Imitation, mirror neurons and autism

Article · Literature Review (PDF Available) inNeuroscience & Biobehavioral Reviews 25(4) · July 2001with317 ReadsDOI: 10.1016/S0149-7634(01)00014-8 · Source: OAI

Justin H G Williams


Thomas Suddendorf

Thomas Suddendorf


Andrew Whiten

David I Perrett47.07

(Häijyn näköistä porukkaa...)



Various deficits in the cognitive functioning of people with autism have been docu-mented in recent years but these provide only partial explanations for the con-dition. We focus instead on an imitative disturbance involving difficulties both in copying actions and in inhibiting more stereotyped mimicking, such as echolalia. A candidate for the neural basis of this disturbance may be found in a recently dis-covered class of neurons in frontal cortex,'mirror neurons' (MNs). These neurons show activity in relation both to specific actions performed by self and matching actions performed by others, providing a potential bridge between minds. MN systems exist in primates without imitative and ‘theory of mind’ abilities and we suggest that in order for them to have become utilized to perform social cognitive functions, sophisticated cortical neuronal systems have evolved in which MNs function as key elements. Early developmental failures of MN systems are likely to result in a consequent cascade of developmental impairments characterised by the clinical syndrome of autism.

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1. Introduction: the basis of autism ...........................................................287
2. The role of early imitation ......................................................................288
3. Imitation in autism ....................................................................... .........289
4. Neurobiology of imitation .................................................................. .....289
5. The functional signi®cance of mirror neurons ...................................... 290
5.1. Speech ............................................................................ ...................290
5.2. Theory of mind ..................................................................... ............. 290
5.3. More basic intersubjective phenomena: emotional contagion and shared attention.................................................................................................... 290
5.4. Imitation ..............................................................................................291
6. Mirror neurons and autism ................................................................... 291
7. Autism, executive functions and mirror neurons ................................. .291
8. Neuroimaging mirror neurons and `theory of mind' ............................. .292
9. Testing the hypothesis ......................................................................... 292
10. Conclusion ......................................................................................... 293
References ............................................................................................... 293

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1. Introduction: the basis of autism
The autistic spectrum disorders are increasingly being recognised as an important cause of social disability [1]´and have been the focus of a ¯urry of research in the last decade [2± 5]. Here, we suggest that juxtaposing some of these psychological ®ndings with recent discoveries in neurobiology offers the prospect of a new and potentially powerful model of both early social functioning and the disorders in it that are associated with autism.
The autistic spectrum disorders are characterised by impairments in social interaction, imaginative ability and not specific to the condition such as global developmental delay, aggression or sleep disturbance.
2. The role of early imitation
The possibility that deficits in imitation might be particularly intimately connected with the earliest developmental stages of autism was ®rst set out systematically
by Rogers and Pennington [21]. According to these authors, imitation might fill at least two of the three gaps left by the ToM explanation noted above: first, imitation has characteristics suggesting that the mechanisms underlying it could be precur- sors (perhaps the first that can be identified in infancy) to full ToM; and second, imitation may also be fundamental to the other, broader kinds of social deficits seen in autism. The relationship between imitation and the third group of (largely non-social) deficits listed above is one we shall discuss once other parts of our model have been explained.
Rogers and Pennington [21] collated existing empirical evidence of imitation defi-cits in autism, which we discuss in the following section. First, however, some key theoretical bases for a link between imitation mechanisms and later developing ToM need to be recognised.
Imitation and the attribution of mental states bear some fundamental resemblan-ces [22,23]. Both involve translating from the perspective of another individual to oneself. Thus in accurately reading the belief of another, one essentially copies the belief into one's own brain, creating a `second-order' representation of the other's primary representation of the world (and, of course, not confusing it with one's own beliefs, at least in the normal case). Conversely, in imitating, one must convert an action plan originating from the other's perspective into one's own. A more specific linkage between imitation and ToM is implied by the fact that one of the two principal models of how ToM operates is designated the `simulation' theory [24]. Its rival is the `theory theory', which sees the child acting somewhat like a young scientist, observing patterns of behaviour in others, and developing theories about mental states to explain and predict them. The simulation theory instead proposes that children come to read minds by `putting themselves in the other's shoes', and using their own minds to simulate the mental processes that are likely to be operating in the other.
`Acting as if you are the other's simulation is thus at the covert, mental level akin to what is involved at the overt level in imitation. Current views include the possi-bility that both `simulation theory' and `theory-theory' processes are at work in the human case [25].
Meltzoff and Gopnik [26] reviewed evidence for imitation in the earliest phase of infancy and proposed that this could provide a key starting-state for the develop-ment of ToM. The nub of their hypothesis is that the new-born's capacity to trans-late between the seen behaviour of others and what it is like to perform that same behaviour offers a crucial basis for recognising the linkage between mental states and actions.
There are, thus,substantial theoretical reasons for considering imitation as a prime candidate for the building of a ToM. Rogers and Pennington's theory [21] was that at the root of autism is `impaired formation/co-ordination of specific self-other re-presentations', manifest first in impaired imitation,followed by a cascade of impair- ments in emotion-sharing, joint attention and pretend play (thus including the broad range of socialde®cits), and ToM. What, then, is the evidence for imitation being affected in autism?
3. Imitation in autism
Evidence for an imitative de®cit in autism has been reviewed elsewhere [21, 27 ± 29]. None of these reviews is comprehensive,but together they cite 21 experimen-tal studies of the imitative competence of individuals with autism.The studies have been heterogeneous with respect to the mental ages tested, the types of control groups used and the imitation tests themselves, but only two studies did not find an imitative deficit in the autistic samples and then possibly because of the simpli-city of the tasks,leading to ceiling effects. Smith and Bryson [27] conclude that the literature shows a `consistent fnding that people with autism do not readily imitate the actions of others'. Furthermore it is worth noting the magnitude of the imitative deficit. For instance, Rogers et al.[30] detected group differences of approximately 1.5 standard deviations between the autistic and control group means. More re-cently, Hobson and Lee [31] found that only 1 out of 16 (6%) subjects imitated the style of one of their tasks, compared to 12 out of 16 (75%) controls. A number of studies have detected significant group differences with just 10 subjects per group. The magnitude of this deficit then can be at least as great if not greater than the `theory of mind' deficit. Rogers [28] additionally notes the difficulties faced by carers in intensively teaching imitation to young children with autism.
Deficits in the imitation of `symbolic' elements (such as pantomiming brushing one's teeth with a non-existent toothbrush) might be expected in view of the dia-gnostic criteria; thus of special interest are those concerning basic body move-ments or gestures. These were first demonstrated by DeMeyer et al. [32] and have since been replicated in at least nine further studies [27±29].
Rogers [28] concludes that `every methodologically rigorous study so far pub-lished has found an autism-specific de®cit in motor imitation'. The conclusion that the imitative deficit may be operating at such a fundamental level is important to our synthesis with neurobiological findings discussed further below.
The reason for difficulties in imitation associated with autism remains unclear but some clues may come from an examination of the type of imitative deficit present.
Firstly, imitation of meaningless gestures would appear to be affected more than imitations of actions with objects [30].
Perhaps the use of objects in some tests may offer a `prop', helping to shape a matching response; by contrast, difficulties in copying raw gestures underlines the more basic nature of the imitative de®cit referred to earlier [33].
Secondly, when children with autism were asked to imitate an unconventional action with a common object (such as drinking from a teapot) they were more like-ly to make errors [27]. This again provides evidence for an imitative deficit more fundamental than that expected on the basis of other known impairments. Thirdly are reversal errors [27,29];for example,in `copying' the action of holding the hands up palm away, grasping the thumb of one hand with the other hand, autistic sub-jects tended to hold their palm towards themselves, recreating the hand view they had seen (sometimes also failing to grasp the thumb) instead of translating the perspective the other had seen [25]. Finally there are greater group differences with respect to sequences of actions than when single actions alone are being imitated [30].Together,these kinds of errors suggest that deficits may be occurring in the basic ability to map actions of others onto an imitative match by oneself [29] especially when such actions are complex.
Finally, there is a curious aspect of imitation-like phenomena in relation to autism, that concerns the well-known repetitive and stereotyped behaviours and speech
that may occur. These may be copied from others, including words and phrases (echolalia) and sometimes actions, that are mimicked without regard to their nor-mal goals and meanings.At first sight these phenomena seem contradictory to the notion of an imitative de®cit, but they may instead offer clues to the underlying neural dysfunction. We will discuss this in a later section, in integration with the findings on neurobiology to which we now turn.
4. Neurobiology of imitation
Patients with left frontal lobe lesions may show imitative dyspraxia [33,34]. These patients are unable to repeat actions performed by others, despite demonstrating
adequate motor control of their limbs. Furthermore, they are unable to replicate such gestures on a manikin [35].
This is consistent with the idea that imitation may normally rely on representation of action at a `supramodal' level [36], which is unavailable to these patients; the same lesion site will accordingly disrupt the replication of a gesture whether on the self or on another body.
Work at the neuronal level in non-human primates has started to indicate the path-ways by which representation of such actions may be built up. A number of diffe-rent types of specialised neuron have been identified in the superior temporal sul-cus (STS) of monkeys that are dedicated to visual processing of information about the actions of others.
Particular populations of cells code the posture or the movements of the face, limbs or whole body [37±41].Other classes of neurons appear to code movements as goal-directed actions and are sensitive to hand and body movements relative to objects or goals of the movements (e.g. reaching for, manipulating or tearing an object) [42 ± 45].
Of special relevance to our model is a subset of such action-coding neurons iden-tified in the prefrontal cortex (area F5) in monkeys [46, 47]. Such neurons will fire when the monkey performs a speci®c action, such as a precision grip, but also when an equivalent action (a precision grip, in this example) is performed by an individual the monkey is watching. These have been called `mirror neurons' (MNs) [47]. Their potential relevance to imitation is signalled by another label: `monkey see, monkey do' neurons [48]. F5 cell activity, however, does not automatically lead to motor responses and action performance, otherwise seeing actions performed would lead to obligatory copying (echopraxia).
The execution of actions when F5 cells are activated by the sight of actions of others, may be inhibited by mechanisms operating elsewhere in the motor pathway [49] and perhaps involving orbitofrontal cortex [50].
Although MNs cannot be studied directly in the same way in humans, the exis-tence of a system with the properties of MNs is supported by ingenious alternative approaches [47,51] including the use of transcranial magnetic stimulation (TMS) of human motor cortex to produce electromyographic potentials in muscle groups [52]. Observing actions involving distal finger movements but not proximal whole
arm movements selectively lowered the threshold for TMS to induce electromyographic activity in distal musculature.
This demonstrates input from the sight of movements to the neural system involved in motor control of the same movements.
Several functional imaging studies have noted that the sight of hand actions pro-duces activity in frontal regions (premotor cortex and Broca's area) [53,54], which may be homologous to F5 in the monkey [49]. In a recent fMRI study, activation of the left Broca's area during observation of finger movements became more intense when that same action was executed simultaneously [55]. These imaging
studies also reveal activity in parietal cortex. This area, along with possibly the superior temporal sulcus, also shows some evidence of mirror neuron activity ([56] and M. Iacoboni (pers. com.)).
5. The functional significance of mirror neurons
MNs appear to have the capacity to embody a `supramodal representation' of action, functioning as a bridge between higher visual processing areas and motor cortex (between seeing and doing). As yet, MNs have been investigated with res-pect to hand actions, but it seems likely that others are concerned with different actions, such as facial expression and speech, and perhaps eye movements and the higher-level abstractions [41, 42]. However, MNs have only recently been dis-covered. Their precise significance is not yet known, but some specific suggestions are particularly relevant to our discussion.
5.1. Speech
Rizzolatti and Arbib [49] have suggested that the part of the monkey brain which contains MNs dealing with hand actions has evolved to subserve speech in hu-mans, with language building on top of a `prelinguistic grammar of actions' already existing in the primate brain. By acting as a bridge between perceived and per-formed action and speech, the MN system is thus suggested to have provided
the foundations for the evolution of dialogue. Furthermore,if MNs do process audi- tory representations as they do visual ones,they may be important in representing the relationships between words and their speaker like the personal pronouns.
If this is true, the MN system may also provide crucial foundations ontogenetically, particularly with respect to the development of the pragmatic aspects of speech, and thence more complex aspects of language. However, not only the pragmatics of speech may depend on a functional mirror neuron system. Lack of invariance in the physical structure of phonemes gave rise to the motor theory of speech per-ception, which suggests that we hear sounds according to how we produce them [57, 58]. If MNs are an important link between the production and perception of speech or between sender and receiver [49]Ð then an intact MN system may be important for other stages of language development as well.
5.2. Theory of mind
Gallese and Goldman [59] have suggested that it may be possible to predict and also `retrodict' an observed person's mental state by constructing the appropriate mental correlates of an act once it is `reconstituted' in the observer's own MN system.They suggest that MN activation can permit the generation of an executive plan to perform an action like the one being watched, thereby getting the observer `into the mental shoes' of the observed (but see also Gallese [60]).
They also note this is a process that requires an ability for controlled inhibition to prevent concomitant execution of an observed action. They argue that such a mechanism is in keeping with the `simulation' model of ToM, which also requires that observed action sequences are represented in the observer `off-line' to prevent automatic copying, as well as to facilitate further processing of this high-level social information.
5.3. More basic intersubjective phenomena:emotional contagion and shared attention
Before moving on to consider the possible role of mirror neurons in autism, it is important to note that there seems no reason in principle why MNs should not address a wide range of actions and the mental states they connote. For example, since emotional states are closely linked to certain facial expressions, observation of a facial expression might result in mirrored (but mainly inhibited) pre-motor acti-vation in the observer and a corresponding `retrodicted' emotional state. Such a process might help to explain the phenomenon of emotional contagion, in which people automatically mirror the postures and moods of others [61]. This seems particularly likely in view of the close connections between STS neurons, the mir-ror neuron circuits and the amygdala [43]. Indeed, there is direct electromyogra-phic evidence that observers adopt facial muscle activity congruent with expressions witnessed even when this process is not at an overt level [62].
Like emotion reading [20], a capacity for shared attention has been proposed as an important precursor to full theory of mind, partly on the basis of evidence that deficits in this capacity are apparent early in the life of individuals with autism, their occurrence thus being explored as an early warning sign [16,63,64]. Here we note simply that being able to identify the focus of attention of another, or to be able to consider drawing their attention to the focus of one's own attention, is another case of being able to `stand in the other's shoes'. In shared attention, each individual's attentional focus mirrors the other, raising the prospect that MNs
could play a role in this achievement.
5.4. Imitation
In discussing the possible role of MNs in each of the above capacities, some references to imitative-like phenomena (`standing in the others shoes') have been made. It might be thought that the obvious functional role of MNs would indeed lie in imitation (in which case MN outputs would not be inhibited). However, noting that there is little evidence of imitation in monkeys [65,66] Gallese and Goldman [59] suggested that in the monkeys in which they have been identified, MNs are functioning to facilitate social understanding of others (to the extent the monkey `stands in the same `mental shoes' as the other, as Gallese and Goldman put it).
This is not argued to amount to ToM (for which there is also little evidence in monkeys [22,23]), but it may nevertheless represent the kind of foundation which permitted the evolution of ToM in humans [59].
However, we note there is better evidence for imitation in apes than in monkeys, and of course imitation is both evident and functionally important in our own species [66,67]. We suggest that the evolution of imitation in humans is likely to have utilised an existing MN system, even if its prior uses lay in more generalised kinds of social understanding. As mentioned earlier, fMRI with human subjects during a simple imitation task did indeed find activation in area 44 as well as in parietal cortex, suggesting that the MN system is involved in imitation in humans.
If Gallese and Goldman are right about the function of MNs in monkeys, certain additional capacities had to evolve before MNs could support either imitative or more advanced ToM functions. We may guess that these additional factors reject
the increased cortical volumes of great apes and humans and the representatio-nal capacities associated with them; their precise nature is a question for future research. For now, the critical hypothesis is that MNs provide a key foundation for the building of imitative and mindreading competencies.
Accordingly, if Rogers and Pennington were right about the linkage between imi-tation and ToM, we should, thus,expect that MNs play important roles in the whole ontogenetic cascade from early imitation to elaborated ToM. This would clearly be consistent also with Gallese and Goldmann's [59] hypothesis that MNs and ToM are linked.
6. Mirror neurons and autism
These ideas lead directly to our hypothesis that some dysfunction in the MN sys-tem might be implicated in the generation of the constellation of clinical features which constitute the autistic syndrome. The most basic hypothesis would be that there is a failure or distortion in the development of the mirror neuron system. This could be due to genetic or other endogenous causes, to external conditions ad- verse to MN functioning,or some interaction between these. Such factors might af- fect all MN groups or be confined to just certain groups such as those in the parie-tal cortex. Complete failure is not necessarily implied, for there might be merely a degree of delay or incomplete development.
Considering the factors discussed in previous sections, such dysfunction could prevent or interfere with imitation, or perhaps more fundamentally, lead to the `impaired formation/co-ordination of speci®c self-other representations' proposed to lie at the root of the cascade of autistic problems [21]. This in turn could explain the failure to develop reciprocal social abilities including shared/joint attention, gestural recognition and language (particularly the social/pragmatic aspects that Rogers and Pennington [21] note are the most affected), as well as breakdowns in
the development of empathy and a full ToM.
Such a simple `MN-dysfunction, imitation-dysfunction' model is unlikely to provide the whole story, however, insofar as we also need to explain features of repetitive, in¯exible and stereotyped behaviour and language that appears to incorporate some copying from others, in some patients with autism.
We would suggest that in fact these latter features are testimony to the per-ception-action linkage problems that occur in autism; they are consistent with the hypothesis that in autism, the mirror neuron system is as a whole malfunctioning. In these cases the system might be evidencing poor modulation.
Recall that it has been suggested that a controlled inhibitory system is essential for allowing MN's to operate `off-line' for simulation ToM to function and develop. If damage extends to such inhibitory components, then certain forms of mimicry
might occur, yet be oddly performed.
7. Autism, executive functions and mirror neurons
In recent years it has been shown that autistic individuals experience difficulties in executive functions like planning [68 ± 72]. It tends to be assumed that executive functions such as planning ability and attentional shifting are the product of deve-lopmental processes largely restricted to the individual. But it is also possible that the child learns something of these functions from others, perhaps initially in rela-tively concrete contexts, such as playing with building bricks in infancy,and then at higher levels of abstraction and over longer time frames, such as planning meals. The initial stages in such a process might correspond to some kind of `program-level' imitation [73]. There is evidence for this in three-year-old children who are able to acquire, by imitation, alternative hierarchical plans for running off a sequence of actions to complete a functional task [74]. Insofar as MNs code for actions on objects, directed towards a goal, they could be key elements in such a process [75], helping to translate perceived executive functions into praxis and then generalising them to similar situations.
With poor MN development, the key building blocks permitting planning functions to be acquired from the external culture might be unavailable.
If mirror neurons play a part in the development of executive function as well as ToM,one would expect to see a correlation between performance on tests of each of the two abilities. This has recently been demonstrated [76].The same principles may apply to the acquisition of other executive functions, such as approaches to problem solving and attentional shifting,which can be a problem for autistic child- ren [68,69]. Evidence in favour of this proposition comes from Griffiths et al. [77]. They found that apart from tests requiring rule reversal, there was no deficit of executive function in children under 4 years of age with autism. This suggests that the executive deficits are not primary but arise later on in a disrupted pattern of development. Some executive functions, including inhibition and possibly visual working memory appear to be spared in autism [4,67,78,79]. These might be functions much less easily learnt by imitation.
Autistic children show not only characteristic ToM and planning deficits, but also impairment in reconstructing the personal past [80]. Suddendorf [81 ± 83] has pro-posed that the executive capacity to disengage or dissociate from one's actual current state (putting it of¯ine, as it were) in order to simulate alternative states un-derlies both `theory of mind' and mental `time-travel' the ability to mentally con-struct possible (e.g. planned) events in the future and reconstruct personal events from the past. Thus, in this account mirror neurons may be implied through simulation and executive functions.
8. Neuroimaging mirror neurons and `theory of mind'
If ToM and related social de®cits in autism are the result of a poorly functioning system of mirror neurons, this might be manifest in recent neuroimaging studies
with relevant tasks. The mirror neuron region has been implicated in reading facial emotion in a normal population [84]. Similarly, a task that involved reading emotio- nal expressions from looking at images of eyes, found that individuals with autism showed less involvement of areas normally activated during emotional interpre-tation, namely the left putative mirror-neuron region (BA 44/45), the superior tem-poral gyrus (BA 22) bilaterally, the right insula and the left amygdala [85]. A recent review [86] of studies of both typical individuals and those with autism, seeking to identify sites active in ToM functions found that a well demarcated area of the pa-racingulate gyrus has been consistently implicated, as have areas of the anterior cingulate cortex but not the mirror neuron regions. The paracingulate gyrus and the anterior cingulate cortex are closely linked and receive dense serotonergic innervation, consistent with them performing a modulatory function and this could explain their involvement. One possible reason for the failure of these tasks to activate MN regions may be related to the control tasks that have been used. As these have been predominantly action-based such as following an action-based story, they would be expected to activate the MN regions as much as the ToM task, so discounting their apparent relevance.
9. Testing the hypothesis
From our hypothesis, several testable predictions ¯ow.
First, imitative de®cits should be apparent in autism especially where studies take place in the earliest years such as in the study by Charman et al. [87]. Particular aspects of imitation expected to be most susceptible are those where imitation involves a co-ordinated activity between different modes of sensory input, different groups of action-coding neurons and self-other visual transformations.
Secondly, we suggest that the McGurk effect [88] whereby the perceived sound is altered by perceiving lip movements making a different sound,may be the result of MN functioning. In this case we predict that on testing groups of children with autism, non-standard McGurk effects will be apparent.
A third prediction can be related to the work of Baron-Cohen et al. [64] using the CHAT screening test for autism.
These authors found that joint attention at 18 months was a predictive screening item for autism (focussing on siblings of individuals with autism). Our hypothesis predicts that even earlier, appropriately-sensitive screening for an imitative deficit would be predictive in this way.
Fourth, we would predict that imaging studies will indicate altered activation of putative MN regions in the brain during imitation tasks attempted by subjects with autism. Similarly, electrophysiologic studies will show altered muscle activity during the observation of actions, whether facial, vocal or with the hands
One recent study has attempted to examine mirror neurone activity in Asperger's syndrome [89].Magnetoencephalography was used to detect a decrease in the 20 Hz activity that occurred in the MN region during median nerve stimulation whilst subjects viewed an action. The study did not find a significant difference between the five Aspergers' participants and a control group. Our analysis predicts that
more extensive testing of people with autism will reveal such a difference.With the small sample size and small expected effect size (the hypothesis was tested in older individuals with the milder form of the disorder) this first study had minimal power and there was a high risk of a type two error. It is therefore important that further work is extended to larger groups with other characteristics.
10. Conclusion
The discovery of mirror neurons offers a potential neural mechanism for the imitation of actions as well as other aspects of understanding social others.
Evolution of this system may have been critical in the emergence of proto-culture and Machiavellian manoeuvring in the most encephalized non-human primates, followed by elaborate ToM and language in humans [90]. In the development of the human child, mirror neurons may be key elements facilitating the early imi-tation of actions, the development of language, executive function and the many components of ToM. A failure to develop an intact, sensitively regulated, mirror neuron system may therefore impair the development of these important human capabilities.
Our exploration of this hypothesis highlights numerous aspects of our ignorance.
Unanswered questions include:
1. What other cognitive and neural capacities work in conjunction with MNs to support imitation and ToM functions?
2. How do MNs relate to other social information processing neurons in performing social cognitive functions?
3. How physically extensive are MN functions which relate to autism? Do they just exist in Broca's area or are there such groups in locations such as parietal cortex, paracingulate gyrus and superior temporal sulcus?
4. Do MNs have functions in non-visual modalities as preliminary reports suggest (C. Keysers, E. Kohler, A. Umilta, V. Gallese and G. Rizzolatti, personal commu-
nication; Baker and Perrett, unpublished studies)? For example, is the sound of an action (or vocal utterance) mirrored by the same neurons as those which mirror its sight? What is the range of actions addressed by MNs?
Despite the various candidates suggested in the literature, a `prime mover' source of the complex cascade of impairments that characterise autism has so far proved elusive. We are suggesting that developmental delay or distortion of a mirroring system with an early age of onset could be such `prime mover'. The heterogeneity of the autistic condition may argue against a single cause, yet the commonalities of the clinical syndrome nevertheless permit the possibility of a core dysfunctional mechanism. If this mechanism is normally a precursor to a cascade of effects on other variable systems, then its dysfunction is likely to result in a quite variable cli-nical picture. Our proposal offers such a mechanism, together with some prelimi-nary evidence for its existence and empirically testable hypotheses. If it gains further empirical support, this may suggest important new avenues for both psychological and pharmacological remediative strategies.
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Sari Avikainen nojaa tähän aivopieruun väitöskirjassaan 2005:



6.1.4 Functional role of the MNS

MNS function is based, according to the direct-matching hypothesis (Rizzolatti et al. 2001), on mapping of the visual representation of an action onto the observer’s own motor representation of the same action. This matching function has been suggested to be in involved in different behaviors, such as action understanding, imitation, attributing mental states, and even in some aspects of language. In action understanding, the motor knowledge of the observer is used for understan-ding and recognizing actions of others (Rizzolatti et al. 2001). In line with this as-sumption, in a PET study by Grezes et al. (1998) the premotor areas were stron-ger activated during observation of meaningful arm actions, when the subjects had to undertand the purpose of the actions than when they just had to imitate the actions.

The term imitation can be used to describe many kind of functions in biology, sociology and psychology. When simple defined as copying by an observer of an action performed by a model, the underlying neural mechanism has been pro-posed to be based on the MNS (Iacoboni et al. 1999; Nishitani and Hari 2000; Rizzolatti et al. 2001; Nishitani and Hari 2002; Wohlschläger and Bekkering 2002). The function of the MNS may involve different imitative phenomena, such as ‘res-ponse facilitation’ (an automatic tendency to reproduce observed movements) in-cluding release phenomena in birds and yawning, laughing and neonatal imitation in humans (Meltzoff and Moore 1977), further to higher order imitation and imitative learning (Rizzolatti et al. 2001; Wohlschläger and Bekkering 2002).

The possible role of the MNS in other complex cognitive functions, such as lan-guage (Rizzolatti and Arbib 1998) and mind-reading (Gallese and Goldman 1998), has also been discussed.In line with the motor theory of speech perception (Liber- man and Mattingly 1985; Liberman and Whalen 2000), suggesting that successful linguistic communication is not dependent on sound, but rather on a neural link between the sender and the receiver that allows production of phonetic gestures, Rizzolatti and Arbib (1998) proposed that the action execution/observation mat-ching system could have served as the neural prequisite for the development of interindividual communication and finally speech. Interestingly, in a recent study by Petitto et al. (2001), babies with profoundly deaf parents were shown to convey a kind of silent linguistic babling with their hand movements.


Gallese and Goldman (1998) have proposed that the ability to detect and recog-nize mental states of others could have evolved from the MNS. According to one of the dominant mind-reading theories, the simulation theory (Davies and Stone 1995), other person’s mental states are detected by matching their states with resonant states of one’s own. Shared representations of different actions could serve as the basis of getting the observer into the same ‘mental shoes’ as the target (Gallese and Goldman 1998).

According to the simulation theory, all mental states requiring TOM, irrespective of whether they are are attributed to others or to oneself, should involve same neuro-nal system. However, in a fMRI study by Vogeley et al.(2001), modeling ones own mental-states activated at least in part dintinct brain regions than modeling the mental-states of others, opposed to the basic idea of simulation.

Although the relation of the MNS to different cognitive functions is still merely spe-culative, the discovery of the mirror neurons has offered a new tool to investigate brain function in our social enviroment. Future goals in this field include mapping of all brain areas involved in the mirror-neuron system and obtaining more infor-mation about their precise role in it. Futhermore,more information is needed about different stimulus types and modalities that are able to evoke mirror-neuron type activation, about the connection of the mirror-neuron system with different cogni-tive capacities, and about the possible role of a dysfunctional mirror-neuron system in different patient groups.

6.2 Autism

The autism spectrum disorders are a group of neurodevelopmental disorders that have a great variability in their clinical presentation but alltogether share some core symptoms, such as social impairment, deficits in communication, and restric-tive pattern of behaviour. Autism has been a great challenge for neuroscience during the last decade.

Although a lot has been learned since the time when it was thought to be a psy-chogenic syndrome caused by “refrigerator mothers”, the rapidly growing body of literature reports very heterogenous findings and theories about the basis of autism.

Abnormalities have been observed in many brain regions. However, not all sub-jects with autism show any abnormalities e.g. in structural or functional brain ima-ging, and none of the found abnormalities characterizes all subjects.In spite of the intensive research, we still don’t know whether autism is a single syndrome vary-ing in severity or whether the autism spectrum of disorders have multiple etiologies that nonetheless lead into similar core symptoms.


Autism is a rather common syndrome affecting about 0.7% of the general popu-lation of children and adolescents (Gillberg and Wing 1999). Since it is a lifelong disorder with severe deficits in social interaction and communication and since many of the subjects have psychiatric and neurologic comorbidities, there is a great need for long-term institutional, medical, educational and psycho-social care. The costs for the individuals, the families and the society are significant. Even subjects at the able end of the disorder often have problems in coping in-dependently due to the social deficits that make their every-day life difficult. Sofar the treatment in autism merely includes rehabilitation and symptomatic medi-cation, no curative treatment exists. Although these means can of course relieve comorbid symptoms and help the subjects and families to manage in every-day life, there is evidence (Gillberg and Billstedt 2000) that the core features of autism do not change much over time. On the other hand, most of the intensive rehabili-tation has only been performed during the last decade, and randomised follow-up studies of these interventios are merely lacking. Most effective results have sofar been obtained from early and highly intensive intervention programmes (Howlin et al. 1995).

6.2.1 Autism and mirror neurons

None of the cognitive theories of autism (such TOM, weak central coherence and executive function deficit) has proven to be exclusive and none has been able to explain the whole range of symptoms found in autism. Most theories focus on so-cial symptoms, since in spite of the wide clinical variation all subjects with autism spectrum disorders suffer from social deficits. However, the neural basis of the deficit is largely unknown.

The discovery of mirror neurons has lead to hypothesis of their role in social cog-nition (Gallese and Goldman 1998; Rizzolatti et al.2001; Williams et al.2001). Es-pecially, when evidence of the human counterpart of the monkey mirror neurons was found, a question of the possible dysfunction of the MNS in conditions associ-ated with social impairments, such as autism, was raised. Dysfunction of the MNS could lead in impairments in imitation, action understanding and further in difficul-ties in using and understanding body-language, mentalising, joint attention and even some aspects of language (Williams et al. 2001).


Total dysfunction, partial dysfunction, a dysfunction in certain parts of the MNS, or a developmental delay could all be in question.

In Studies II, V, and VI the hypothesis of possible connection between MNS and autism was tested. Study II showed rather normal activation of the primary motor cortex in a group of AS subjects both during observation and execution of manipu-lative hand actions, in spite of the deficit in their TOM abilities. The results exluded the possibility of a total dysfunction of the MNS in Asperger subjects.Furthermore, no evidence was found of the connection between a TOM deficit and MNS dys-function. However, the number of subjects was small (N = 5) and although no sta-tistically significant differences were observed, a slight tendency was evident toward a weaker activation of the M1 in AS subjects.

In Study V, the AS and HFA subjects’ imitation abilities were examined by using a behavioural task. Recent evidence suggests that human imitation is based on the mirror-neuron system (Iacoboni et al. 1999; Nishitani and Hari 2000; Wohlschläger and Bekkering 2002). Normally people tend to imitate as in looking at a mirror (Bekkering et al. 2000; Iacoboni et al. 2001) and observation of movements in a mirror-image view speeds up performance also in non-imitative tasks (Brass et al. 2000; Brass et al. 2001).

However, Study V showed that AS and HFA subjects are impaired in goal-direc-ted imitation, when the imitation occurs in a mirror-image fashion. As certain as-pects of imitation, such as imitation requiring self-other visual transformations, are most susceptible for MNS function (Williams et al. 2001), a developmental delay or adysfunction of the MNS could explain the observed results.

In Study VI, the hypothesis of a MNS dysfunction in autism was tested further by recording cortical activations while AS subjects imitated orofacial gestures. The results showed abnormal activation in the IF and M1 areas. As the the human mirror-neuron areas (the inferior parietal region, the Broca’s region and the M1) are activated in sequence, dysfunction of both frontal and parietal part of the MNS could explain the delayed and weaker activation of the IF and M1 areas. Broca’s region, the homologue of monkey F5 area, is activated during observation, exe-cution and imitation of hand and mouth movements (Iacoboni et al.1999; Nishitani and Hari 2000; Nishitani and Hari 2002) and considered as an essential part of the human MNS. Dysfunction of the IF part of the MNS could affect social abilities via connections to the orbitofrontal cortex and to the anterior ventral medial frontal region that are considered to contribute to theory of mind.


The STS region is closely connected to the MNS function and it has an important role in perception of many kind of socially relevant visual stimuli (for a review, see Allison et al. 2000; Puce and Perrett 2003). Interestigly, the STS region is also ac-tivated in tasks requiring mentalising (McGuire et al. 1996; Gallagher et al. 2000). In line with these results, autistic children, have been shown to be impaired in vi-sual recognition of biological motion (Blake et al. 2003). In a PET study by Castelli et al. (2000), activations of the STS and medial prefrontal cortex were weaker in autistic than in control subjects during a mentalising task, whereas the activity of the exstrastriate cortices did not differ from the controls. However, in Study VI ac-tivation of the occipital and STS areas did not differ between AS and control sub-jects. This discrepancy probably reflects different activation cascades within the STS region; perception of an mouth and hand actions in order to imitate might be intact in the STS level in AS subjects, whereas processing of more abstract and complex social stimuli (such as cartoons and stories of TOM) could be affected. Accordingly, perception of goal-directed hand actions was found to activate the caudal STS and the intraparietal sulcus, whereas perception of expressive whole-body motion activated the rostrocaudal STS, as well as the limbic structures, including the amygdala (Bonda et al. 1996).

Subjects in Studies II, V, and VI were adults and had AS (except one subject in Study II and two subjects in Study V who were autistic) representing the able end of the autism spectrum disorders. This subject group was chosen, since MEG re-cordings require some co-operation from the subjects, especially when tasks in-volve active participation. Additionally, the subjects have to keep their heads stea-dy during the measurement to avoid movement artefacts and to enable identifi-cation of accurate source locations. Futhermore, in the AS group the amount of other factors that could affect the results, such as medication, comorbidities and language problems, is at minimum. Adult subjects were studied, because the knowledge of MEG responses in children and adolescents is still rather limited. However, in adults with the most “mildest” form of the disorder, the size of the effect could be smaller than in more severely affected subjects. On the other hand, although most AS and high-functioning autistic subjects, are of normal intelligence, they suffer from social difficulties, which according to the MNS hypothesis are just the symptoms that are linked with the MNS function.

Altogether, the results from Studies II and VI suggest that MNS dysfunction can account for a part of the imitation and social impairments in subjects with Asperger’s syndrome.


Since we only studied able adult subjects, it would be interesting in the future to examine MNS function in more affected and younger subjects. Furthermore, modulatory influences from the prefrontal theory-of-mind regions on the MNS should be evaluated.

In autism research, lack of replication of studies, small and heterogenous experi-mental groups and poor control of other confounding variables have for long been a problem, therefore future studies should attempt to investigate more homoge-neous subgroups within the autism spectrum disorders. Effective communication between reseachers on this field will help to integrate and update the diagnostic criteria for the different subgroups. The studies should also aim at integrating in-formation from different fields of the research, such as genetics, functional ima-ging and neuropsychology. Hopefully, in the near future we are able to understand much better the biological mechanisms underlying the mystery of autism.





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FOXP2 and the mirror system



An inherited deficit in spoken language has been associated with a mutation in the forkhead box P2 ( FOXP2) gene on chromosome 7. A recent functional magnetic resonance imaging study has linked the deficit to underactivity in Broca's area during word generation, which in turn suggests a possible link between FOXP2 and the mirror-neuron system observed in the primate homologue of Broca's area. This link might have implications for the evolution of Broca's area and its role in speech.


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DOI: 10.1016/j.tics.2004.01.007



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Mice carrying a "humanized version" of a gene believed to influence speech and language may not actually talk, but they nonetheless do have a lot to say about our evolutionary past, according to a report in the May 29th issue of the journal Cell, a Cell Press publication.

Read more at:
Mice carrying a "humanized version" of a gene believed to influence speech and language may not actually talk, but they nonetheless do have a lot to say about our evolutionary past, according to a report in the May 29th issue of the journal Cell, a Cell Press publication.

Read more at:

Mice carrying a "humanized version" of a gene believed to influence speech and language may not actually talk, but they nonetheless do have a lot to say about our evolutionary past, according to a report in the May 29th issue of the journal Cell, a Cell Press publication.


"In the last decade or so, we've come to realize that the mouse is really similar to humans," said Wolfgang Enard of the Max-Planck Institute for Evolutionary Anthropology. "The genes are essentially the same and they also work similarly." Because of that, scientists have learned a tremendous amount about the biology of human diseases by studying mice.

"With this study, we get the first glimpse that mice can be used to study not only disease, but also our own history."

Enard said his team is generally interested in the genomic differences that set humans apart from their primate relatives. One important difference between humans and chimpanzees they have studied are two amino acid substitutions in FOXP2. Those changes became fixed after the human lineage split from chimpanzees and earlier studies have yielded evidence that the gene underwent positive selection. That evolutionary change is thought to reflect selection for some important aspects of speech and language.




No Evidence for Recent Selection at FOXP2 among Diverse Human Populations Graphical

Sohini Ramachandran et. al.

No support for positive selection at FOXP2 in large genomic datasets.

Sample composition and genomic scale significantly affect

An intronic ROI within FOXP2 is expressed in human brain cells and cortical tissue

This ROI contains a large amount of constrained, human-specific polymorphisms