates broader social cognitive processes, in-
may underlie ASD (i.e., the broken mirror hypothesis) (6–8). Evi-
utism spectrum disorder (ASD) is characterized by severe
social, communicative, and behavioral impairments. The
precise neuropathophysiology of ASD is unclear, but a re-
dence for reduced activation of elements of the mirror system in
autism comes from a range of noninvasive techniques, including
fMRI (9), structural magnetic resonance imaging (10,11), EEG indi-
ces of mu suppression (12–14), and TMS indices of corticospinal
excitability during action observation (15). Stimuli used to elicit a
mirror neuron response in these studies have been similarly varied
but include static emotional facial expressions (9), static nonemo-
tional facial expressions (16), and intransitive hand movements
(12,13,15,17). Another study demonstrated that the observation of
an action led to mirrored activity of a muscle that was soon to be
of mouth-opening mylohyoid muscle when viewing an object
grasped for the purpose of eating) but that this mirrored anticipa-
tion was absent in ASD (18); this implies a deficit in linking or
with social relating (9), these studies have nevertheless been char-
acterized by small sample sizes, thereby limiting further analyses
More recently, Bastiaansen et al. (19) used fMRI to investigate
were no overall group differences, the authors found reductions in
(mean age: 22 years) and an age-related increase in IFG activity for
the ASD group. These age patterns were not apparent among the
it suggests that individuals with ASD may outgrow any mirror neu-
ron deficit by early-mid adulthood, raising questions about the
importance of the mirror neuron system (MNS) among adults with
ASD, many of whom nevertheless continue to experience pro-
nounced social difficulties.
Despite this evidence for a mirror neuron impairment, ASD is
perspectives, as a heterogeneous group of disorders. Accordingly,
one neurobiological model, such as the mirror neuron account, is
unlikely to provide an explanatory account that applies to all indi-
of Psychology and Psychiatry, Monash University and the Alfred, Mel-
sity, Clayton, Australia; and Centre for Addiction and Mental Health
(ZJD), University of Toronto, Toronto, Canada.
Address correspondence to Peter G. Enticott, Ph.D., Monash University and
the Alfred, School of Psychology and Psychiatry, Monash Alfred Psychi-
Victoria, 3004, Australia; E-mail: firstname.lastname@example.org.
Received Jul 12, 2011; revised Aug 31, 2011; accepted Sep 1, 2011.
BIOL PSYCHIATRY 2012;71:427–433
© 2012 Society of Biological Psychiatry
viduals with ASD. It is therefore possible that only a subgroup of
ity, which would be crucial to future efforts to individualize treat-
uals with ASD in regions thought to comprise the MNS (9), while
others provide evidence to suggest enhanced activation of the
MNS in ASD (17) or no mirror neuron deficit in ASD at all (20,21).
Whether a lack of mirror neuron activity in ASD is associated with a
different clinical profile (e.g., more pronounced social-relating im-
pairments) to those with ASD who do not show evidence for a
mirror neuron deficit is not clear.
in ASD. To our knowledge, there has been only one other study that
istered TMS to 10 adults with ASD and 10 matched control subjects
during the observation of intransitive thumb and index finger move-
tric (other) perspectives. Motor evoked potentials (MEPs) were re-
corded from the contralateral first dorsal interosseous (FDI; index
authors suggest that this may reflect a mirror-related deficit in self-
via regression analyses, associations with potential modulating vari-
ables, including social relating and age. Transcranial magnetic stimu-
individual, whether or not there is evidence of MNS activity. Specifi-
cally, increased motor corticospinal excitability (CSE) during action
observation (compared with CSE during a control condition) is
whereas unchanged or decreased CSE amplitude does not (22–24).
observed movement) (24,25). The current study employed transitive
stimuli (i.e., hand interacting with object in a goal-directed fashion),
esized that individuals with ASD would be associated with reduced
positive modulation of CSE during the observation of a transitive
movement and that this would be negatively associated with age. It
was also hypothesized that in ASD, greater social symptom severity
Methods and Materials
Participants were 34 individuals diagnosed with ASD (either high-
functioning autism or Asperger’s disorder) and 36 neurotypical (NT)
(healthy) control subjects matched for gender and age. Individuals
with ASD were recruited via the Monash Alfred Psychiatry Research
Centre participant database (comprised of clinically diagnosed re-
tion to future research) and advertisements in ASD support group
newsletters and websites. All clinical participants had a confirmed
DSM-IV diagnosis of autistic disorder or Asperger’s disorder. Where a
participant had not been diagnosed through our clinical service, the
diagnosis was confirmed by participants providing a copy of their
nosing clinician (psychiatrist, pediatrician, or psychologist). Eleven of
hibitor [SSRI], 2 SSRI/atypical antipsychotic [AP], 2 SSRI/atypical AP/
benzodiazepine, 1 tetracyclic antidepressant, 1 atypical AP, 1 sero-
tonin-norepinephrine reuptake inhibitor). Neurotypical participants
logical illness and were recruited via advertisements placed at The
Alfred Hospital and Monash University. Demographics are presented
assessed by the Kaufman Brief Intelligence Test, Second Edition). All
participants were screened to ensure that they did not meet safety-
based exclusion criteria for TMS (26). Written informed consent was
18). The project was approved by the research ethics committees of
Participants (and their parents for those under 18) completed
Autism Spectrum Quotient (AQ)/Autism Spectrum Quotient Ado-
Scale (for those aged 18 or above) (30), and the parent-completed
Consistent with previous research (22–24), putative mirror neu-
ron activity was assessed via the administration of TMS to the left
primary motor cortex (and subsequent electromyography [EMG]
recordings of the contralateral FDI muscle) during the observation
of a series of short video clips depicting a static hand or a hand
the presentation of a transitive (i.e., goal-directed, object-related)
ron response among healthy individuals.
Single pulse TMS (Magstim-200 stimulator, Magstim Company
Ltd., United Kingdom) was administered to the primary motor cor-
tex using a hand-held, 70 mm figure-of-eight coil that was placed
against the scalp in the conventional manner. The site of the pri-
Table 1. Participant Demographics
Formal Education (Years)a
Handedness (EHI) (R : L : ambi)
DBC Autism Screen
Standard deviations in parentheses.
ambi, ambidextrous; AQ, Autism Spectrum Quotient; ASD, autism spec-
trum disorder; DBC, Developmental Behaviour Checklist; EHI, Edinburgh
Handedness Inventory; F, female; FSIQ, full-scale intelligence quotient;
KBIT-2, Kaufman Brief Intelligence Test, Second Edition; L, left; M, male; NT,
neurotypical; PIQ, performance (nonverbal) intelligence quotient; R, right;
RAADS, Ritvo Autism-Aspergers Diagnostic Scale; VIQ, verbal intelligence
ap ? .01.
bp ? .001.
428 BIOL PSYCHIATRY 2012;71:427–433
P.G. Enticott et al.
mary motor cortical stimulation was that which, following stimula-
tion, produced the greatest EMG response in the contralateral FDI
muscle. Resting motor threshold was the lowest stimulator inten-
sity at which at least three out of five consecutive pulses elicited a
response of at least 50 ?V.
adhesive electrodes. All EMG signals were amplified and filtered
ments, Colorado Springs, Colorado) and sampled via a CED Micro
1401 mk II analog-to-digital converting unit (Cambridge Electronic
Design, Cambridge, United Kingdom).
Briefly, participants viewed a quasi-random sequence of five
mug present, a pantomimed grasping motion, a pantomimed
where the hand grasped the handle of the mug (see Enticott et al.
 for screen shots of each condition and further details). All
(120% resting motor threshold) was delivered during each clip; for
the motion videos, this was immediately before the completion of
the grasp (which is the phase in this movement that is typically
associated with the most pronounced increase in CSE) (25). Each
clip was of 3 seconds duration and presented 10 times, with the
entire sequence of 4 minutes 39 seconds duration. Stimuli were
presented on a 22-inch LCD monitor (aspect ratio: 16:9) that was
positioned at eye level and 120 cm ahead of the participant.
Participants were monitored by a second experimenter
throughout the video presentation to ensure that visual gaze was
directed toward the monitor. Participants were also asked a series
of questions at the conclusion of the video presentation, for which
ing to the videos (e.g., name the object present in the videos,
imitate the hand movement seen). All participants were able to
answer these questions successfully.
Consistent with our previous study, in which enhanced CSE
among NT individuals was only seen during the observation of a
ity) (23), median MEP responses were extracted for the static hand
observation of a transitive hand movement was then converted to
observation of a static hand. The formula for calculating this vari-
able is presented below:
This provides not only an index of relative mirror neuron
activity but also the opportunity to differentiate between those
who do show evidence of mirror neuron activity (i.e., MEP-PC ?
(i.e., MEP-PC ? 0).
Standard and logistic regression were used to investigate the
effect of group (ASD vs. NT) on our index of mirror system activity
(i.e., MEP-PC). Additional predictors that have been shown or spec-
ulated to modulate mirror neuron activity in ASD (verbal IQ, age,
and gender) were also added to the model. Because of multicol-
linearity, the ASD diagnosis and self-reported social-relating im-
pairments (i.e., social relating subscale of AQ/Autism Spectrum
Quotient Adolescent Version) were considered in separate regres-
AQ social relating, gender, verbal IQ, and age. We examined both
the mirror neuron response (i.e., CSE increase during action obser-
vation) and the presence or absence of a mirror neuron response
(i.e., whether or not CSE was increased during action observation);
the former assesses a spectrum view of mirror neuron activity,
whereas the latter assesses the possibility of abnormal mirror neu-
ron activity (i.e., absent MNS response) as a possible neurobiologi-
cal subtype of ASD.
Results of the regression analyses are presented in Tables 2, 3,
associated with reduced MEP-PC during transitive action observa-
tion (Figure 1), thus providing support for reduced mirror system
ysis of all five observation conditions by group is presented in
Figure S1 in Supplement 1.) Within this model, there was no effect
of age, verbal IQ, or gender.
When examining predictors of MEP-PC during action observa-
scatter plot), while the remaining variables, verbal IQ, gender, and
Table 2. Regression Examining the Influence of Four Predictors, Group
(ASD Versus Control), Verbal IQ, Gender, and Age, on MEP-PC
IVMEP-PC ? (p)
ASD, autism spectrum disorder; IQ, intelligence quotient; IV, indepen-
dent variable; MEP-PC, motor evoked potentials-percentage change.
Table 3. Regression for Examining, Among All Participants, the Effect of
Predictors AQ Social, Verbal IQ, Gender, and Age on MEP-PC and Logistic
Regression Examining the Effect of These Same Predictors on the
Presence/Absence of a Putative MNS Response
IV MEP-PC ? (p)MNS Response Odds Ratio (p)
AQ, Autism Spectrum Quotient; IQ, intelligence quotient; IV, indepen-
dent variable; MEP-PC, motor evoked potentials-percentage change; MNS,
mirror neuron system.
Table 4. Logistic Regression Examining, Separately for Each Group, the
Influence of Predictors on the Presence or Absence of Putative MNS
ASD Control Subjects
MNS Response Odds
MNS Response Odds
ASD, autism spectrum disorder; AQ, Autism Spectrum Quotient; IQ, in-
telligence quotient; IV, independent variable; MNS, mirror neuron system.
P.G. Enticott et al.
BIOL PSYCHIATRY 2012;71:427–433 429
age, were again not associated. When, however, examining the
influence of factors on the presence or absence of a mirror neuron
suggesting that having a discernable mirror neuron response is
associated with an increased score on the AQ social relating sub-
scale, but there was no effect of verbal IQ, gender, or age.
When considering ASD and control groups separately (Table 4),
there was an effect of social on the MNS response for the ASD
group, suggesting that the absence of a putative mirror neuron
effect of verbal IQ, gender, or age. By contrast, among control
subjects, there was no effect of any of the variables AQ social relat-
ing, verbal IQ, gender, and age, suggesting that the presence or
absence of recordable putative mirror neuron activity has no rela-
tionship to these variables among this group. (Remaining scatter
plots and bar charts presenting relationships described here are
presented in Figures S2–S16 in Supplement 1.)
among individuals with ASD. When viewing a human hand per-
forming a transitive action, individuals with ASD showed reduced
CSE (relative to viewing a static hand) when compared with NT
individuals. Although we did not compare different visual orienta-
tions, because our videos were presented from an egocentric per-
spective, this should be considered consistent with the findings of
Theoret et al. (15). Among ASD participants, self-reported social
activity, a relationship that did not exist among control subjects.
Finally, unlike Bastiaansen et al. (19), we found no association with
age, nor did we find any link to gender or verbal IQ. Although we
recording technique and stimulus presentation, our results are not
in agreement with the view that any mirror neuron impairment in
ASD is absent or corrected by early-mid adulthood.
There is good evidence, both in primates and humans, that the
MNS plays a vital role in allowing a first-hand understanding of the
goals and intentions associated with others’ behavior (32). From a
theoretical perspective, then, our findings add strong support to
the broken mirror hypothesis of autism, specifically, that a deficit
within mirror neurons, or impairment within the broader MNS,
significantly limits one’s ability to understand the behavior of oth-
ties. As demonstrated by Cattaneo et al. (18), this presumably in-
Figure 1. Motor evoked potentials-percentage change (? standard error)
during observation of a transitive hand movement for autism spectrum
disorder and neurotypical groups. ASD, autism spectrum disorder; MEP-PC,
motor evoked potentials-percentage change; NT, neurotypical.
Figure 2. Scatter plot demonstrating relationship between motor evoked potentials-percentage change and Autism Spectrum Quotient social for all
participants. AQ, Autism Spectrum Quotient; MEP-PC, motor evoked potentials-percentage change.
430 BIOL PSYCHIATRY 2012;71:427–433
P.G. Enticott et al.
cludes the ability to infer intention by linking motor events to infer
goals and intentions. The MNS is therefore considered integral to
the neuropathophysiology of social-relating impairments in ASD,
where the ability to infer others’ intentions is impaired.
Beyond intention understanding and in further support of our
results within the broken mirror hypothesis, there is also evidence
to support a link between the MNS and higher-order social cogni-
tive processes related to action and emotion understanding. For
tered Botox to block automatic facial mimicry, a presumed conse-
to successfully infer others’ emotional facial expressions. Further-
and higher-order social cognitive processes that are typically im-
paired in ASD, such as empathy (34–36), facial affect recognition
(37,38), and the interpretation of action (26). Thus, mirror neurons
opercularis) disrupts subsequent imitation (39), which has been
(40). Thus, our findings of reduced MNS activity in ASD and an
association with social relating seem entirely consistent with the
broken mirror model.
The neuropathophysiology of the broken mirror account might
be best understood in the context of motor impairments in ASD;
mirror neurons, after all, are also motor neurons. Although not a
core symptom, impaired motor coordination is widely recognized
and review). This includes, for example, dyspraxia (42,43), distur-
bances of gait and posture (44), and impaired movement prepara-
tion (45,46). Neuroimaging and electrophysiological research has
allowed our understanding of this dysfunction to extend to struc-
premotor cortex, supplementary motor area, basal ganglia, thala-
in the current study, dyspraxia in ASD is associated with clinical
characteristics, including impaired social relating (42,43). Thus, the
observed mirror neuron deficit may reflect, at a cortical level, im-
paired motor function in ASD and result from the disrupted devel-
opment of neural circuitry involving key motor regions. Related to
tivity in ASD (52), a possibility that we have previously discussed in
relation to both ASD and schizophrenia (53). This does not argue
against the broken mirror hypothesis, but it does provide a sound
neurobiological basis for reduced mirror neuron activity in ASD.
Despite our findings, it cannot be conclusively suggested that
dysfunctional mirror systems cause some forms of autism or that
who display no evidence of mirror system activity. The broken
mirror hypothesis of autism has been highly controversial since its
inception, largely because of what it attempts to explain and the
limitations of extant research, and a number of researchers have
suggested that a mirror neuron-based explanation of autism is
premature or grossly undersupported (54,55). In the broken mirror
social cognition, providing an embodied simulation of others’
minds that allows interpersonal understanding. A recent, alterna-
Hebbian sensorimotor associations, whereby the mirror properties
and the observation of these same or similar motor actions often
co-occur (e.g., parental imitation of a child in infancy, visually self-
guided motor movements) (55). Within this association model, it is
conceivable that there is an underlying nonmirror mechanism in
autism that produces the social and communicative impairments
but that these impairments also prevent the necessary social ori-
enting and attention toward others that are crucial to the effective
formation of these mirror associations. The data from the current
rimotor model seems less well equipped to account for findings
substantial testing in relation to the broken mirror hypothesis of
models, claiming an important role for experience in the develop-
ment of mirror neurons but attesting to their capacity to under-
stand goals and other aspects of behavior (27).
Accordingly, the issue of causation in this study remains unre-
solved, with mirror neuron impairment either a cause or conse-
quence of social impairments in ASD. This uncertainty, however, is
not specific to the broken mirror hypothesis. The correlational na-
clinical populations ensures that we must be cautious when at-
tempting to infer causality. In another example, the apparent re-
ductions in structural and functional connectivity between certain
brain regions in ASD (52) may actually be a product of a lifelong
pattern of altered engagement with one’s environment, social and
otherwise. Large-scale longitudinal studies will be critical to ad-
dressing these concerns.
a continuous variable (i.e., MEP amplitude when observing transi-
tive relative to static videos) and as a categorical variable (i.e.,
whether or not the MEP amplitude was greater for transitive than
static videos). That a significant association was seen for social
ron index may speak to the heterogeneous nature of ASD; that is,
ASD, it may indicate a neurobiological subtype of ASD that is asso-
ever, that the influence of AQ social on the continuous mirror neu-
ron variable approached significance. While this finding might be
seen as supporting the broken mirror hypothesis, it could also be
viewed as consistent with a sensorimotor learning account,
whereby greater social impairments might prohibit the effective
movements and others’ movements (i.e., mirror neurons). In any
neurobiological subtypes of ASD is of particular importance to de-
veloping biomedical treatments.
Limitations to this study include investigation of only one cere-
bral hemisphere, the inclusion of some medicated participants (al-
though the impact of psychotropic medication on recordings of
age range of participants. It might be argued that our results could
reflect attentional impairments (i.e., that the group that did not
show facilitation displayed poorer attention to the stimuli); this is
questions about the stimuli and the monitoring of participant eye
gaze. The use of self-report for determining symptom severity
might also be criticized; however, we lack strong measures for
third-party symptom ratings in ASD that are appropriate for both
children and adults. Furthermore, many of our adult participants
live alone, and in this respect self-report was considered most ap-
propriate. Nevertheless, the current findings provide support for
P.G. Enticott et al.
BIOL PSYCHIATRY 2012;71:427–433 431
the contention that, on the whole, there is an MNS impairment in
ASD. This impairment does not appear to affect all individuals with
need to determine the neurobiological source of this impairment
(e.g., motor systems, neural connectivity, neurotransmitter sys-
of this impairment (which will arise through continued study of
mirror neuron activity in both healthy and disordered human pop-
ulations). This will allow us to decide whether the human MNS
should be pursued in relation to developing new ways of diagnos-
ing and treating autism and associated disorders, or simply be
considered a by-product of impaired social relating.
This work was supported by a National Health and Medical Re-
Canadian Institutes of Health Research Clinician Scientist Award and
by Constance and Stephen Lieber through a National Alliance for Re-
search on Schizophrenia and Depression Lieber Young Investigator
We thank all those who took part in the study and those who as-
Freeman (Wesley College Melbourne), Ms. Pam Langford, Dr. Kerryn
Saunders, Ms. Linke Smedts-Kreskas (Supporting Parents of Children
with Autism & Asperger’s Syndrome, Community Living & Respite Ser-
tism Spectrum Australia, and the Asperger Syndrome Support Net-
Bradshaw, and Dr. Taffe reported no biomedical financial interests or
potential conflicts of interest. Dr. Daskalakis has received external
funding through Neuronetics, Inc. and Aspect Medical, Inc. and travel
support through Pfizer, Inc. Professor Fitzgerald has received equip-
1. Rizzolatti G, Fabbri-Destro M (2010): Mirror neurons: From discovery to
standing motor events: A neurophysiological study. Exp Brain Res 91:
3. Rizzolatti G, Craighero L (2004): The mirror-neuron system. Annu Rev
4. Keysers C, Gazzola V (2009): Expanding the mirror: Vicarious activity for
actions, emotions, and sensations. Curr Opin Neurobiol 19:666–671.
5. Gallese V (2007): Before and below ’theory of mind’: Embodied simula-
Frith C, editors. Social Intelligence: From Brain to Culture. New York: Ox-
ford University Press.
6. Williams JHG, Whiten A, Suddendorf T, Perrett DI (2001): Imitation, mir-
ror neurons and autism. Neurosci Biobehav Rev 25:287–295.
7. Oberman LM, Ramachandran VS (2007): The stimulating social mind:
The role of the mirror neuron system and simulation in the social and
communicative deficits of autism spectrum disorders. Psychol Bull 133:
8. Iacoboni M, Dapretto M (2006): The mirror neuron system and the
consequences of its dysfunction. Nat Rev Neurosci 7:942–951.
9. Dapretto M, Davies MS, Pfeifer JH, Scott AA, Sigman M, Bookheimer SY,
Iacoboni M (2006): Understanding emotions in others: Mirror neuron
dysfunction in children with autism spectrum disorders. Nat Neurosci
autism. Cereb Cortex 16:1276–1282.
Reduced gray matter volume of pars opercularis is associated with
impaired social communication in high-functioning autism spectrum
disorders. Biol Psychiatry 68:1141–1147.
12. Oberman LM, Hubbard EM, McCleery JP, Altschuler EL, Ramachandran
VS, Pineda JA (2005): EEG evidence for mirror neuron dysfunction in
13. Raymaekers R, Wiersema JR, Roeyers H (2009): EEG study of the mirror
14. Bernier R, Dawson G, Webb S, Murias M (2007): EEG mu rhythm and
imitation impairments in individuals with autism spectrum disorder.
individuals with autism spectrum disorder. Curr Biol 15:R84–R85.
16. Hadjikhani N, Joseph RM, Snyder J, Tager-Flusberg H (2007): Abnormal
activation of the social brain during face perception in autism. Hum
17. Martineau J, Andersson F, Barthelemy C, Cottier JP, Destrieux C (2010):
Atypical activation of the mirror neuron system during perception of
hand motion in autism. Brain Res 1320:168–175.
18. Cattaneo L, Fabbri-Destro M, Boria S, Pieraccini C, Monti A, Cossu G,
Rizzolatti G (2007): Impairment of actions chains in autism and its pos-
19. Bastiaansen JA, Thioux M, Nanetti L, van der Gaag C, Ketelaars C, Mind-
eraa R, Keysers C (2011): Age-related increase in inferior frontal gyrus
activity and social functioning in autism spectrum disorder. Biol Psychi-
20. Fan Y-T, Decety J, Yang C-Y, Liu J-L, Cheng Y (2010): Unbroken mirror
21. Dinstein I, Thomas C, Humphreys K, Minshew N, Behrmann M, Heeger
DJ (2010): Normal movement selectivity in autism.Neuron 66:461–469.
22. Fadiga L, Craighero L, Olivier E (2005): Human motor cortex excitability
Understanding mirror neurons: Evidence for enhanced corticospinal
excitability during the observation of transitive but not intransitive
hand gestures. Neuropsychologia 48:2675–2680.
24. Gangitano M, Mottaghy FM, Pascual-Leone A (2004): Modulation of
premotor mirror neuron activity during observation of unpredictable
25. Gangitano M, Mottaghy FM, Pascual-Leone A (2001): Phase-specific
modulation of cortical motor output during movement observation.
26. Ocampo B, Kritikos A (2011): Interpreting actions: The goal behind mir-
ror neuron function. Brain Res Rev 67:260–267.
view [published online ahead of print April 5]. Neuroscientist.
28. Baron-Cohen S, Hoekstra RA, Knickmeyer R, Wheelwright S (2006): The
Autism-Spectrum Quotient (AQ)-Adolescent Version. J Autism Dev Dis-
Autism Spectrum Quotient (AQ): Evidence from Asperger Syndrome/
high functioning autism, males and females, scientists and mathemati-
scale to assist with the diagnosis of autism and Asperger’s disorder
(RAADS): A pilot study. J Autism Dev Disord 38:213–223.
31. Einfeld SL, Tonge BJ (2002): Manual for the Developmental Behaviour
atry, University of New South Wales.
mirror circuit: Interpretations and misinterpretations. Nat Rev Neurosci
fying and dampening facial feedback modulates emotion perception
of corticospinal excitability during action observation. Eur J Neurosci
432 BIOL PSYCHIATRY 2012;71:427–433
P.G. Enticott et al.
35. Pfeifer JH, Iacoboni M, Mazziotta JC, Dapretto M (2008): Mirroring oth- Download full-text
ers’ emotions relates to empathy and interpersonal competence in
children. Neuroimage 39:2076–2085.
36. Gazzola V, Aziz-Zadeh L, Keysers C (2006): Empathy and the somato-
topic auditory mirror system in humans. Curr Biol 16:1824–1829.
neuron activation is associated with facial emotion processing. Neuro-
38. Oberman LM, Winkielman P, Ramachandran VS (2007): Face to face:
Blocking facial mimicry can selectively impair recognition of emotional
expressions. Soc Neurosci 2:167–178.
39. Heiser M, Iacoboni M, Maeda F, Marcus J, Mazziotta JC (2003): The
essential role of Broca’s area in imitation. Eur J Neurosci 17:1123–1128.
40. Rogers SJ, Cook I, Meryl A (2005): Imitation and play in autism. In:
Volkmar FR, Paul R, Klin A, Cohen D, editors. Handbook of Autism and
Pervasive Developmental Disorders, 3rd ed. Hoboken, NJ: John Wiley &
41. Fournier KA, Hass CJ, Naik SK, Lodha N, Cauraugh JH (2010): Motor
coordination in autism spectrum disorders: A synthesis and meta-anal-
42. Dowell LR, Mahone EM, Mostofsky SH (2009): Associations of postural
knowledge and basic motor skill with dyspraxia in autism: Implication
for abnormalities in distributed connectivity and motor learning. Neu-
sky SH (2007): Dyspraxia in autism: Association with motor, social, and
44. Rinehart NJ, Tonge BJ, Bradshaw JL, Iansek R, Enticott PG, McGinley J
(2006): Gait function in high-functioning autism and Asperger’s disor-
der: Evidence for basal-ganglia and cerebellar involvement? Eur Child
45. Glazebrook CM, Elliott D, Szatmari P (2008): How do individuals with
autism plan their movements? J Autism Dev Disord 38:114–126.
46. Rinehart NJ, Bradshaw JL, Brereton AV, Tonge BJ (2001): Movement
47. Enticott PG, Bradshaw JL, Iansek R, Tonge BJ, Rinehart NJ (2009): Elec-
trophysiological signs of supplementary motor area deficits in high-
functioning autism but not Asperger’s disorder: An examination of in-
ternally cued movement-related potentials. Dev Med Child Neurol 51:
48. Rinehart NJ, Tonge BJ, Bradshaw JL, Iansek R, Enticott PG, Johnson KA
(2006): Movement-related potentials in high-functioning autism and
49. Muller RA, Pierce K, Ambrose JB, Allen G, Courchesne E (2001): Atypical
patterns of cerebral motor activation in autism: A functional magnetic
resonance study. Biol Psychiatry 49:665–676.
50. Allen G, Muller R-A, Courchesne E (2004): Cerebellar function in autism:
task. Biol Psychiatry 56:269–278.
51. Verhoeven JS, De Cock P, Lagae L, Sunaert S (2010): Neuroimaging of
autism. Neuroradiology 52:3–14.
tivity in autism. Brain Cogn 75:18–28.
(2008): Reduced motor facilitation during action observation in schizo-
phrenia: A mirror neuron deficit? Schizophr Res 102:116–121.
54. Hickok G (2008): Eight problems for the mirror neuron theory of action
P.G. Enticott et al.
BIOL PSYCHIATRY 2012;71:427–433 433