Tämä  puoskaritiede on lähtenyt liikkeelle jo aikanakin 12 vuotta aikai-semmin Britanniasta NATO-tieteen Euroopan-keskuksesta (hyvässä ja pahassa, olen itsekin käynyt luennoimassa ja julkistamassa tutkimustulok-siani siellä, motkaissut olan takaa oman alan "eurotiedettä", ettei sen puoleen...), jo 8 vuotta ennen Giacomo Rizzolattin ilmeisiä väärennösha-vaintoja (2) samalla, alun perin Ragnar Granitin kehittämällä elektrodi-menetelmällä, saman porukan ja lisäksi tamperelaisen Jari K. Hietasen toimesta, tästä tarkemmin lopussa. (1)


Imitation, mirror neurons and autism

Article · Literature Review (PDF Available)  in Neuroscience & Biobehavioral Reviews 25(4) · July 2001 with 317 ReadsDOI: 10.1016/S0149-7634(01)00014-8 · Source: OAI

https://www.researchgate.net/publication/28763620_Imitation_mirror_neurons_and_autism

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Justin H G Williams
Institution
Department

 

Thomas Suddendorf

Thomas Suddendorf

The University of Queensland | UQ · School of Psychology

 

Andrew Whiten

ImportedProfilePhoto.jpg

Andrew Whiten

David I Perrett47.07

Perrettmedium.jpg

David I. Perrett
 

Institution
Department

(Häijyn näköistä porukkaa...)

 

Abstract

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 condition. 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 discovered 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.


(PDF) Imitation, mirror neurons and autism.

Available from:

https://www.researchgate.net/publication/28763620_Imitation_mirror_neurons_and_autism [accessed Aug 05 2018].

Contents
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


(PDF) Imitation, mirror neurons and autism. Available from:

https://www.researchgate.net/publication/28763620_Imitation_mirror_neurons_and_autism [accessed Aug 05 2018].

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 findings 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 first 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 precursors (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 deficits in autism, which we discuss in the following section. First, however,some key theore- tical 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 resemblances [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 re-presentation 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 pat-terns of beha-viour 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 possibility 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 in-fancy and proposed that this could provide a key starting-state for the development of ToM. The nub of their hypothesis is that the new-born's capacity to translate bet-ween 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 represen-tations', manifest first in impaired imitation,followed by a cascade of impairments 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 deficit in autism has been reviewed elsewhere [21,27 ± 29]. None of these reviews is comprehensive, but together they cite 21 experimental stu-dies 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 simplicity 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, Ro-gers et al. [30] detected group differences of approximately 1.5 standard deviations between the autistic and control group means. More recently, Hobson and Lee [31] found that only 1 out of 16 (6%) subjects imitated the style of one of their tasks, com-pared 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 diagnostic criteria;thus of special interest are those concerning basic body movements 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 published 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 mat-ching 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 likely to make errors [27]. This again provides evidence for an imitative deficit more funda-mental 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 subjects 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 perspec-tive 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 (echola-lia) and sometimes actions, that are mimicked without regard to their normal goals and meanings. At first sight these phenomena seem contradictory to the notion of an imitative deficit,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 different types of specialised neuron have been identified in the superior temporal sulcus (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 identi-fied in the prefrontal cortex (area F5) in monkeys [46,47].Such neurons will fire when the monkey performs a specific 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 po-tential relevance to imitation is signalled by another label: `monkey see, monkey do' neurons [48]. F5 cell activity, however, does not automatically lead to motor respon-ses 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 existence of a system with the properties of MNs is supported by ingenious alternative approa-ches [47, 51] including the use of transcranial magnetic stimulation (TMS) of human motor cortex to produce electromyographic potentials in muscle groups [52]. Obser-ving actions involving distal finger movements but not proximal whole arm move-ments 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 produ-ces 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 respect 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 discovered. 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 humans, 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 performed action and speech, the MN system is thus suggested to have provided the foundations for the evolution of dialogue. Furthermore,if MNs do process auditory 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 perception, 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 sys-tem.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 me-chanism 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 im-portant 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 emo-tional states are closely linked to certain facial expressions, observation of a facial expression might result in mirrored (but mainly inhibited) pre-motor activation in the observer and a corresponding ´retrodicted' emotional state. Such a process might help to explain the phenomenon of emotional contagion, in which people automati-cally mirror the postures and moods of others [61]. This seems particularly likely in view of the close connections between STS neurons, the mirror neuron circuits and the amygdala [43]. Indeed, there is direct electromyographic 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 occur-rence 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 referen-ces 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 un-derstanding.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 in-creased cortical volumes of great apes and humans and the representational capa-cities 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 imitation and ToM, we should, thus,expect that MNs play important roles in the whole ontoge-netic cascade from early imitation to elaborated ToM. This would clearly be consis-tent 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 system 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 adverse to MN functioning, or some interaction between these. Such factors might affect all MN groups or be confined to just certain groups such as those in the parietal 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 pre-vent 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, inexible 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 perception-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 develop-mental processes largely restricted to the individual. But it is also possible that the child learns something of these functions from others, perhaps initially in relatively 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 com-plete a functional task [74]. Insofar as MNs code for actions on objects, directed to-wards 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 children [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 execu-tive 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 im-pairment in reconstructing the personal past [80]. Suddendorf [81± 83] has proposed that the executive capacity to disengage or dissociate from one's actual current state (putting it offline, as it were) in order to simulate alternative states underlies both `theory of mind' and mental `time-travel' the ability to mentally construct 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 deficits in autism are the result of a poorly functioning sys-tem of mirror neurons, this might be manifest in recent neuroimaging studies with re-levant tasks. The mirror neuron region has been implicated in reading facial emotion in a normal population [84]. Similarly, a task that involved reading emotional expres-sions from looking at images of eyes, found that individuals with autism showed less involvement of areas normally activated during emotional interpretation, namely the left putative mirror-neuron region (BA 44/45), the superior temporal gyrus (BA 22) bi-laterally, 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 paracingulate 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 per-forming 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 as-pects 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 puta-tive 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 indi- viduals 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 imitation 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 communication; 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 elu-sive. 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 au-tistic 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 sys-tems,then its dysfunction is likely to result in a quite variable clinical picture. Our pro- posal offers such a mechanism, together with some preliminary evidence for its exis-tence 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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[HM: Tuo "Pierret(ys)" ON SIIS "TUTKINUT" 10 VUOTTA AIKAISEMMIN PILKUL-LEEN SAMAA ONGELMAA SAMOIN KEINOIN KUN "TIETEEN MULLISTAJA" GIACOMO RIZZOLATTI, SIIS JUURI "PEILINEURONEJA" (= "AJATUS KEENIN EXPRESSIONA, PÖLHÖ-KANDEL!) - MITÄPÄ MUUTAKAAN! SAAMATTA KUI-TENKAAN ODOTETTUA TULOSTA "REHELLISESTI"! Kun homma meni havain-noissakin huijaamiseksi (eikä vain niiden tulkinnoissa), hommaan valittiin "sopiva" henkilö melko kaukaa infosota"tieteen" "esikunnasta": syntyjään neuvostoliiton-italialainen, pavlovilaisen tutkimustaustan (sen "kumottavan"!) omaava Rizzolatti Parmasta Italiasta!
 
[39] Perrett DI, Harries MH, Benson PJ, Chitty AJ, Mistlin AJ. Retrieval of structure from rigid and biological motion; an analysis of the visual response of neurons in the macaque temporal cortex. In: Troscianko T, Blake A, editors. AI and the eye, Chichester: J. Wiley & Sons, 1990. p. 181± 201.
[40] Oram MW, Perrett DI. Responses of anterior superior temporal polysensory (STP) neurons to `biological motion' stimuli. J Cog Neurosci 1994; 6: 99± 116.
[41] Perrett DI, Harries MH, Bevan R, Thomas S, Benson PJ, Mistlin AJ,Chitty AJ, Hietanen J, Ortega JE. Frameworks of analysis for the neural representation of animate objects and actions. J Exp Biol 1989; 146:87 ± 114.

[Tosi vanha pieru: Tuo "Pierret" näyttää olevan primus motor; tuolloin ei kuitenkaan ole "tiedetty peilineuroneista"... vai "onko"? HM]

 
[42] Perrett DI, Emery NJ.Understanding the intentions of others from visual signals: neurophysiological evidence. Curr Psychol Cog 1994; 13: 683 ± 94.
[43] Emergy NJ, Perrett DI. How can studies of the monkey brain help us understand `theory of mind' and autism in humans. In:Baron-Cohen S,Tager-Flus-berg H, Cohen DJ, editors. Understanding other minds perspectives from develop-mental cognitive neuroscience, 2nd ed. Oxford: Oxford University Press, 2000.
[44] Jellema T, Oram MW, Baker CI, Perrett DI. Cell populations in the banks of the superior temporal sulcus of the macaque and imitation. In:Meltzoff A,Prinz W, editors. The imitative mind:development, evolution, and brain bases, 2001 (in press).
[45] Jellema T, Baker CI, Wicker B, Perrett DI. Neural representation for the perception of the intentionality of hand actions. Brain Cog 2001; 44: 280 ± 302.
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[47] Rizzolatti G, Fadiga L, Matelli M, Bettinardi V, Paulesu E, Perani D, Fazio F. Lo-calisation of grasp representations in humans by PETÐ1: observation vs execution. Exp Brain Res 1996; 111: 246 ± 52.
[48] Carey DP. `Monkey see, monkey do' cells. Current Biol 1996; 6:1087 ± 8.
[49] Rizzolatti G, Arbib MA. Language within our grasp. Trends Neurosci 1998; 21: 188 ± 94.

HM: Michael Arbib oli ensimmäinen joka loikkasi ulos tuosta sisäpiiristä vaatien Rizzolattin koepöytäkirjoja julkisiksi ja näin myös antaen ymmärtää, että "kokeet" oli-vat joko väärennettyjä.Ne eivät siis olleet ryhmän jäsenillekään julkisia! Tämä tapah- tui sen jälkeen, kun ilmeni, ettei Rizzolattin "kokeita" pystytä elektrodimenetelmällä toistamaan millään lajilla. Valitettavasti Arbib siirtyi sittemmin toisen HUUHAAn, "ajattelevien tietokoneiden" pariin,eikä oikeaan tieteeseen,kuten toinen "auktoriteetti" Michael Tomasello, joka omissa kokeissaan huomasi, että IHMISAPINOILLA EI OLEKAAN MITÄÄN "MIELENTEORIAA", oletuksia toisten aikomuksista! "Sellainen" on vain ihmisellä - ihminen niitä ajatuksia ja suunnitelmia sitten olettaa muiden elä-vien päihin, perusteettomasti. Kahden hölynpölläriryhmän, "aitojen ja keinotekoisten peilineuronien, todella ajattelevien tietokneiden", ero on metodologinen: ensimmäi-nen yrittää "löytää luoonosta" oletutensa mukaisen informaatisystemminen, jälkim-mäinen taas "rakentaa sellaisen" ensin keinotekoisesti - ja sitten väitää, että "se on se, millä myös luonto toimii".
 
[50] Stevens JA, Fonlupt P, Shiffrar M, Decety J. New aspects of motion perception: selective neural encoding of apparent human movements. Neuroreport 2000; 11: 109 ± 15.
[51] Hari R, Forss N, Avikainen S, Kirveskari E, Salenius S,Rizzolatti G. Activation of human primary motor cortex during action observation: a neuromagnetic study. Proc Natl Acad Sci 1998; 95: 15061 ± 5.
[52] Fadiga L, Fogassi G, Pavesi G, Rizzolatti G. Motor Facilitation during action observation: a magnetic stimulation study. J Neurophysiol 1995; 73: 2608 ± 11.
[53] Grafton ST, Arbib MA, Fagdiga L, Rizzolatti G. Localization of grasp represen-tations in humans by positron emission tomography 2: observation compared with imagination. Exp Brain Res 1996; 112: 103 ± 11.
[54] Rizzolatti G,Fadiga L,Gallese V,Fogassi L. Premotor cortex and the recognition of motor actions. Cog Brain Res 1996; 3: 131 ± 41.
[55] Iacoboni M, Woods RP, Brass M, Bekkering H, Mazziota JC, Rizzolatti G. Cortical mechanisms of human imitation. Science 1999; 286: 2526 ± 8.
[56] Fogassi L, Gallese V, Fadiga L, Rizzolatti G. Neurons responding to the sight of goal-directed hand/arm actions in the parietal area PF (7b) of the macaque monkey. Soc Neurosci Abstracts 1998; 257(5): 654.
[57] Liberman AM, Cooper F, Shankweiler M, Studdert-Kennedy M. Perception of the speech code. Psychol Rev 1967; 74: 431 ± 61.
[58] Liberman AM, Whalen DH. On the relation of speech to language. Trends in Cognitive Sciences 2000;4:187± 96.
[59] Gallese V, Goldman A. Mirror neurons and the simulation theory of mind-reading. Trends Cog Sci 1998; 2: 493±501.
[60] Gallese V. Agency and motor representations:new perspectives on intersubjecti- vity. ISC working papers 2000-6. Workshop on Autism and the Theory of Mind, Lyon, 18th May, 2000. http://www.isc.cnrs.fr/wp/wp00-6.htm.
[61] Hatfield E, Caciopoo JT, Rapson RL. Emotional contagion. New York: Cambridge University Press, 1994.
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Sari Avikainen nojaa tähän aivopieruun väitöskirjassaan 2005:

 

http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/avikainen/cortical.pdf

 

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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, attri-buting mental states,and even in some aspects of language.In action understanding, the motor knowledge of the observer is used for understanding and recognizing actions of others (Rizzolatti et al.2001).In line with this assumption,in a PET study by Grezes et al. (1998) the premotor areas were stronger 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, socio-logy and psychology. When simple defined as copying by an observer of an action performed by a model,the underlying neural mechanism has been proposed to be based on the MNS (Iacoboni et al. 1999; Nishitani and Hari 2000; Rizzolatti et al. 2001; Ni-shitani 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 phe-nomena 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 language (Rizzolatti and Arbib 1998) and mind-reading (Gallese and Goldman 1998), has also been discussed. In line with the motor theory of speech perception (Liberman 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 matching system could have served as the neural prequisite for the development of interindividual communi-cation 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.

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Gallese and Goldman (1998) have proposed that the ability to detect and recognize 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 neuronal system. However, in a fMRI study by Vogeley et al. (2001), modeling ones own men-tal-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 specu-lative, 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 information 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 cognitive 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 restrictive pat-tern 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 psycho-genic 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 subjects with autism show any abnormalities e.g. in structural or functional brain imaging, and none of the found abnormalities characterizes all subjects.In spite of the intensive re-search, we still don’t know whether autism is a single syndrome varying in severity or whether the autism spectrum of disorders have multiple etiologies that nonetheless lead into similar core symptoms.

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Autism is a rather common syndrome affecting about 0.7% of the general population 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 indi-viduals, the families and the society are significant. Even subjects at the able end of the disorder often have problems in coping independently due to the social deficits that make their every-day life difficult. Sofar the treatment in autism merely includes rehabilitation and symptomatic medication, no curative treatment exists. Although these means can of course relieve comorbid symptoms and help the sub-jects and families to manage in every-day life, there is evidence (Gillberg and Bill-stedt 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 lac-king. 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 social symptoms, since in spite of the wide clinical variation all subjects with autism spect-rum 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). Espe-cially, when evidence of the human counterpart of the monkey mirror neurons was found, a question of the possible dysfunction of the MNS in conditions associated with social impairments, such as autism, was raised. Dysfunction of the MNS could lead in impairments in imitation, action understanding and further in difficulties in using and understanding body-language, mentalising, joint attention and even some aspects of language (Williams et al. 2001).

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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 au-tism 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 manipulative 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 dysfunction. However, the number of subjects was small (N = 5) and although no statistically sig-nificant 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 (Bek-kering 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-directed imitation, when the imitation occurs in a mirror-image fashion. As certain aspects 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 re-cording 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 se-quence,dysfunction of both frontal and parietal part of the MNS could explain the de-layed 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.

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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 acti-vated 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 visual 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 exstra-striate corti-ces did not differ from the controls. However,in Study VI activation of the occipital and STS areas did not differ between AS and control subjects. This discre-pancy probably reflects different activation cascades within the STS region; per-ception 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 intraparie-tal sulcus, whereas perception of expressive whole-body motion activated the rostro-caudal 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 recordings require some co-operation from the subjects, especially when tasks involve active participation. Additionally, the subjects have to keep their heads steady during the measurement to avoid movement artefacts and to enable identification 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 “mil-dest” form of the disorder,the size of the effect could be smaller than in more severe- ly affected subjects. On the other hand,although most AS and high-functioning autis- tic subjects, are of normal intelligence,they suffer from social difficulties,which accor- ding 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.

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Since we only studied able adult subjects, it would be interesting in the future to exa-mine 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 homogeneous 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 information from different fields of the research,such as genetics,functional imaging and neuropsy-chology. Hopefully, in the near future we are able to understand much better the biological mechanisms underlying the mystery of autism.

...

 

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[HM: Rizzo puhuu "suupeilineuroneista" jo 1981, 15 vuotta ennen "yllättäviä peilineuronilöytöjä"...]

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https://www.cell.com/trends/cognitive-sciences/abstract/S1364-6613(04)00024-5

FOXP2 and the mirror system

DOI: https://doi.org/10.1016/j.tics.2004.01.007
 

Abstract

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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Article Info

IDENTIFICATION

DOI: 10.1016/j.tics.2004.01.007

Copyright

© 2004 Elsevier Science Ltd. Published by Elsevier Inc. All rights reserved.

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"In the last decade or so, we've come to realize that the mouse is really similar to hu-mans," said Wolfgang Enard of the Max-Planck Institute for Evolutionary Anthropolo-gy. "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 hu-mans 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.


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https://reader.elsevier.com/reader/sd/7DE13466AC245BB500CFA9E5BF4B0D7CA9B77A5497E0CAB7195C2E30C95A4DF34AA279646AED38680CED4D2443079BED

 

Article

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


Ingressin viitteet
 
 
(1) http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.110.8731&rep=rep1&type=pdf

" J. exp. Biol. 146, 87-113 (1989)
 
87 Printed in Great Britain © The Company of Biologists Limited 1989
 
FRAMEWORKS OF ANALYSIS FOR THE NEURAL REPRESENTA-TION OF ANIMATE OBJECTS AND ACTIONS BY D. I. PERRETT, M. H. HARRIES, R. BEVAN, S. THOMAS, P. J. BENSON, A.J. MISTLIN, A. J. CHTTTY, J. K. HIETANEN AND J. E. ORTEGA
 
Department of Psychology, University of St Andrews, St Andrews, Fife KY16 9JU, Scotland

Summary

A variety of cell types exist in the temporal cortex providing high-level visual descrip-tions of bodies and their movements. We have investiga-ted the sensitivity of such cells to different viewing conditions to determine the frame(s) of reference utilized in processing. The responses of the majority of cells in the upper bank ofthe superior temporal sulcus (areas TPO and PGa) found to be sensitive to staticand dynamic information about the body were selective for one perspective view (e.g. right profile, reaching right or walking left). These cells can be considered toprovide viewer-centred descriptions because they depend on the observer's vantage point. Viewer-centred descriptions could be used in gui-ding behaviour. They could also be used as an in-termediate step for establishing view-in-dependent responses of other cell types which responded to many or all perspective views selectively of the same object (e.g. head) or movement. These cells have the properties of object-centred descriptions, where the object viewed provides theframe of reference for describing the disposition of object parts and movements (e.g. head on top of shoulders, reaching across the body, walking forward 'following the nose'). For some cells in the lower bank of the superior temporal sulcus (area TEa) the responses to body movements were related to the object orgoal of the move-ments (e.g. reaching for or walking towards a specific place). This goal-centred sensitivity to interaction allowed the cells to be selec-tively activatedin situations where human subjects would attribute causal and intentional relationships.
 
Introduction
 
This paper describes the response properties of cells in different re-gions of thetemporal association cortex of the macaque monkey. It is the aim of the paper to summarize the sensitivity of cells in this brain area to different types of biologically important visual stimuli. A paral-lel aim is to consider frameworks for visual processing which are ap-propriate for making explicit different types of informationabout ani-mate objects and hence for achieving a more complete understanding ofthe world.

Key words: temporal cortex, single cell, face, action.
 
88 D.I. PERRETT AND OTHERS
 
The first section of the paper focuses on cells in one region of the higher-asso-ciation cortex (the upper bank of the superior temporal sulcus, areas TPO and PGa of Seltzer & Pandya, 1978; Pandya & Yeterian, 1985) which appear to be involved in the recognition of individuals (Fig. 1, left column) and how these individuals are moving (Perrett etal. 1985a, b; Baylis et al. 1985).
 
This region has received extensive study since it was realised that it contained cells selectivelyre sponsive to faces (Bruce et al. 1981; Perrett et al. 1982, 1984, 1987; Rolls, 1984; Desimone etal.1984; Mikami & Nakamura, 1988). The second section focuses oncoding in an adjacent section of cortex in the lower bank of the same sulcus (area TEa of Seltzer & Pandya, 1978).
 
Populations of cells in this region appear to be involved in the recognition of ac-tions, that is, how other individuals are interacting with the environment (Fig. 1, middle column). Studies of action coding have been mainly restricted to actions of the hand but there are indications that the framework for such processing applies to actions of the whole body (Perrett et al.1989a, b, e).
 
Physiological methods
 
Standard single-unit recording techniques were employed to study cells indiffe-rent regions of the temporal cortex of awake, behaving rhesus macaquemonkeys (for details see Perrett et al. 1985a,b). A large-aperture shutter was usedto present different types of visual stimuli.These included real faces and bodies, two-dimen- sional slides of monkeys and humans in different postures,videotapes of different actions and a variety of simple and complex three-dimensional stimuli. Respon-ses to these stimuli were measured by analysing the number of actionpotentials from individual cells in a 0-25 s period beginning 100 ms after the shutteropened. This period of analysis was chosen because it is relatively uncontaminated with eye movements and visual responses in the temporal cortex generally have latencies greater than 100 ms.Viewer- and object-centred descriptions
 
General characteristics of face
 
Within the cortex of the superior temporal sulcus (STS) popu-lations of cellshave been studied that respond more to the sight of faces than to a variety ofsimple sti-muli (e.g.bars or gratings) or complex,potentially arousing stimuli (e.g.hands, ba- nanas, pictures of snakes and birds of prey) (Bruce et al. 1981; Penett etal. 1982). Most such cells are sensitive to the general characteristics of faces andrespond to a variety of faces regardless of their species (human or monkey). Thesecells also show a remarkable tolerance for changes in viewing conditions andrespond to faces despite change in retinal size, orientation and position (Perrett etal. 1982, 1984, 1988, 1989d; Bruce et al. 1981; Rolls & Baylis, 1986). This generalization indicates that the cells' discriminative responses to faces are notdependent direct-ly on simple visual attributes (e.g. position and orientation oflocal edges, spatial frequency components) which change from display to display.
... "

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Publications (11)

Publication Preview
Source
Use of preferential inspection to define the viewing sphere and characteristic views of an arbitrary machined tool part
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  • Perception
  •  
Measurements were made of the way human subjects visually inspected an idea-lized machined tool part (a 'widget') while learning the three-dimensional shape of the object. Subjects were free to rotate the object about any axis. Inspection was not evenly distributed across all views. Subjects focused on views where the faces of the object were orthogonal to the line of sight and the edges of the object were aligned parallel or at right angles to the gravitational axis. These 'face' or 'plan' views were also the easiest for subjects to bring to mind in a mental imagery task. By contrast, when subjects were instructed to imagine the views displaying the most structural information they visualized views lying midway between face views.
 
Publication Preview
Source
Viewer-centred and object-centred coding of heads in the macaque temporal cortex
Article
Full-text available
  • Feb 1991
  • Experimental Brain Research
An investigation was made into the sensitivity of cells in the macaque superior tem-poral sulcus (STS) to the sight of different perspective views of the head. This allowed assessment of (a) whether coding was 'viewer-centred' (view specific) or 'object-centred' (view invariant) and (b) whether viewer-centred cells were preferen-tially tuned to 'characteristic' views of the head.The majority of cells (110) were found to be viewer-centred and exhibited unimodal tuning to one view. 5 cells displayed object-centred coding responding equally to all views of the head. A further 5 cells showed 'mixed' properties,responding to all views of the head but also discriminating between views. 6 out of 56 viewer and object-centred cells exhibited selectivity for face identity or species. Tuning to view varied in sharpness. For most (54/73) cells the angle of per-spective rotation reducing response to half maximal was 45-70 de-grees but for 19/73 it was greater than 90 degrees. More cells were optimally tuned to characteristic views of the head (the full face or profile) than to other views. Some cells were, however, found tuned to intermediate views throughout the full 360 deg-ree range. This coding of many distinct head views may have a role in the analysis of social signals based on the interpretation of the direction of other individuals' attention.
 
Publication Preview
Source
Preferential inspection of views of 3-D model heads
Article
  • Feb 1991
  • Perception
The importance of different perspective views for the recognition of model heads was studied.
 
In experiment 1 subjects were instructed to learn the appearance of six heads placed individually on a turntable free to rotate through 360 degrees. Subjects did not distri-bute their time evenly but focussed their inspection on particular views (the full face view and a view close to the profile).Despite differential inspection of these two views during the learning phase, the face, half profile, and profile views were recognized with equal efficiency in a subsequent recognition task with static views.
 
Experiment 2 used the inspection paradigm to investigate view preference during the recognition of heads from memory. In this experiment subjects were asked to learn the appearance of three heads each seen rotating at an even speed. In a subse-quent retrieval task the subjects actively inspected six model heads on the turntable and were asked to differentiate the three heads previously seen rotating from three novel heads. The pattern of inspection in this retrieval task was equivalent to that in experiment 1. Results suggest that during the encoding into memory subjects con-struct descriptions of specific prototypical views of the head and that descriptions of these same views are preferentially utilised during recognition.
 
Publication Preview
Visual Processing of Faces in Temporal Cortex:Physiological Evidence for a Modular Organization and Possible Anatomical Correlates
Article
  • Jan 1991
  • Journal of Cognitive Neuroscience
Physiological recordings along the length of the upper bank of the superior temporal sulcus (STS) revealed cells each of which was selectively responsive to a particular view of the head and body.Such cells were grouped in large patches 3-4 mm across. The patches were separated by regions of cortex containing cells responsive to other stimuli. The distribution of cells projecting from temporal cortex to the posterior regions of the inferior parietal lobe was studied with retrogradely transported fluores-cent dyes. A strong temporoparietal projection was found originating from the upper bank of the STS. Cells projecting to the parietal cortex occurred in large patches or bands. The size and periodicity of modules defined through anatomical connections matched the functional subdivisions of the STS cortex involved in face processing evident in physiological recordings. It is speculated that the temporoparietal pro-jections could provide a route through which temporal lobe analysis of facial signals about the direction of others' attention can be passed to parietal systems concerned with spatial awareness.
 
Publication Preview
Social signals analyzed at the single cell level: Someone is looking at me, something touched me, something moved!
Article
  • Jan 1990
  • International journal of comparative psychology / ISCP; sponsored by the International Society for Comparative Psychology and the University of Calabria
Conducted 2 experiments that examined the behavioral significance of tactile and motion sensitive cells in the superior temporal sulcus (STS) of the macaque brain. In the awake, behaving monkey ,the critical dimension for polymodal coding was whether or not the sensations were expected. Tactile stimulation out of sight could not be predicted and elicited neuronal responses. By contrast, when the monkey could see and, therefore, predict impending contact, or when the monkey touched a familiar surface in a predictable location, cell responses were reduced or abolished. In an analogous way some cells were unresponsive to the sight of the monkey's own limbs moving, but responded to the sight of other moving stimuli.
(PsycINFO Database Record (c) 2012 APA, all rights reserved)
 
Publication Preview
Understanding the visual appearance and consequence of hand action
 
Article
  • Jan 1990
 
Publication Preview
Three stages in the classification of body movements by visual neurons.
Article
  • Jan 1990
we have suggested that there are three ways in which body movements are classi-fied by nerve cells in the temporal lobe / by referring the movements to three diffe-rent frames of reference, the viewer, the object viewed or the goal of an action,in this classification a comprehensive understanding of the nature and intention of move-ment can be derived (PsycINFO Database Record (c) 2012 APA, all rights reserved)
 
Publication Preview
Source
Frameworks of analysis for the neural representation of animate objects and actions
Article
Full-text available
  • Oct 1989
  • Journal of Experimental Biology
A variety of cell types exist in the temporal cortex providing high-level visual descrip-tions of bodies and their movements. We have investigated the sensitivity of such cells to different viewing conditions to determine the frame(s) of reference utilized in processing. The responses of the majority of cells in the upper bank of the superior temporal sulcus (areas TPO and PGa) found to be sensitive to static and dynamic information about the body were selective for one perspective view (e.g. right profile, reaching right or walking left). These cells can be considered to provide viewer-cent-red descriptions because they depend on the observer's vantage point. Viewer-cent-red descriptions could be used in guiding behaviour. They could also be used as an intermediate step for establishing view-independent responses of other cell types which responded to many or all perspective views selectively of the same object (e. g.head) or movement.These cells have the properties of object-centred descriptions, where the object viewed provides the frame of reference for describing the dispo-sition of object parts and movements (e.g. head on top of shoulders, reaching across the body, walking forward 'following the nose'). For some cells in the lower bank of the superior temporal sulcus (area TEa) the responses to body movements were related to the object or goal of the movements (e.g. reaching for or walking towards a specific place). This goal-centred sensitivity to interaction allowed the cells to be selectively activated in situations where human subjects would attribute causal and intentional relationships.
 
Publication Preview
Source
 
Specialized face processing and hemispheric asymmetry in man and monkey: Evidence from single unit and reaction time studies
 
Article
  • Sep 1988
  • Behavioural Brain Research
Experimental and clinical studies have generally shown that the neural mechanisms for face processing in man are (1) designed to deal with the configuration of upright faces and (2) located predominantly in the right cerebral hemisphere.Monkeys would seem to process faces in a different manner to humans since they appear to show no hemispheric asymmetry and to treat upright and inverted faces equivalently. We re-examine these claims. Our reaction time studies reveal that monkeys do behave like human subjects since they process facial configuration faster when stimuli are pre-sented upright as compared with horizontal or inverted. Single unit studies in the monkey reveal patches of neurones responsive to faces in the upper bank and fun-dus of the left superior temporal sulcus (STS). Recording from the right hemisphere also reveals cells responsive to faces but in this hemisphere such cells appear less numerous.These cells process upright faces faster than inverted faces. Face proces-sing in monkeys and man appears to utilize qualitatively similar mechanisms, but the extent and/or direction of cerebral asymmetry in these mechanisms may not be similar.
 
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Source
 
Characteristic views and the visual inspection of simple faceted and smooth objects: Tetrahedra and potatoes
 
Article
  • Feb 1988
  • Perception
The way in which human subjects distribute their time when attempting to learn the surface appearance of objects placed on a stand free to rotate about its vertical axis was investigated. Experiments were undertaken to establish whether observers con-centrate their time on particular views and, if so, to determine the image characteris-tics of the preferred views. For tetrahedra,subjects concentrated on views which pre-sented a face or an edge centred on the line of sight. Both of these views were sym-metric about the vertical axis. For potatoes as examples of opaque smooth objects, subjects concentrated on four views in which the object's principal (long) axis was oriented side-on or end-on to their line of sight. For such views the horizontal width (and surface area) of the object's image had maximum and minimum values. Preferred views were not systematically related to views defined as stable from the appearance of surface boundaries or 'singularities'.
 
Publication Preview
Neuronal mechanisms of face perception and their pathology
Article
 

Citations (1,297)

... This region has been associated with visual-spatial attention, in particular atten-tional shifts (Corbetta, 1998; Corbetta et al., 1995; Haxby et al., 1994). Further, tem-poral-parietal connections may play a role in transferring expressive, changeable fa-cial features (e.g.,facial expressions,gaze directions) from the temporal to the parietal regions for spatial attention (Harries and Perrett, 1991). This might partially explain the difference noted between the parietal ROI and the occipito-temporal ROI. ...
 
Reference:
Integrating high-density ERP and fMRI measures of face-elicited brain activity in 9-12 year-old children: An ERP source localization study
 
Visual Processing of Faces in Temporal Cortex: Physiological Evidence for a Modular Organization and Possible Anatomical Correlates
Citing article
  • Jan 1991
View
 
... They found that their participants spent time exploring "plan" views, namely views that were on-axis or orthogonal and parallel to the object's structural axis. Perrett et al. [10,11] found a similar preference for "plan" views in tool-like as well as "novel" objects. The mixed evidence could be due to the fact that view-canonicity can be ex-pressed by the multiple factors [12]:goodness for recognition (a good view for recog-nition shows the most salient and significant features, and it is stable with respect to small transformations, and it avoids a high number of occluded features), familiarity (recognition is influenced by the views that are encountered more frequently and du-ring the initial learning), functionality (recognition is influenced by the views that are most relevant for how we interact with an object), and aesthetic criteria (preferred views can be influenced by geometric proportions). ...
 
Reference: A Survey of Viewpoint Selection Methods for Polygonal Models
 
Characteristic views and the visual inspection of simple faceted and smooth objects:
 
Tetrahedra and potatoes
 
Citing article
 
  • Feb 1988
  • PubMed
View
... First, the task demand and stimuli used in prior studies might be critical in the ob-servation of this deficit. In line with this claim, abnormal processing of gaze direction has been reported in both acquired and developmental prosopagnosia in studies using face pictures with a deviated head orientation faces (McConachie,1976; Perrett et al., 1988;De Haan & Campbell,1991) but not with a frontal head orientation (as in Duchaine et al.,2009;Burra et al.,2017). In addition,despite being able to discriminate gaze direction explicitly (left, right, center), prosopagnosia patients failed to respond automatically to gaze direction (Burra, Kerzel, & Ramon, 2017). ...
 
Reference: Eye gaze direction perception in a case of acquired prosopagnosia
 
Neuronal mechanisms of face perception and their pathology
 
Citing article
 
  • Invalid date
View
 
... These findings suggest that facial information from the subcortical system might affect the cortical visual system in early infants with premature cortical visual systems. Furthermore, previous behavioral studies have reported that monkeys and humans display behavioral sensitivity to face orientations (Perrett et al., 1990) and that great apes follow the directions of a human experimenter based mainly on the human's face orientation with eye direction also playing a role (Tomasello et al., 2007). These findings suggest that frontal faces with their face orientation directed to the subjects are important social signals regardless of gaze direction. ...
 
Reference:
Population Coding of Facial Information in the Monkey Superior Colliculus and Pulvinar
 
Understanding the visual appearance and consequence of hand action
 
Citing article
  • Jan 1990
View
 
...Perception of 3D orientation has been systematically studied for objects and faces. For example, rigid 3D objects and faces can be best recognized from canonical views (Blanz, Tarr & Bülthoff,1999), and humans tend to choose preferred views when learning 3D objects and faces (Harries, Perrett, & Lavender, 1991; Peissig & Tarr, 2006; Perrett & Harries, 1988). It has also been shown that local and global strategies are combined in a flexible manner when judging the facing in depth of 3D objects (Foster & Gilson, 2002; Troje & B ¨ulthoff, 1996; Watson, Johnston, Hill, & Troje, 2005). ...
Reference: Depth perception from point-light biological motion displays
 
Preferential inspection of views of 3-D model heads
 
Citing article
 
  • Feb 1991
  • PubMed
View
... We localized OFA in the lateral inferior occipital gyrus ( Gauthier et al., 2000), FFA in the mid-fusiform gyrus ( Kanwisher et al., 1997;McCarthy et al., 2003), and STS in the posterior part of the superior temporal sulcus. Since studies reported differences in face processing mechanisms across hemispheres ( Perrett et al., 1988;Kanwisher et al., 1997;Ishai et al., 1999;Haxby et al., 2000;Rossion et al., 2003;Kanwisher and Yovel, 2006;Meng et al., 2012), we defined face-sensitive areas separately for each hemisphere to assess differences in activation between the two hemispheres. ...
 
Reference:
Task-dependent enhancement of facial expression and identity representations in human cortex
 
Specialized face processing and hemispheric asymmetry in man and monkey:
 
Evidence from single unit and reaction time studies
 
Citing article
  • Sep 1988
  • PubMed
View
 
... They found that their participants spent time exploring "plan" views, namely views that were on-axis or orthogonal and parallel to the object's structural axis. Perrett et al. [10,11] found a similar preference for "plan" views in tool-like as well as "novel" objects. The mixed evidence could be due to the fact that view-canonicity can be ex-pressed by the multiple factors [12]:goodness for recognition (a good view for recog-nition shows the most salient and significant features, and it is stable with respect to small transformations, and it avoids a high number of occluded features), familiarity (recognition is influenced by the views that are encountered more frequently and du-ring the initial learning), functionality (recognition is influenced by the views that are most relevant for how we interact with an object), and aesthetic criteria (preferred views can be influenced by geometric proportions). ...
 
Reference: A Survey of Viewpoint Selection Methods for Polygonal Models
 
Use of preferential inspection to define the viewing sphere and characteristic views of an arbitrary machined tool part
Citing article
  • Feb 1992
  • PubMed
  •  
View
...The shapes and the parameters of each tuning curve are usually dependent on the specific neuron and stimulus. We highlight the work performed by Perret et al. in [79] and the work of Newsome and Salzman in [80] that investigated the firing patterns in reaching motions, and which we base our work upon. We extracted their results and used the functions they proposed in designing our Gaussian functions within the population are defined. ...
 
Reference: Dynamic contextualization and comparison as the basis of biologically inspired action understanding
 
Viewer-centred and object-centred coding of heads in the macaque temporal cortex
 
Citing article
  • Feb 1991
  • PubMed
View full-text
... Additional mirror neurons were later found within monkey parietal regions, which innervate the premotor cortex (Gallese, Fadiga, Fogassi, & Rizzolatti, 2002). With the incorporation of superior temporal re- gions, which are involved in recognizing biolo-gical motion (Perrett et al., 1990) and are reciprocally connected to parietal regions, a putative macaque imitation system has emerged Gallese et al., 1996). However, one significant limitation of the mirror neuron system model of imitation in macaque mon-keys is the simple fact that the available data indicate that the imita-tive abilities of species within this genus are notably limited (Visalberghi & Fragaszy, 2002). ...
 
Reference: Changes in fronto-parieto-temporal connectivity following Do-As-I-Do imitation training in chimpanzees (Pan troglodytes)
 
Social signals analyzed at the single cell level: Someone is looking at me, something touched me, something moved!
 
Citing article
 
  • Jan 1990
View
 
... The interest in the brain networks underlying others' observed action processing has been triggered by the discovery, in the monkey ventral premotor area F5, of the so-called "mirror neu- rons," which respond during both action execution and others' action observation (di Pellegrino et al.1992;Gallese et al. 1996;Rizzolatti et al. 1996). This finding demonstrated that observed action processing is not limited to visual brain areas (Perrett et al. 1989; Vangeneugden et al. 2009; Singer and Sheinberg 2010), but involves frontoparietal areas belonging to the motor system as well (see Materials and Methods for the anatomo- functional criteria defining the areas of inte-rest). Subsequently, neurons responding to the observation of another individual's action have been described in 2 parietal areas: PFG, in the infe- rior parietal lobule (IPL) convexity ( Fogassi et al. 2005;Rozzi et al. 2008;Bonini et al. 2010) and the anterior intraparietal (AIP) area ( Pani et al. 2014;Maeda et al. 2015). ...
 
Reference:
Anterior Intraparietal Area: A Hub in the Observed Manipulative Action Network
 
Frameworks of analysis for the neural representation of animate objects and actions
 
Citing article
  • Oct 1989
  • PubMed
 
****


http://keskustelu.skepsis.fi/Message/FlatMessageIndex/176429?page=1#176429
 
RK
16.06.2005 01:47:09
176429

Rizzolattin "peiliSOLUhavaintoja" ei ole pystytty vahvistamaan.

Harmis löysi viestissä 176090 milenkiintoisen linkin sosiobiologistikirkon sisäiseen keskusteluun ”peilisoluista”:

Harmaa.Eminenssi kirjoitti 12.06.2005 (176090)...

>Tällaista keskustelua aiheesta muualla:

>http://www.interdisciplines.org/mirror/papers/4/pr

RK (176097): Antipavlovistikirkon sisäistä jargoonia.

Mutta ERITTÄIN MIELENKIINTOISTA heti ensimmäisessä jutussa,että nimenomaan SOLUTASON ilmiöitä (ehdollistuneita tai muita) EI OLE EDES HAVAITTU muualla kuin Rizzolatti makaki-apinoilla!

Ja itse asiassa, kaikki muu tohina huomioiden tuon asian ympärillä, SIIHENKÄÄN "HAVAINTOON" EI TAIDA OLLA KAUHEASTI LUOTTAMISTA!

Arbib myös pulputtaa kovasti matkimisesta apinoilla,ja löytää siihen alkeellisilla api-noilla rudimentaarisen ehdottoman (tai leimaus-) refleksinkin, VAIKKA "PEILISOLU-TEORIAN" ISÄT Goldmann ja Gallese kategorisesti "KIELTÄVÄT" MATKIMISILMIÖIDEN OLEMASSAOLON apinoilla ja laajemminkin luonnossa” :

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/175827?page=1#175827

Otetaanpa muutama kommentti tuolta tarkastelun alle.

Michael Arbib:

” 1) Much of the discussion of “mirror neurons” is based on metaphorical discussion of “mirror systems” rather than on analysis of actual neurophysiological data.

Mirror neurons have only been measured in macaque monkeys. Human brain ima-ging data only provide evidence for mirror systems – i.e., neural regions active both during the execution of a class of actions and during the observation of actions from that class. A mirror system need not contain mirror neurons, though it is generally assumed that it will. “

Kommenttini yllä.

“2) My own work with Rizzolatti has suggested an evolutionary path from a mirror system for grasping via a mirror system that supports imitation [not present in more than rudimentary form in monkeys] to a mirror system that can support language [unique to humans]. But this is a theory. As far as I know, there is no evidence that mirror neurons are involved in language, imitation, or intersubjectivity. Rather, there is suggestive evidence that mirror systems may be related to these functions. “

RK: On olemassa ja tutkittuna myös ihan muita ja parempia selityksiä kielen tunnis-tamiselle ja oppimisella, jotka eivät TARVITSE YHTÄÄN SE ENEMPÄÄ ainakaan geneettisiä ”PEILISYSTEEMEITÄ” kuin ”-SOLUJAKAAN”:

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/162827?page=1#162827

Kuten Arbibkin tavallista rehellisempänä sosiobiologistina aiheellisesti mainitsee.

” ) In computer science and engineering, simulation involves the ability to predict a trajectory in quantitative detail. However, if we look at data on mirror neurons, there is no evidence of simulation at such a level of detail. Even worse, to reiterate one of Csibra’s points, many a mirror neuron is only “broadly congruent”. Again, we know there are mirror neurons that fire both when the monkey breaks a peanut and when he hears the sound of a peanut breaking (Kohler et al., 2002). But since the sound gives no information about the manner of breaking, it is unclear what justifies calling this “simulation” rather than just “classification”. If this concern is accepted, one must ask whether the “classification” theory of intersubjectivity loses any essential features of the “simulation” theory. “

Olen jossakin hieman erheellisesti maininnut, että ehdollistumisteorian mukainen mielenteoria kuuluu ”peilisolu- / -systeemiteoreetikkojen” kategoriaan ”simulaatioteoriat” (enemmänkin kuin Goldmannin kategoriaan ”teoriateoriat”).

Nyt niillä on kuitenkin uusi kategoria ”luokitteluteoria” (classification theory), johon se vasta istuukin hyvin, esimerkkinä juuri pähkinänkuoren rikkomisprodeduuri, joka ak-tivoituu myös rikkontuvan pähkinänkuoren aiheuttamasta äänestä,eikä vain sellaisen työn tekemisestä tai katselemisesta! (Itse asiassa siitä on vain yksi kukonaskel sym-bolifunktioon, että pähkinänkuoren rikkomisääni yhdistetään johonkin kellonkilauk-seen, tai SANAAN, joka tuo sen koko ehdollisen refleksin erilaisine variaationeen aktiiviseksi.)

” 4) Which leads into the observation that “classification” in the sense of mere “pattern recognition” in no way equals understanding or empathy. “

Arbib erehtyy siinä, että tuo refleksin aktivoituminen toiminnan äänestä ei olenkaan liittyisi YMMÄRTÄMISEEN: se ei vain liity, vaan se suorastan ON sitä!

Mutta EMPATIAAN sen ei todellakaan tarvitse liittyä millään tavalla: yhdistetynä muihin toiminalisiin kuvioihin se ”ymmärtäminen” voi aiheuttaa esimerkisi reaktion, joka ihmisllä vastaisi osapuilleen seuravaa: ”nyt se p..le löysi kumminkin sen mun piilottamani pähkinän, ja rikkoi sen! Turpiin tulee!"

” In other words,it is not the mirror neuron firing itself that is crucial, but rather activity in a widely distributed neural system of which the mirror neurons are part – and it is not even established that mirror neurons are more significant than quasi-mirror neurons in this regard. ”

“Peilisolusta” pidetään kuitenkin kiinni kuin sika limpusta, vaikka sitä EI TARVITA MIHINKÄÄN,ja HAVAINTOKIN niistä on asetettu kyseenalaiseksi! Lisäksi kehitellään uusia stiiknafuuliota, kuten ”kvasipeilisoluja” (jotka aktivoituvat havaitessa, mutta eivät tehdessä)!

SENKÖ TÄYTISEEN tarvitaan (vielä lisää) tuollaisia VALEKÄSITTEITÄ, se alkupe-räinen ”peilisolun” valekäsite oli fysiologisesti tarpeeton, koska jokainen aivokuoren pinnan solu olisi sen mukaan ainakin jonkin asian ”peilisolu”, mutta tuo ”kvasipeiliso- lu” on jo LOOGISESTIKIN saman tason "käsite" kuin vanhaa lasten vitsiä lainatakse-ni ”saippuan nimittäminen ´valeoravaksi´”, koska ”saippualla ja oravalla on yhteinen ominaisuus, että molemmat pääsevät puuhun, paitsi saippua”!

” 5) We must distinguish what the macaque data from Parma tell us about mirror neurons from what we tend to claim they tell us. “

OLOSUHTEET HUOMIOON OTTAEN: terävästi päätelty…: on pidettävä erillään se, mitä tulokset kertovat, ja mitä "me" (="sosiobiologistikirkko") HALUAMME USKOA niiden tarkoittavan!

Ei käynyt niin kuin pikku Kallelle, kun USKONNON opettaja kysyi, että "mikä on rus-kea ja karvainen ja hyppii oksalta oksalle". Kalle vastasi,että ”Ensin tuli vähän muuta mieleen, mutta OLOSUHTEET HUOMIOIDEN vastaan, että se on Jeesus-lapsi”.

(Vastaavalla odotusarvojen yodennäköisyystasolla ovat ehdollistumisteorian (”orava”) ja ”peilisolutoerian” (”Jeesus-lapsi”) edustamat tulkinnat neurofysiologisista kokeista….)

” 6) [Gerely] Csibra suggests that “a plausible counter-hypothesis for the role of MNs would be that they are involved in the prediction or anticipation of subsequent — rather than in the simulation of concurrent — actions of the observed individual.”

MITEN tuo on muka “peilisoluteorian” vastahypoteesi?

Jos siellä ”peilisolussa” on jokin TOIMINTA koodattuna, niin sehän on sitä juuri ”toimenpiteiden seurantona”, miten se muuten siellä voisi olla?

Mutta helvetin paljon yksinkertaisemmin tuollainen selittyy ehdollistumisteorialla ja ILMAN SOLUTASON KOODAUSTA, koska kullakin niillä osatoiminnoilla voi olla ja on oma refleksikaarensa SAMASSA "PROSESORISSA", ja niiden välille tarvitaan vain järjestävä yhteys, jotta niistä saadaan ”koko toiminnan refleksikaari” seurantoi-neen! Tuohon viime mainittuun voi sitten ärsykkenä viitata sana tai vaikka pähkinän-kuoren tietynlainen risahdus apinan salavarastolla. Tämä on sitä ehdollisten reflek-sien SYSTEEMISYYTTÄ, että ”ylin” ja ”abstraktein” taso määrää, ja ohjaa hierarki-sesti niihin alempiin , perustavampiin, alkupeäisempiin. Sellaista ei esiinny genetti-sillä erillisillä ehdoTTOMilla reflekseillä, joissa taas ”alin määrää” . (Esimerkiksi vaikka olisi kuinka herkullisia ruokia ja kuinka kauhea nälkä, mutta sormi pistetään kurkkuun, niin yrjö tulee. ”Vieras esine kurkussa, jota ei voi nielaista” on nimittäin originaalinen laukaiseva ärsyke).

” 7) Finally, let me note that simulation theorists seldom address the fact that we may be observing others while still going about our own lives. To address this, the simu-lation theorist must explain how the same neural circuitry could support the simula-tions of the others at the same time as it supports our own actions, and how it solves the binding problem of keeping the neural representations of agents and actions properly paired as the drama unfolds. “

Tässäkään ei ole ehdollistumisteorian valossa mitään ihmellistä: kaksi eri toimintoa voi hyödyntää yhtä aikaa samaa aktivoitua refleksikaarta, siitä on usein vain hyötyä, jos se on muutakin kautta aktiivisena (sanotaan vaikka bändisoitossa tai pariluiste-lussa, missä on toisella silmällä tai korvalla seurattava naapureiden suoritusta, tuol-lainen ei oikein automatisoitunesti muuten onnistuisikaan). Mutta jos kaksi henkilöä tekee samaa proseduuria hiukan eri tahtiin ja havainnoi toisiaan, niin sitten voi sekaanusta sattua, esimerkiksi siten, että jäljessä oleva jättää pois jonkin vaiheen ja jatkaa erehdykdessä samasta kohdasta missä se toinen suorittaja on.

Sillä, ovatko aktivoituvat ilmiöt ”solutason simulaatiota” vai suhteellisesti objektivoitunutta "toimnnan vakiomallia", on olennainen merkitys tukinnan kannalta.

Siitä nämä Gergely Csibran kommentit:

” 1. The existence of "mirror systems" does not tell us anything about simulation. Simulation theories require not only that the same neural substrate be involved in the execution and observation of actions, but also that the actual representations match between these domains. The claim that mirror neurons "mirror" actions has implicitly (and sometimes explicitly) been extended to "mirror systems" by analogy and terminology. As Arbib notes, there is no evidence supporting this claim. “

Ilman “mätsäystä” ei ole, tai ei tarvita, “peilisolujakaan”…

Nyt tullaan siihen, mikä olisi luokitteluteorian (joka siis sopii ehdollistumisteorian ja kielellisen ajateluteoriankin kanssa, jos sen ei oleteta olevan keenissä) ja ”simulaatioteorian” ero:

2. Arbib asks "whether the 'classification' theory of intersubjectivity loses any essen-tial features of the 'simulation' theory." Yes, it does - it loses its main point. If an action is 'classified' without simulation, then it is understood without simulation, and it is no longer "devoid of meaning" (Rizzolatti et al., 2001), however this meaning is elaborated by further processes.

“Simulaatioteorialla” voi pyyhkäistä tiettyä paikkaa ”luokitteluteorian” hyväksi, ja saman tien ”automaattisella mielenlukemisella”.

Jos esiintyy ”simuloivaa mielenlukemista” se on yhteisen harjoittelun tulos jossakin useamman henkilön työ- tmv. prosessissa. Ja se koskee pelkästään sitä tiettyä, yhteistä suoritusta edellyttävää prosessia.

Seuraavat pykälää kovempien "peisoluteorian" kannatajien "kriittiset kommentit" näistä osin kerettiläisistä huomiosta ovat mielenkiintoista paljastavaa luettavaa "peilisolutoerian" kannalta...

Pätkaisen tähän tällä kertaa, ja palaanniihin tuonnempana, inshallah...

RK

 
Arbibin Wiki-sivulla mainitaan hänen roollinsa Rizzolattin "peilineurooniryhmässä", MUTTA EI PUHUTA MITÄÄN HÄNEN KYLMISTÄ JÄLKIKÄTEISTERVEISISTÄÄN SILLE!

" With Richard Didday, he developed one of the first winner-take-all neural net-works in 1970. More recently, with Giacomo Rizzolatti, the leader of research team that discovered mirror neurons, he proposed an evolutionary link between mirror neurons, imitation, and the evolution of language. "


Vieläkin kaemmaksi rikostutkinassa päästään:

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/150509?page=1#150670

RK
14.09.2004 00:11:10
150670

Re: perustosiasiat, "peilisolut" on jo 1968 hahmoteltua poliittista "eurotiedettä

H5 kirjoitti 12.09.2004 (150560)...

>Hyvä RK

>Tietääkseni ainakaan missään neurologisissa julkaisuissa ei ole vielä >nimenomaisesti väitetty että ns. peilisolut olisivat rakenteeltaan mitenkään erilaisia >muista saman alueen (F5) soluista ts. nimenomaan tiettyjen geenien aktivoituminen >juuri näissä neuroneissa tekisi niistä peilisoluja. Kerro jos tiedät jotain muuta.

“Peilisolun” käsite on kopioitu kritiikittömästi Rizzolattilta, ja sitä pidetään apinoilla ”todistettuna”, vaikka Rizzolatti ei mitään sellaista ole todistanut (ja aivan tarkasti ottaen ei niin edes välitä tehneensä):

http://www.cercor.oupjournals.org/cgi/content/full/12/8/847

“PeiliSOLUUN”,siis mineomaan SOLUUN eikä esimerkiksi hermokudoksen synapsi- yhteyksiin,on muka ”koodattuna toimintaa” (tarkasti ottaen käytetään ilmausta ”solun koodaamaa”, kuin se olisi jokin ”itsenäinen subjekti”, äärimmäisen sekavaa ja epä-määräistä kielenkäyttöä, kuten näissä yhteyksissä tavaksi on tullut, muistettakoon vain vaikkapa Tooby&Cosmidesin houru ”EP Primer):

“ Within area F5 there is a class of neurons, known as mirror neurons, that respond to the sight of another monkey or experimenter performing the same type of action encoded by that neuron (Di Pellegrino et al., 1992 ; Rizzolatti et al., 1996a ). “

Erittäin kummallista jopa “evoluutiopsykologiankin teorian” kannalta tässä yhteydes-sä on että ”KYKY ON KEHITTÄNYT” sen (”pienen” , ”spesialisoituneen” á la Tooby & Cosmides) ”laitteen”, JOLLE SE ITSE KYKY SITTEN KUITENKIN PERUSTUU (ei-vätkä ne OLEKAAN ”kehittyneet yhdessä” evoluutiossa, kuten sisnsä houru T&C:kin edelyttäisi:

“ Mirror neurons are characterized by their response to both observation and exe-cution of the same action. It has been proposed that the ***human ability to imitate evolved out of the mirror system***, with its capacity to match directly observed and executed actions (Arbib, 2002 ). !

Jossakin on nyt matoja jopa “E.P::nkin kannalta…tieteestä puhumattakaan. >:-]

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0V-3T70Y2D-4&_coverDate=05%2F01%2F1998&_alid=200452853&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=4872&_sort=d&view=c&_acct=C000049137&_version=1&_urlVersion=0&_userid=950195&md5=cdf2ec9c552db02dce5a31201b9465d2

Ja täältä sitten löytyvät ne ankarat antipavlovistit Chomskyt ja Pinkerit, joiden tuotanosta voi haulla etsiä nimeltä asiantuntevaa keskustelua tältäkin palstalta.

57. N. Chomsky. Knowledge of Language: Its Nature, Origin and Use, Praeger (1986).

59. S. Pinker and P. Bloom. Behav. Brain Sci. 12 (1990), pp. 707–784. Abstract-PsycINFO | $Order Document

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WVC-446CP4R-39C&_user=950195&_coverDate=01%2F01%2F1900&_fmt=summary&_orig=search&_qd=1&_cdi=7099&view=c&_acct=C000049137&_version=1&_urlVersion=0&_userid=950195&md5=50b3f03e9e80a80357dede88fcbd7aac&ref=full

Rizzolattin ja “peilisoluteorian” takana on EU:n jo 1968 organisoima sosiobiologisti-nen seura, jonka sääntöjenmukaisena toimenkuvana on edistää ”aivolaitteiden (mechanism) ja käyttäytymisen suhteiden tutkimusta”.

Joten ”huippututkijoita” riittää kehuskelemaan toistensa ”löytöjä”…

Eivär ne ”pienet evoluution luomat spesialisoituneet laitteet” siis olekaan Tooby & Cosmidesin ”keksintöä”, eikä edes amerikalaista alkuperää, vaan poliitinen ohjelma selaisten etsimiseksi on esitetty fas… ei kun europiireistä jo 1968, ennen kuin E. O. WILSONKAAN oli ”sosiobiologiaansa” esitellyt!

Kova on ollut paine ”keksiä jotakin”…  >:-]

https://www.ebbs-science.org/bylaws.php

http://www.ebbs-science.org/RULES.htm

“The object of the Society shall be the furtherance of scientific enquiry within the field of the ***interrelationships of brain mechanisms and behaviour*** …

>Yksi teoria peilisolujen syntymisestä on se että lapsena tapahtuvat käsien >tarrautumisliikkeet ja niiden visuaalinen havaitseminen muokkaavat osan >aivosoluista niin että ne pystyvät myöhemmin aiheuttamaan saman reaktion kun >toinenkin ihminen tekee vastaavan liikkeen .

Tuo on ehdollistumisteorian mukainen selitys eri aistinten informaation ja myös muiden toimia koskevien havaintojen yhdistämiselle. Ei TÄMÄ edelytä minkäänlaisia erikoisspesialisoituneita "pelisoluja".

>(tämä voisi ehkä selittää sen miksi ei-kädellisillä vastaavat kyvyt ovat heikommat, >peilisolujärjestelmä ei pääse kehittymään kovin hyväksi jos eläin ei pääse >seuraamaan omien ruumiinosiensa liikettä kasvojensa edessä jatkuvasti)

Höpölöpö. Tietysti peili on yksi apuväline muiden joukossa parantaa havaintokyky-ään, mutta kyllä se on ihmisellä hyvin uusi keksintö varrattuna muihin "etuihimme" apinoihin nähden...

>Toisaalta ei myöskään ole perusteltua vielä väittää, että peilisolujärjestelmän >kehityksessä ei myös geeneillä olisi osuutensa.

Kun sellaisia ei ole, niitä "peilisoluja", eivätkä nuo tutkimusmenetelmät edes mene solutasolle...

>Esim. pienet muutokset neuronien >signaloitinopeuksissa, haarakkeiden >pituuksissa, reagoimisessa välittäjäaineisiin ym. vaikuttavat ratkaisevasti >neuroplastisuuteen ja peilisolujen tapauksessa ehkä osaltaan autismin syntyyn.

Voivat vaikuttaa suoraan autismin syntyyn, jos niissä jossakin on jotakin hyvin poikkeuksellista, ei SIIHENKÄÄN tarvita erityisiä "peilisoluja"...

>Ihmisen peilisolujärjestelmä on huomattavan monimutkainen.

Grrr....

>Se aktivoituu selvästi määritellyssä ajallisessa järjestyksessä noin 250 ms >kuluessa: näköaivokuori -> STS - >> päälaenlohkon alaosa -> Brocan alue - >> >liikeaivokuori. Brocan alue aktivoituu selvästi voimakkaammin liikeaivokuori. >Brocan alue jäljittelyn aikana kuin sormen tai suun liikkeiden suorittamisen >yhteydessä.

Ähhh... Brocan alueen aktivoituminen perustuu siihen perusfaktaan, että AJATTELU ON KIELELLISTÄ.

Venäläiset sitä aktivoitumista yrittivät kovasti silloisilla laitteilla näyttää toteen, mutta toiset, esimerkiksi behavioristit, eivät ottaneet uskoakseen näyttöön...

Mutta nyt uskovat,ja tietävät pilkulleen, mistä on kysymys, toisin kuin harit...

>On täysin mahdollista, että on olemassa geenejä joita ilman pelisolujärjestelmän >syntyminen ei olisi mahdollista.

Grrr...

>Ei tarvita kuin tiraus liikaa tai liian vähän dopamiinia tietyille aivoalueille ja tulevat >peilisolut opettelevatkin jonkun muun tehtävän.

Sitten ne EIVÄT OLE "OIKEITA PEILISOLUJA", vaan tavallisia ehdollisten refleksien hermostollisia solmualueita!

>Peilisolut ovat kiistatta neurotieteen merkittävin löytö pitkään aikaan.

Ne ovat samanlainen "merkittävä löytö" kuin Chomskyn "kielielin"...

>Nyt vain pitää oppia niiden toiminta, kehitys ja rakenne paljon paremmin.

Ei haaskata nyt rahaa hölynpölyteoriapohjalta lähtevään tutkimukseen, vaan tämä asia on pantava kansainväliseen syyniin, ja sitten pitää jatkaa niillä Lounasmaan hienoilla laitteilla tieteellisesti kestävältä teoriapohjalta.

RK

Muokannut: , 1/27/2013 2:13:36 PM

 

RK
14.09.2004 00:11:17
150677

Koko ja peilisolut...

Koko-gorillakin, jonka “älykkysosamääräksi on mainittu 90”, todistaa geenipeilisolujen puolesta:

http://nationalzoo.si.edu/publications/zoogoer/2002/4/primatethink.cfm

“ Frontal areas of the neocortex may also be involved in the use of visual information to plan and execute fine motor movements. When a monkey performs an action like reaching out and grasping a small object with its fingers, neurons in a certain part of the frontal neocortex “fire” wildly. Interestingly, Giacomo Rizzolatti from the University of Parma found that these same neurons fire when the monkey simply observes another monkey, or even a human, performing the same action. These mirror cells, as Rizzolatti dubbed them, may play a role in imitative behavior and learning through observation.

As the phrase “monkey see, monkey do” suggests,primates seem quite good at aping each other. In fact, striking examples of what appears to be observational learning come from studies of tool use in great apes. Primatologist Jane Goodall reported that infant and juvenile chimpanzees at Gombe National Park in Tanzania watch intently as their mothers break off small branches and poke them into holes, fishing for termites. The young chimps then make awkward attempts to copy their mothers. “

 

RK
14.09.2004 00:11:19
150679

Perustosiasiat: "peilisoluteoria" on "evoluutiopsykologiaa"

H5 kirjoitti 12.09.2004 (150560)...

>Hyvä RK

>Peilisolut ovat kiistatta neurotieteen merkttävin löytö pitkään aikaan. Nyt vain pitää >oppia niiden toiminta, kehitys ja rakenne paljon paremmin.

Näistä linkeitä ilmenee, että "peilisoluteoria" on kuin onkin tavaramerkin luojien Tooby & Cosmidesinkin tunnustamaa "evoluutiopsykologiaa" (ns. "kosmista tuubaa"):

http://www.cogweb.ucla.edu/ep/Conceptual-3.html

Täällä on se "asiayhteys", josta edellinen on poimittu.

http://www.cogweb.ucla.edu/ep/index.html

Ja täältä löytyy, mitä sitten se asiayhteys "todella on":

http://keskustelu.skepsis.fi/Message/FlatMessageIndex/144845?page=2#144946

RK

Muokannut: , 1/27/2013 2:16:02 PM

 

***

Ja varsin mahdollinen LOPPUJUTTU!

https://journals.sagepub.com/doi/full/10.1177/1745691621990638

What Happened to Mirror Neurons?

 
Cecilia Heyesorcid.png, Caroline Catmur

First Published July 9, 2021

Abstract

Ten years ago, Perspectives in Psychological Science published the Mirror Neuron Forum, in which authors debated the role of mirror neurons in action understanding, speech, imitation, and autism and asked whether mirror neurons are acquired through visual-motor learning. Subsequent research on these themes has made significant advances, which should encourage further, more systematic research.

For action understanding, multivoxel pattern analysis, patient studies, and brain sti-mulation suggest that mirror-neuron brain areas contribute to low-level processing of observed actions (e.g., distinguishing types of grip) but not to high-level action inter-pretation (e.g.,inferring actors’ intentions). In the area of speech perception, although it remains unclear whether mirror neurons play a specific, causal role in speech per-ception, there is compelling evidence for the involvement of the motor system in the discrimination of speech in perceptually noisy conditions.For imitation,there is strong evidence from patient, brain-stimulation, and brain-imaging studies that mirror-neu-ron brain areas play a causal role in copying of body movement topography. In the area of autism, studies using behavioral and neurological measures have tried and failed to find evidence supporting the “broken-mirror theory” of autism. Furthermore, research on the origin of mirror neurons has confirmed the importance of domain-general visual-motor associative learning rather than canalized visual-motor learning, or motor learning alone.

Keywords
 

Ten years ago, mirror neurons were everywhere. In 2011, when Perspectives on Psychological Science published a forum focused on the functions and origins of these fascinating cells (Gallese et al., 2011; Glenberg, 2011a,2011b), mirror neurons featured in Time magazine and The New York Times,programs about mirror neurons were broadcast by CNN and the BBC, and more than 200 articles were published in academic journals implicating mirror neurons in,among other functions, action under- standing, alexithymia, autism, business management, empathy, imitation, language comprehension, language production, literary mimesis,posttraumatic stress disorder, and schizophrenia. Measured by number of academic publications, interest in mirror neurons peaked 2 years later in 2013 and then began to decline (Fig. 1). Of course, the numbers in Figure 1 are not an infallible measure of scientific interest in mirror neurons. Since 2013, researchers may have begun to use other terms for the same targets of investigation. However, Figure 1 suggests that cognitive scientists are no longer working as actively in this field, or that the mirror-neuron “brand” is losing its appeal, or both and therefore raises the question of what happened to mirror neurons.

10.1177_1745691621990638-fig1.jpg

Fig. 1. Number of articles published per year from 1996 to 2020 that included the words “mirror neuron” in the title, abstract, or keywords. Data from Scopus, January 8, 2021.

 

Given the extent of public interest in mirror neurons and the liveliness of the contro-versy they provoked among scientists and philosophers, this question could be fruit-fully interpreted in an historical and sociological way.We could ask about the currents in Western society and in contemporary cognitive science that first made mirror neu-rons “mesmerising” (Heyes, 2010) and then weakened their appeal. But this article takes a more straightforward, natural science approach. After a brief introduction to mirror neurons,we use the questions discussed in the Mirror Neuron Forum (Gallese et al., 2011), concerning the functions and origins of mirror neurons, to structure a succinct survey of research published in the past 10 years. We then consider whe-ther these recent findings have taken the shine off mirror neurons and, if so, whether that reaction is appropriate. We conclude that although the results of careful empiri-cal research were bound to be disappointing relative to the more grandiose claims, recent work on mirror neurons should encourage further systematic investigation.

 

Mirror Neuron Basics

Mirror neurons were discovered by chance in monkeys in 1992 and given their evo-cative name 4 years later (di Pellegrino et al., 1992; Gallese et al., 1996). Early stu-dies of the field properties of mirror neurons — the sensory and motoric conditions in which they fire — revealed three basic types. Strictly congruent mirror neurons dis-charge during execution and observation of the same action, for example, when the monkey performs a precision grip and when it passively observes a precision grip performed by another agent. Broadly congruent mirror neurons are typically active during the execution of one action (e.g., precision grip) and during the observation of one or more similar, but not identical, actions (e.g.,power grip alone,or precision grip, power grip, and grasping with the mouth). Logically related mirror neurons respond to different actions in observe and execute conditions. For example, they fire during the observation of an experimenter placing food in front of the monkey and when the monkey grasps the food to eat it (di Pellegrino et al., 1992). Strictly and broadly con-gruent mirror neurons were, from the beginning,of primary interest,and they are what we and most other researchers mean when we use the term “mirror neuron.” These cells are intriguing because,like a mirror, they match observed and executed actions; they code both “my action” and “your action.”

Monkey mirror neurons are responsive to the observation and execution of hand and mouth actions. The hand actions include grasping, placing, manipulating with the fin-gers, and holding (di Pellegrino et al., 1992; Gallese et al., 1996). The mouth actions include ingestive behaviors such as breaking food items, chewing, and sucking and communicative gestures such as lip smacking, lip protrusion, and tongue protrusion (Ferrari et al., 2003).

Mirror neurons were originally found using single-cell recording in area F5 of the ventral premotor cortex (di Pellegrino et al., 1992; Gallese et al., 1996) and the inferior parietal lobule (Bonini et al., 2010; Fogassi et al., 2005) of the monkey brain. Subsequently, they were found not only in these “classical” areas but also in nonclassical areas, including primary motor cortex (Dushanova & Donoghue, 2010; Tkach et al., 2007) and dorsal premotor cortex (Tkach et al., 2007).

Early research with human participants used functional MRI (fMRI) to show spatial overlap in the areas of ventral premotor cortex and inferior parietal lobule that are active when people observe and execute movements (Buccino et al., 2001; Decety et al., 1997; Grezes & Decety, 2001; Rizzolatti et al., 1996). This was not conclusive evidence of the existence of human mirror neurons because the spatial overlap could have been due not to neurons that each respond both to observation and exe-cution of action (mirror neurons) but to clusters of neurons each responding either to action observation or to action execution (Dinstein, 2008; Dinstein et al., 2007). By 2011, doubts about the presence of mirror neurons in the human brain had been as-suaged by studies using single-cell recording in presurgical patients (Mukamel et al., 2010) and the repetition suppression fMRI procedure in healthy volunteers (Kilner et al., 2009). Like monkey mirror neurons,evidence consistent with the existence of hu- man mirror neurons has been found in both classical areas — ventral premotor cor-tex and inferior parietal lobule — and nonclassical areas, including dorsal premotor cortex, superior parietal lobule,cerebellum (Molenberghs et al.,2012), supplementary motor area, and medial temporal lobe (Mukamel et al., 2010).

Research using single-cell recording (and to some extent, repetition suppression) suggests that mirror neurons are typically present in adult human brains. However, this research does not license the inference that mirror neurons are always or usual-ly responsible for spatial overlap in fMRI responses during the observation and exe-cution of action. Consequently,it has become common to use terms such as “the mirror-neuron system” and “mirror-neuron brain areas” to refer to regions of the brain that are active during action observation and execution and/or for which there is evi-dence of the presence of mirror neurons. As reviewers, we have adopted the latter of these conventions, but note that these terms are unsatisfactory in at least two re-spects. First, it is not clear in what sense the areas containing mirror neurons consti-tute a system.Second,it is likely that only a few of the neurons in each of these areas have mirror properties.For example,fewer than 10% of the neurons studied in di Pel-legrino et al.’s (1992) seminal article showed “strict” or “broad” congruence in their fi-ring patterns to observed and executed actions, and although some single-unit stu-dies have reported higher proportions of mirror neurons, the nature of the single-unit technique makes it problematic to estimate the true prevalence of mirror neurons in any brain area (see also Kilner & Lemon, 2013). These issues should be borne in mind when considering the results of neuroimaging and neurostimulation studies discussed in this review.

From their discovery in 1992, theorizing about the function of mirror neurons was do-minated not by computational modeling and experimental intervention but by consi-deration of their field properties. Defining functions broadly and in everyday langu-age, researchers reflected on what neurons responsive to similar observed and exe-cuted actions would be “good for,” what kinds of psychological tasks they might be able to fulfill. In some cases, this strategy produced hyperbole. Mirror neurons were hailed as “cells that read minds” (Blakesee, 2006), “the neurons that shaped civili-zation” (Ramachandran, 2009), and a “revolution” in understanding social behavior (Iacoboni, 2008). But most researchers, including the group in Parma that disco-vered mirror neurons, focused on four realistic possibilities: action understanding, speech perception, imitation, and their potential dysfunction in autism. Each of these four hypotheses about the function of mirror neurons was debated in the Mirror Neu-ron Forum (Gallese et al., 2011; referred to hereafter as the forum) alongside a key question about their origins: Do mirror neurons get their characteristic visual-motor matching properties from learning?

 

Functions

Action understanding

In his lucid summary analysis of the forum, Glenberg (2011b) concluded in relation to action understanding that there was broad agreement that mirror neurons, or a mirror-neuron system, “plays some role in action processing” (p. 408) but no consen-sus about what that role might be. It could be relatively low level; mirror neurons may contribute to action selection or to action recognition, helping to distinguish one type of action from another (e.g., precision grip from power grip). Alternatively, mirror neu-rons may have a high-level function in action processing, enabling “understanding from within” (Rizzolatti & Sinigaglia, 2010) or inferences about actors’ mental states. Since 2011, advances in addressing this issue have come mainly from two broad lines of evidence: the use of multivoxel pattern analysis in fMRI to “decode” the infor-mation represented within and across brain areas and the use of patient studies and neurostimulation to investigate the causal role of mirror-neuron brain areas for action understanding.

Multivoxel pattern analysis has revealed that “mirror” areas including premotor cor-tex encode concrete representations of observed actions (e.g., the action involved in opening a particular bottle) rather than abstract, higher level representations (e.g., the goal “to open”; Wurm & Caramazza, 2019; Wurm & Lingnau, 2015). These fin-dings are consistent with the involvement of mirror neurons in lower level processing of observed actions.

However, any such involvement does not entail that mirror neurons play a causal role in action processing. The evidence in this case is still rather mixed. Studies of individuals born without upper limbs indicate that action recognition can take place without motor representations of the relevant effectors (Vannuscorps & Caramazza, 2016), and some stroke patients can identify actions despite damage to mirror-neu-ron brain areas (Tarhan et al., 2015), although a meta-analysis of previous findings indicates that such patients do show impairments in action identification (Urgesi et al., 2014).

Patient studies can be hard to interpret, however, because of heterogeneity in the damage incurred and the acquisition over time of compensatory strategies. Tempo-rary disruption of brain function using neurostimulation can therefore provide conver-gent evidence that a particular brain area plays a causal role in relation to a particu-lar cognitive function. One prominent neurostimulation study indicated that premotor cortex was necessary for identification of the intentions underlying observed actions (Michael et al., 2014). However, in that study, premotor cortex stimulation also dis-rupted perceptual matching of the observed actions. It is possible, therefore, that the disruption to intention identification was the result of disruption to low-level action processing and that premotor cortex does not play a direct, causal role in intention reading (Catmur, 2014).

On the basis of evidence including that summarized above, Thompson and col-leagues’ (2019) recent review of the putative contribution of mirror neurons to action understanding concluded that any involvement of mirror neurons appears to be con-fined to lower level processing of observed actions (e.g., aiding action discrimination or recognition). In particular, they found no compelling evidence for the involvement of mirror neurons, or mirror-neuron brain areas, in higher level processes such as inferring other people’s intentions from their observed actions.

Speech perception

Four contributors to the forum (Gallese et al.,2011) — Gernsbacher, Gallese, Hickok, and Iacoboni — agreed that the motor system has some role in speech perception, but they disagreed about the type and magnitude of the motor system’s role and about whether mirror neurons in particular are important (Glenberg, 2011b).

Neuroimaging data indicate that mirror-neuron brain areas respond during speech perception. For example,Callan and colleagues (2014) demonstrated that responses in ventral premotor cortex during a vowel-identification task were enhanced when the signal-to-noise ratio was reduced, suggesting that such responses may improve speech discrimination in perceptually noisy conditions. Measurement of motor cortex excitability has also been used to investigate the involvement of motor areas in speech perception. Motor cortical representations of speech effectors (e.g., lips or tongue) are enhanced during the perception of speech in noise (Nuttall et al., 2016, 2017; but see Panouilleres et al., 2018, for a contrasting result). This enhancement may have functional implications for speech perception ability: Participants with greater motor mirroring of perceived speech showed better ability to discriminate speech in noise (d’Ausilio et al., 2014).

However, evidence from patient studies casts doubt on whether the motor system is causally involved in speech perception. If speech perception requires perceived speech to be matched with motor commands for the production of speech, then one should find speech perception impairments in patients who have impairments in speech production as a result of brain lesions. In contrast to this prediction, a series of studies has demonstrated intact speech sound discrimination in patients with speech production difficulties (Hickok et al., 2011; Rogalsky et al., 2011; Stasenko et al., 2015).

A final line of evidence comes from brain-stimulation studies. Restle and colleagues (2012) demonstrated that facilitatory brain stimulation to the inferior frontal gyrus — a classical mirror-neuron brain area — improved participants’ accuracy in repeating unfamiliar foreign speech sounds. They argued that this indicates the role of the in-ferior frontal gyrus in matching perceived speech to produced speech, but this result cannot reveal whether the crucial role of this brain area is in speech perception, speech production, or the matching process itself. Furthermore, because this study did not include a control task, it is unclear whether stimulation of this brain area had a specific effect on speech processing or whether any complex sensorimotor task might have been improved by such stimulation. However, a series of subsequent studies has shown that stimulation of motor (Rogers et al., 2014; Smalle et al., 2015) or premotor cortex (Nuttall et al., 2018) affects speech perception ability, in particular for distorted speech (Nuttall et al., 2018), and one of these studies included a control task, which permits the conclusion that the stimulation had a specific effect on perception of speech but not nonspeech sounds (Rogers et al., 2014).

In summary, there appears to be reasonably strong evidence for the involvement of the motor system (including premotor mirror-neuron brain areas as well as motor cortex) in the discrimination of speech in perceptually noisy conditions. However, this conclusion is not yet supported by the patient data. A priority for future research, therefore, is to test whether patients with premotor lesions are impaired at discrimination of speech from noise.

Imitation

Of the functions discussed in the forum, imitation attracted the strongest consensus. It was agreed that although early work on the relationship between mirror neurons and imitation had involved some dubious definitions and inferences, “when imitation [is] defined in terms of action topography [how body parts move relative to one an-other], most agree mirror neurons contribute” (Glenberg, 2011b,p.409). This consen- sus was due in large measure to two studies showing that repetitive transcranial magnetic stimulation, a disruptive intervention, of the inferior frontal gyrus, a mirror-neuron brain area, selectively impaired imitative behavior (Catmur et al., 2009; Heiser et al., 2003).

Causal methodologies, including brain-stimulation and patient studies, have conti-nued to support the consensus that mirror-neuron brain areas contribute to imitation. Two studies in which facilitatory brain stimulation to inferior frontal gyrus were used demonstrated improvements in vocal imitation and naturalistic mimicry (Hogeveen et al., 2015; Restle et al., 2012), whereas inhibitory stimulation to the inferior parietal lobule slowed participants in an instructed imitation task (Reader et al., 2018). Inhibitory stimulation of the inferior frontal gyrus also disrupted automatic imitation (Newman-Norlund et al., 2010), but this effect was not specific to human body movements, and similar disruption was found for nonbiological stimuli.

Binder and colleagues (2017) demonstrated that patients with apraxia were impaired on an instructed imitation task and that this impairment was associated with lesions to a set of brain areas thought to contain mirror neurons, including the left postcent-ral gyrus, intraparietal sulcus, and inferior frontal cortex.A similar result was reported by Frenkel-Toledo et al. (2016), who found imitation impairments to be associated with lesions to the left inferior and superior parietal lobules and postcentral gyrus.

Data from causal studies such as these have been complemented by a series of fMRI studies over the past decade, which demonstrate greater responses in mirror-neuron brain areas during imitation than during other closely matched tasks (e.g., Campbell et al., 2018; Mainieri et al., 2013; Mengotti et al., 2012; Ocampo et al., 2011).

Autism

In marked contrast with imitation, the forum unearthed “huge disagreement on autism” (Glenberg, 2011b). Although Gallese defended the view that “impaired motor cognition,” rather than mirror neurons, contributes to the autistic1 phenotype, Iaco-boni stood by the more specific “broken-mirror theory” (Iacoboni & Dapretto, 2006; Oberman & Ramachandran, 2007; Williams et al., 2001; but see Southgate & Hamil-ton, 2008),citing a range of brain-imaging studies suggesting that people with autism have abnormal activity in mirror-neuron areas of the brain. Gernsbacher contested all of this evidence, highlighting methodological problems and replication failures, whereas Heyes, also skeptical about the broken-mirror theory, focused on evidence that people with autism show intact (Bird et al.,2007; J. L. Cook & Bird, 2012; Gowen et al., 2008; Press et al., 2010) and sometimes exaggerated (Spengler et al., 2010) automatic imitation.

A systematic review in 2013 of neuroscientific evidence concluded that there was “little evidence for a global dysfunction of the mirror system in autism” (Hamilton, 2013, p. 91). Studies published since that review, in which a range of techniques were used to investigate neural responses to observed actions and imitation (the cognitive function thought to rely most strongly on such responses), support this conclusion.

A popular technique to measure motor system responses during action observation is mu suppression, an electroencephalographic (EEG) measure of the reduction in coherence in certain frequency bands that occurs both when performing and when observing actions. However, the use of this technique to index mirror-neuron respon-ses has been criticized on the grounds that it measures attentional (Hobson & Bishop, 2016, 2017) and somatosensory (Coll et al., 2015, 2017), rather than motor, responses. Notwithstanding these critiques, recent studies of mu suppression during action observation in autism have shown no differences from neurotypical controls (Bernier et al., 2013; Ruysschaert et al., 2014).

In contrast, fMRI of neural responses during action observation indicates some diffe-rences between autistic and neurotypical participants. A recent meta-analysis of six fMRI studies of action observation and imitation indicated that participants with autism showed greater responses in bilateral fronto-parietal regions than participants without autism (Yang & Hofmann, 2016), although another study showed no differen-ces in neural responses during action observation (Pokorny et al., 2015). These data suggest some differences in responses during action observation, but they are not consistent with a broken-mirror account of autism; if anything, they point to greater neural responses in mirror-neuron brain areas during action observation in people with autism compared with those without autism. Furthermore, although these res-ponses are in brain areas thought to contain mirror neurons, none of these resear-chers used techniques that permit the definitive conclusion that such responses are due to mirror neurons instead of other neurons colocated in these brain areas.

Techniques that measure motor representations of specific actions (e.g., grasping) are potentially more informative in this respect. Recent studies in which motor-evoked potentials were used to measure motor cortical excitability during action ob-servation provide mixed evidence for differences between autistic and neurotypical participants. Enticott and colleagues (2012) reported a smaller increase in motor cor-tical excitability in participants with autism compared with neurotypical control partici- pants when viewing hand grasps. However, a later study found no differences on the same measure when observing socially relevant hand actions (Enticott et al., 2013). Previous claims of disrupted mirror responses in autism based on electromyographic evidence (Cattaneo et al., 2007) have also come under scrutiny, and a series of me-thodological critiques has cast doubt on the interpretation of previous data (Pascolo & Cattarinussi, 2012; Ruggiero & Catmur, 2018).

Finally, behavioral measures of imitation have also provided little evidence for a broken-mirror account of autism. Although one study reported some differences in instructed imitation (Cossu et al., 2012), a task with many demands unrelated to mir-ror neurons,the majority of recent studies have found either no difference in imitation between autistic and neurotypical participants or greater imitation in people with autism (Gordon et al., 2020; Schulte-Ruther et al., 2017; Schunke et al., 2016; Sow-den et al.,2016). Overall,therefore, the past 10 years of research have produced no compelling evidence for the claim that autism is associated with mirror-neuron dysfunction.

Origins

Contributors to the forum also debated the origins of mirror neurons, addressing the question of whether mirror neurons get their characteristic visual-motor matching properties from learning. Heyes argued that mirror neurons get their matching pro-perties via standard mechanisms of sensorimotor associative learning.They start out as motor neurons, active only during the performance of action. Then, through corre-lated experience of seeing and doing the same actions—in the context of self-obser-vation (e.g., an infant watches his or her hand own in motion) and social interactions in which the same movements are repeatedly both observed and executed (e.g., pat-a-cake; Heyes, 2001) —  these motor neurons become strongly connected to vi-sual neurons tuned to similar actions. Consequently, what was once a motor neuron becomes a mirror neuron — responsive to both the sight and performance of an ac-tion.Iacoboni agreed that visual-motor learning is likely to be important but saw signs that it is “canalized” by a genetic predisposition to develop mirror neurons (Del Giu-dice et al.,2009). Gallese went further,arguing that there is an “innate” or “genetically pre-determined” (Gallese et al., 2011, p. 384) propensity to develop mirror neurons that is facilitated not primarily by visual-motor learning but by motor experience before and after birth (Gallese et al., 2009). Summarizing the debate about origins, Glenberg (2011b, p. 409) identified as a key question “the degree to which neonatal imitation is a reliable phenomenon.”

Sensorimotor learning

In the past decade,more evidence has emerged that learning plays an important role in the development of mirror neurons (Brunsdon et al.,2020; Catmur et al., 2011; Co- pete et al., 2016; de Klerk et al., 2015; Fitzgibbon et al., 2016; Furukawa et al., 2017; Guidali et al., 2020; Hou et al., 2017; McKyton et al.,2018; Orlandi et al., 2017; Press et al., 2012; Wiggett et al., 2012; Zazio et al.,2019). Some of the recent studies have reported greater activity in mirror-neuron brain areas in pianists and dancers than in people who lack such expertise during observation of musical performance and dance, respectively (Furukawa et al., 2017; Hou et al., 2017; Orlandi et al., 2017). These studies are of interest because they indicate that activity in mirror-neuron brain areas is affected by long-term learning under naturalistic conditions, but they do not indicate what kind of learning is important. For example, dancers may show greater mirror-neuron brain area activity than control participants during dance observation because the dancers have watched more dance movements (sensory learning), performed more dance movements (motor learning), and/or watched more dance movements while performing similar dance movements (sensorimotor learning).

Experiments that were designed to isolate the kind of learning involved in mirror-neuron development have suggested that sensorimotor learning is crucial (Catmur et al., 2011; de Klerk et al., 2015; Fitzgibbon et al., 2016; Guidali et al., 2020; Press et al., 2012; Wiggett et al., 2012). For example, replicating and extending earlier work with a similar design (e.g., Catmur et al., 2007, 2008), Wiggett et al. (2012; see also Brunsdon et al., 2020) found using fMRI that mirror-neuron brain areas were more strongly activated by observation of hand movement sequences in participants who had simultaneously observed and executed the movements (sensorimotor learning) than in participants who had either observed the movements without performing them (sensory learning) or performed the movements without observing them (motor learning). Furthermore, using paired-pulse transcranial magnetic stimulation (TMS), Catmur et al. (2011) confirmed that novel sensorimotor experience of the kind given by Wiggett et al. acts on mirror responses. They showed that “counter-mirror” trai-ning (in which participants performed index-finger movements while observing little-finger movements and vice versa) reversed mirror responses (e.g., resulted in grea-ter activation of an index-finger muscle during observation of little-finger movement than during observation of index-finger movement) via the same connections bet-ween premotor and motor cortex that were responsible for mirror effects before trai-ning (e.g., greater activation of an index-finger muscle during observation of index-finger movement than little-finger movement).

Responding to a study in which counter-mirror training yielded later effects on motor excitability than mirror training (Barchiesi & Cattaneo, 2013; see also Ubaldi et al., 2015), Cavallo et al. (2014), like Catmur et al. (2011), found that mirror responses and counter-mirror responses followed the same time course. Another TMS study found that counter-mirror responses can be induced by instruction alone (Bardi et al., 2015). However, it is unlikely that instructional learning, rather than sensorimotor learning, was responsible for the training effects reviewed above because (a) in the study by Bardi et al. (2015), participants were tested immediately after instruction, whereas in the earlier studies they were tested 24 hr after both instruction and sensorimotor training, and (b) training effects have been observed in uninstructed infants (de Klerk et al., 2015).

The training studies described above involved adult participants, but there is also now evidence that sensorimotor learning is important in the early development of mirror responses. Using EEG recordings of sensorimotor α suppression as an index of mirror-neuron activity, de Klerk et al. (2015) found in 7-month-old infants, who could not yet walk, that mirror responses during observation of stepping movements increased with the amount of sensorimotor experience they had received in earlier training sessions. Infants who had frequently seen their own stepping movements while performing those movements showed greater α suppression than infants who had relatively little correlated experience of seeing and doing the stepping move-ments. De Klerk et al. did not find similar effects of sensory experience (observing stepping) or motor experience (making stepping movements) on α suppression, suggesting that at least in this study, α suppression indexed the sensorimotor matching function of mirror neurons rather than purely attention or arousal.

The idea that motor learning alone is sufficient to change the properties of mirror neurons (Gallese et al., 2009) has not been supported. The study by de Klerk et al. (2015) failed to find a relationship between the frequency with which infants per-formed stepping movements during training and the extent of sensorimotor α sup-pression during observation of stepping movements after training. Yet more striking, using imitation as a behavioral index of mirror-neuron activity, McKyton et al. (2018) found reduced automatic imitation in newly sighted children who suffered from dense bilateral cataracts from early infancy and were surgically treated only years later. These children, who had been deprived of sensory and sensorimotor experience of action but not of motor experience, were less inclined than control children to imitate task-irrelevant hand actions.

In addition to showing that sensorimotor learning is important for mirror-neuron de-velopment, recent research suggests that in everyday life, much of this learning oc-curs in the context of social interactions between infants and their caregivers.The ex-tent to which mothers imitate infant facial expressions at 2 months postpartum pre-dicts EEG α suppression at 9 months during observation of the same facial expres-sions (Rayson et al., 2017; see also Markodimitraki & Kalpidou, 2019; Murray et al., 2018). Furthermore, this relationship is action specific. De Klerk et al. (2019) found that parental imitation of facial expressions predicted infant imitation of facial but not hand movements, implying that parental imitation supports mirror-neuron develop-ment through learning of specific sensorimotor associations (e.g., between the sight and performance of mouth opening) rather than by enhancing attention to body movements or social motivation.

Is the sensorimotor learning genetically canalized?

The importance of sensorimotor learning for the development of mirror neurons is now well established, but questions remain about the character of this learning. The “associative account” maintains that the sensorimotor learning that builds mirror neu-rons is of exactly the same kind as the learning that produces Pavlovian and instru-mental conditioning; it is a computationally undemanding, domain-general process that forges excitatory and inhibitory links between simple event representations (R. Cook et al., 2014; Heyes, 2001; Keysers & Perrett,2004).In contrast,the “canalization account” (Del Giudice et al., 2009; Gallese et al., 2009), supported by Iacoboni and Gallese in the forum, suggests that monkeys and humans genetically inherit a speci-fic propensity to acquire mirror neurons. On this view, the sensorimotor learning that contributes to mirror-neuron development is domain specific — it involves compu-tations distinct from those involved in standard conditioning — and/or the learning is primed for the development of mirror neurons (given a head start by genetically inherited behavioral mechanisms).

A few studies in the past 10 years have addressed the domain generality of the sen-sorimotor learning involved in mirror-neuron development. Consistent with the asso-ciative account, these have indicated that like standard conditioning, mirror-neuron learning depends on contingency as well as contiguity (Cooper et al., 2013) and shows a distinctive pattern of contextual modulation (R. Cook et al., 2012). However, as Glenberg (2011b) predicted, the majority of research bearing on the associative and canalization accounts has focused on neonatal imitation. Given the evidence that mirror neurons contribute to imitation (see above), reliable evidence that newborns can imitate before they have had the opportunity for relevant sensorimotor learning would suggest that the development of mirror neurons is canalized or genetically predetermined.

A set of 10 studies from one research group,eight of them published since the forum, claimed to provide evidence of imitation in newborn monkeys (Ferrari et al., 2006, 2009; Kaburu et al., 2016; Paukner et al., 2011, 2014, 2017; Simpson et al., 2013, 2014, 2016; Wooddell et al., 2019). These studies did not use the “cross-target” pro-cedure, which both enthusiasts and skeptics have agreed is necessary to detect imi-tation in newborns (e.g., Meltzoff, 1996; Meltzoff & Moore, 1977; Oostenbroek et al., 2016; Ray & Heyes, 2011; Redshaw, 2019; Whiten, 2002). For example, when tes-ting for imitation of tongue protrusion and lip smacking, they did not use these beha-viors as controls for one another. Instead of looking for a higher frequency of tongue protrusion than of lip smacking in infants who had just observed tongue protrusion and a higher frequency of lip smacking than of tongue protrusion in infants who had just observed lip smacking, they reported, for example, a higher frequency of tongue protrusion after observation of tongue protrusion than after observation of a rotating disk. An effect of this kind could be due not to imitation of tongue protrusion but to a biological, social stimulus eliciting more behavior of all kinds than a nonbiological, asocial stimulus. Pointing out this problem alongside a number of others (e.g., mul-tiple comparisons without correction), Redshaw (2019) reanalyzed the data from the full corpus of 10 neonatal monkey studies. Applying the cross-target methodology, the reanalysis found no evidence whatever of imitation in newborn monkeys.

Recent work with human neonates points in the same direction. In a study with un-precedented power, conducted in Brisbane, Oostenbroek et al. (2016) tested more than 100 infants longitudinally at 1, 3, 6, and 9 weeks of age in a cross-target proce-dure involving a wide range of targets. They recorded the frequencies of nine target actions — tongue protrusion, mouth opening, happy expressions, sad expressions, index-finger protrusion, grasping, MMM sound, EEE sound,and tongue click — while infants observed 11 movement stimuli — an adult performing each of the nine actions and two object movements (spoon protruding through a tube and box opening). The results of the Brisbane study were wholly negative: In no case did the infants consistently perform a target action more often while observing the same action than while observing all of the alternative actions.

Previous failures to find neonatal imitation have been attributed to methodological factors — for example, the use of an inappropriate model, an inadequate response interval, or suboptimal statistical procedures. In a recent meta-analysis of neonatal imitation research by the Brisbane group,encompassing 336 effect sizes dating back to 1977, researchers sought and did not find a modulating influence of 13 methodo-logical factors previously cited as reasons for replication failure (Davis et al., 2021). However, the meta-analysis did find a modulating effect of “researcher affiliation,” in which a small number of laboratories are more likely than others to find large posi-tive effects. Furthermore, across the whole data set, there was a relationship bet-ween standard error and effect size indicative of publication bias (i.e., suggesting that smaller studies have been conducted, found no evidence of neonatal imitation, and not been published).

Reanalyzing the data from the Brisbane study using a more liberal statistical me-thod, Meltzoff et al. (2018; see also Oostenbroek et al., 2018) found evidence of imi-tation for one of the nine target actions — tongue protrusion.Although consistent with other reviews and meta-analyses of neonatal imitation data (e.g., Anisfeld, 1996; Jones, 2006; Ray & Heyes,2011), this result does not uphold the historical claim that newborns are capable of voluntary imitation of a range of actions (Meltzoff & Moore, 1977; see also Keven & Akins, 2017) or support the view that mirror neurons are learned via a canalized or genetically predetermined process.

Rather than supporting canalization, one study of young human infants provided evi-dence that the development of imitation (and by inference, mirror neurons) depends on unspecialized, unconstrained associative learning. Reeb-Sutherland et al. (2012) found that associative learning ability at 1-month postpartum, measured using a delay-eyeblink-conditioning paradigm, predicted performance on a range of imitation tasks at 9 months of age.

Reflection

In the past 10 years, there has been significant progress in resolving the questions debated in the Mirror Neuron Forum (Gallese et al., 2011). Regarding action under-standing, multivoxel pattern analysis, patient studies, and research using TMS now suggest that mirror-neuron brain areas contribute to low-level processing of observed actions (e.g., distinguishing types of grip) but not directly to high-level action interpretation (e.g., inferring actors’ intentions). In terms of speech perception, although it remains unclear whether mirror neurons play a specific, causal role in speech perception, there is now compelling evidence for the involvement of the mo-tor system (including premotor mirror-neuron brain areas as well as primary motor cortex) in the discrimination of speech in perceptually noisy conditions. Regarding imitation, building on research published before 2011, researchers conducting patient, TMS, and fMRI studies have found strong evidence that mirror-neuron brain areas play a causal role in behavioral copying of body movement topography.

Finally, concerning autism, researchers using behavioral and neurological measures have tried and failed to find evidence for the broken-mirror theory of autism. Instead, there are intriguing signs that under some conditions, people with autism have stron-ger mirror responses than neurotypical control participants. Alongside these deve-lopments, research on the origin of mirror neurons has confirmed the importance of domain-general visual-motor associative learning rather than canalized visual-motor learning or motor learning alone. Specifically, major studies assessing “the degree to which neonatal imitation is a reliable phenomenon” (Glenberg, 2011b) have shown that it is not reliable at all.

These findings are disappointing relative to early newspaper headlines. It turns out that mirror neurons are not “Cells That Read Minds” (Blakesee, 2006), they do not alone explain “what makes humans social” (Lehrer, 2008), and they have not been able to “do for psychology what DNA did for biology” (Ramachandran, 2009). But it is unlikely that any serious cognitive scientist or neuroscientist would be surprised that mirror neurons have not lived up to these sensational claims. The puzzle is why mir-ror neurons have so inflamed the popular imagination. We speculate that two factors are important. First is the deep historical pull of atomism. Mirror neurons are small and apparently indivisible; they combine sensory and motor properties in a single unit. From ancient Greece to particle physics, there is a long tradition in which atoms of this kind are understood to be the building blocks of reality. Immersed in this tra-dition, people may be captivated by the idea that simple, tidy mirror neurons explain the distressing complexities of the social world — including political strife, drug ad-diction, pornography,and responses to media violence (Bocher et al.,2001; Iacoboni, 2008). Second,some descriptions of mirror neurons imply telepathy.If mirror neurons mediate “understanding from within” (Rizzolatti& Sinigaglia, 2010), a “pre-conceptual and pre-linguistic form of understanding,” which can “overcome all linguistic and cul-tural barriers” (Rizzolatti & Sinigaglia, 2008; p. xiii), they allow an effortless, wordless form of communication that is a lot like telepathy. Given ancient links between mir-rors, oracles, and divination (e.g.,Orofino, 1994), even the name mirror neurons may pump the intuition (Dennett, 1984) that these cells give direct, transparent access to other minds (Heyes, 2010).

Figure 1 suggests that even if public enthusiasm for mirror neurons has been sus-tained,scientific interest began to decline in 2014.Two high-profile reviews were pub- lished in that year. One of them, a target article with commentaries in Behavioral and Brain Sciences, did not contest the existence of mirror neurons, or that they contri-bute to social behavior, but marshaled evidence that they are forged by sensorimotor associative learning (R. Cook et al., 2014). This evidence challenged the view that mirror neurons are a biological adaptation — that they evolved via genetic mecha-nisms for action understanding, speech, imitation, or any other function. The other review, a book titled The Myth of Mirror Neurons, was more skeptical. It argued that because mirror neurons are products of associative learning, they could not mediate action understanding or any other cognitive function (Hickok, 2014). The impact of these two publications should not be overestimated. They distilled and developed insights and concerns that had been emerging over the preceding years. But it is plausible that they precipitated the subsequent decline of mirror-neuron research.

Should the decline be resisted, or should it be hoped that the trend apparent in Figure 1 continues until mirror neurons are a thing of the past? We support resis-tance for two reasons. First, even if the mirror-neuron boom was fueled by less than rational currents of thought (e.g., atomism and telepathy) inside as well as outside science,it would not be rational to allow mirror neurons to go bust. This field has pro- duced substantial findings, many summarized in this article, which should not be dis-missed just because mirror neurons are “the most hyped concept in neuroscience” (Jarrett, 2012). Second, in our view, much of the skepticism about mirror neurons is based on a misunderstanding.The discovery that mirror neurons are forged by asso- ciative learning does not imply that they are without function. It suggests they are by-products with respect to genetic evolution, but by-products can be very useful indeed — in the oil business and in the brain. Consider the area of the left fusiform gyrus that mediates identification of visual word forms. Literacy emerged late in human his-tory, only 5000 to 6000 years ago, making it clear that the visual word form area was not designed by genetic evolution to enable reading. It is a by-product of genetic adaptation for the discrimination of visually complex objects — just as mirror neu-rons are a by-product of genetic adaptation for learning about predictive relation-ships — but literacy is hugely important as a means of relating to and learning from other people; literacy is a social cognitive function (Heyes, 2018).

Our review of mirror-neuron research in the past 10 years and the critiques discussed in this section have several implications for future research. In relation to mirror-neuron functions, research on low-level action discrimination is more likely to make progress than continuing effort to find a direct role for mirror neurons in high-level action interpretation. Likewise, imitation looks more promising than speech perception, and — given the strength of the evidence that mirror neurons contribute to imitation and the lack of evidence that autism is due to a broken mirror — dyspra-xias are a more promising target than autism for research with clinical applications.

The idea that mirror neurons contribute to imitation was dismissed at an early stage on the grounds that monkeys, the first species in which mirror neurons were identi-fied, cannot imitate (Rizzolatti & Craighero, 2004). This argument assumed that imi-tation involves copying an entirely novel action guided by understanding of the mo-del’s intentions, a definition so rich that it implies imitation is rare even in adult hu-mans (Heyes,as cited in Gallese et al.,2011). Defining imitation in a way that is more common in cognitive science, as copying the topography of body movement, the associative account of the origin of mirror neurons implies that any animal capable of sensorimotor associative learning has the potential to develop mirror neurons and to imitate. Humans are better imitators than other animals, including monkeys, because sociocultural experience (e.g., synchronous dance and sporting activities, being imitated by others) provides humans with matching sensorimotor experience for a broader range of actions (R. Cook et al., 2014). In retrospect, it seems that the rich definition of imitation diverted attention from one of the most important functions of mirror neurons.

As for future research on the origins of mirror neurons, there is still much to be dis-covered about the sources and developmental timing of the sensorimotor experience that builds mirror neurons, how this varies across cultures, and how this information might be used for clinical and educational interventions. More broadly, investigation of how mirror neurons are woven into computational-neurological systems could pro-vide valuable clues about how other cognitive systems are assembled through lear-ning.When a function is “hardwired” or “innate",the construction work is done by evo- lution acting on genetic variants and lost in the mists of time, but when the construc-tion is done by learning, it can be studied in creatures alive today (Heyes, 2018).

Turning from targets of study to methods, it is clear that causal methodologies, such as TMS, have more power to illuminate functions than correlational methodologies, and if it is concluded that the unitary character of mirror neurons is of crucial impor-tance (see below), the use of more single-unit recording would be desirable. The po-tential for such recording would be greatly expanded by the development of rodent models using sensorimotor training (Heyes, 2013).

Thinking more broadly about methodology, research on mirror neurons would benefit greatly from extension of a system-level, computational approach of the type ad-vanced by Hickok and Poeppel (2015) for language and by Rushworth and collea-gues (e.g., Apps et al., 2016) for other aspects of social cognition. Predictive coding is one potential example of a system-level computational approach to investigating mirror-neuron contributions to social cognition (Kilner et al.,2007; Press et al., 2011). Ideally, in any such approach, each hypothesis about function would specify a part in a psychological process — a process going all the way from peripheral sensory input to overt motor output — that mirror neurons are thought to fulfill and do this in a way that is testable using behavioral and neurophysiological methods. The name given to this part is not important in itself. What is important is that the name does not derive its meaning purely from folk psychology and that the hypothetical function of mirror neurons is distinguished clearly from other components and from the overall pro-cess.For example,movement discrimination or action recognition (component) needs to be distinguished from mentalizing (whole process). Likewise, on the neurological side, we need more specific, testable theories of how mirror neurons work with other types of neurons and the kinds of networks in which they are embedded (including distinguishing whether any differences in function are due to region- or species-spe-cific differences in mirror neurons themselves or the properties of the region or orga-nism in which they are located). The term “mirror-neuron system” is commonly used, but proponents of this term need to specify the sense in which mirror neurons con-stitute a system rather than just cells with similar properties found in interconnected areas of the brain.

At the broadest, conceptual level, we need to think hard about why, if at all, it is im-portant that single neurons have mirror properties. Setting aside the historical appeal of atomism, does it really matter in the context of contemporary psychology and neu-roscience whether individual neurons or small networks of neurons match observed and executed actions? Indeed, in a potentially welcome development, recent single-unit recording studies indicate a move away from considering the properties of indi-vidual neurons and instead focus on population-level encoding. For example, indivi-dual neurons responsive to the observation of others’ manipulative actions (gras-ping, dragging, etc.) in anterior intraparietal area show viewpoint-dependent coding, but as a population, they provide viewpoint-invariant coding of the observed action (Lanzilotto et al., 2020; for a similar demonstration of population encoding of observed actions in presupplementary motor area, see also Livi et al., 2019).

In conclusion, it turns out that mirror neurons contribute to complex control systems rather than dominating such systems or acting alone. Their contributions are at a re-latively low level — for example, to body movement discrimination rather than inten-tion reading. And rather than being immutable units from birth, mirror neurons ac-quire their mirror properties through sensorimotor learning and change them by the same route.Although disappointing relative to some early claims,we argue that these discoveries should not discourage further research on mirror neurons. The findings reviewed in this article suggest that when mirror neurons are studied in the context of system-level theory — as having the potential to fulfill a specified part in a comp-lex process — they can help researchers to understand the categorization of body movements, aspects of speech perception, and the neurological bases of imitation.

Furthermore, the evidence that mirror neurons are forged by sensorimotor experi-ence not only raises important questions about the sources of this experience in everyday life across cultures but also opens up the possibility that other neurocog-nitive mechanisms, once thought to be genetically inherited, are shaped by cultural learning (Heyes, 2018). Mirror neurons should not be tarnished; they are yet to fulfill their true promise.