Category Archives: mirror neuron

On The Agency Cortex

As previously reported, the mirror neuron system is a set of cortical circuits that are active both when an individual performs an act (picking up an apple, say) and when he observes that action being performed by another individual. This collection of cells is clearly important for understanding the intentions of others, and perhaps for learning by imitation. Furthermore, there is quite similar sensory activity associated with both active and passive limb movement (movement imposed on one’s body).

This presents a problem. How do we attribute self-agency to our actions? This is a particularly important question if one subscribes to the theory (mentioned sporadically in this forum), that free will is not the cause of our actions, but the post-hoc assumption of agency for our actions. Even if one does take the stance that free will is the subjective experience of causing thoughts and acts, this question remains relevant since there must be some neural activity which distinguishes self-caused action from passively experienced action.

Of course, there is a wealth of non-cortical activity which accompanies moving one’s arm (signals in the brain-stem and spinal column, in particular) which could provide this signal. However, because of the abstract nature of agency, some have the opinion that there must be a specialized cortical area whose job it is to integrate the diffuse, distributed neural activity associated with a single act and decide whether it was internally generated or externally imposed.

Writing in the pages of the Journal of Neuroscience, Zarinah Agnew and Richard J. S. Wise report that they’ve found an area of the brain that is a candidate for the job of agency detector, the Parietal Operculum1.

This work pushes the boundaries of research into the nature of free will. One class of phenomena which motivates the free-will-as-post-hoc theory is the so-called automatisms: actions which are internally generated but feel as though they were caused by an outside agent. A well known example of automatism is the Ouija Board, where it is possible – most likely due to suggestion and the ability to ascribe agency directly to the other “players” – to feel as though one is not moving a planchette. Another is automatic writing, a phenomenon in which an individual composes pieces (in some cases entire novels) without any feeling of agency.

That the experience of will can break down in these ways is a very direct indication (along with a host of others) that our understanding of the phenomenon is minimal, at best. Localizing the brain areas responsible for the feeling of free will is one step towards understanding it.

1. Agnew Z, Wise RJ. Separate areas for mirror responses and agency within the parietal operculum. J Neurosci 28: 12268-12273, 2008.

On Recognizing Conspecifics

Nature Neuroscience1

Communication with members of ones own species is extremely important for social animals. Non-verbal messages can signal socially significant events such as the presence of a predator or the movement of the group. It is therefore no great surprise that some recent research has found monkey brain areas specialized for recognizing conspecifics1. This is a sensible sensory strategy, one which ensures that individuals are able to distinguish between the various growls and caws that they might be privy to, and pluck out the ones most relevant to their continued survival.

In animals where vocalizations transcend the guttural, even more specialization has been unearthed (unbrained?) in the skull. Work on Zebra finches has demonstrated that there are neurons which are active specifically during the production of an individuals song (they have, after all, only one in a lifetime) or while the animal hears his song being played back. Again we can confidently say that this type of anatomical customization is full of utility since it allows the animal to monitor and potentially modulate its learning. In fact it would be difficult to imagine the learning process without this type of helpful structure.

1. Petkov CI, Kayser C, Steudel T, Whittingstall K, Augath M, Logothetis NK. (2008) A voice region in the monkey brain. Nat Neurosci. 11(3):367-74.
2. Prather JF, Peters S, Nowicki S, Mooney R. (2008) Precise auditory-vocal mirroring in neurons for learned vocal communication. Nature. 451(7176):305-10.

On Making Faces

How do babies learn to make faces? With arm or leg movements, it seems plausible that, as William James suggested, one might gain insight from simply associating observed appendage position with concurrent muscle activation patterns1. However, in contrast to an attempted stirring of limbs, the infant cannot see what results from the activation of his facial muscles. Thus, the learning mechanism cannot rely on sensory confirmation that the indented action was successfull. That new humans very rapidly learn to express their emotional state through a smile, frown or furrowing of brow hints that there is some implicit path to the acquisition of this skill. It has been suggested by some that the Mirror Neuron (MN) system constitutes this road, or at least a map of it2.

In the adult, MNs are cells that respond when an animal performs some act – picking up a piece of fruit, say – and when it observes another individual doing the same thing, even if the observed actor is a member of another species or stranger, a robot. Beyond this, their activation potentiates the pathways that would be involved in the execution of such a movement by the observer: producing measurable sub-threshold responses in the muscles involved. The suggestion that this system is involved in motor learning and imitation from birth amounts to the assumption that MNs are prenatally wired to function as they do in the mature brain. This is a very attractive idea as it removes the need for some external form of reinforcement – like a visual confirmation of the completed movement – to inform the motor-learning process. Instead, the responsibility for being both carrot and stick is shifted internally, to the MNs. The proposition is that the genetically defined circuitry imbues the MNs with a “knowledge” of the pattern of muscle activity associated with both an observed or executed behavior.

This, unsurprisingly, presents a further question: if the MN system is present from birth and possesses such information as described above, why do infants need to learn how to move at all? This is where we must tread a bit into the realm of informed speculation. First, the MN system cannot know how to execute every movement possible: for instance it certainly cannot know at birth the set of motor commands associated with performing some complex gymnastic move, say a double backflip. If the MN is an artifact of evolution, then it is likely that there is a continuum of innate interpretability, from simple acts like smiles that are well known to the MN system to more rare or contemporary behaviors like figure skating or fixing a bicycle. Thus, using the MN system as a template, of sorts, can only be effective for behaviors on the oft-encountered end of the spectrum. Second, since babies sadly do not leap from the the womb as masters of muscular control, the wiring of the MN system must itself develop at a pace commensurate with the time-course of an individual’s behavioral procurement.

How is it then, that this internal electro-cultivation proceeds in lock-step with the infant’s newfound agility? It has been well documented that humans lose half the total number of neurons in their central nervous system by the time they’ve reached six months of age. This pruning is a synaptic refinement process, also termed neural darwinism4. It is quite beneficial to the newborn animal, since his neural connectivity is far too manifest, too spatially noisy, and must be cleaned up. This happens in all areas of cerebral cortex. For example, in the visual system, molecular cues guide the axons of nearby retinal ganglion cells to adjacent targets in the thalamus while the animal is still in the womb in a gross way, but it is the activity arising from visual stimulation which pares down the connections to the state we see them in the adult. the exquisite spatial precision of connections between the retina and thalamus cells in the retina are connected to cells in the thalamus with exquisite spatial precision because of visual experience. It was Hebb who pointed out that cells that “fire together wire together.5” This means that if two retinal cells fire at the same time, they will tend to be connected to the same post-synaptic target. That is not to say that any two cells that fire at the same time anywhere in the brain will inevitably be connected to each-other, but rather that in deciding which of the molecularly defined crude connections to keep, a post synaptic cell will retain those which tend to fire at the same time in response to stimulation. The stimuli that cause the retinal cells to fire are not simply sets of independently fluctuating pixels; rather they are full of spatial correlations. If a single vertical line passed across your field of vision, a single line of cells in the retina would be stimulated at once as the line moved by. It is almost never the case that two abutting photoreceptors see completely uncorrelated (in time) patterns of illumination. In this way, the spatial relationships in the image translate into spatial relationships in the connections in the brain.

The goings-on I’ve outlined above might generally be termed activity dependent synaptic refinement (ADSR). What I’m hypothesizing is that, as with vision, some form of ADSR is at work in those cortical-areas involved in learning how to move: that the very act of generating motor output leads to more stereotyped action through application of the Hebbian “fire together wire together” motif. The commonality between vision and movement, and indeed the unifying principle behind ADSR, is that the systems are exploiting the presence of underlying statistical content. While the MN system is biasing motor output towards certain configurations, the motor cortex is learning about the possible relationships between muscle tensions, lengths and contractile velocities. It is thought that the brain might use such a mechanism universally as an attempt at maximizing efficiency. For example: if you always listen to symphonic classical music, you might set your stereo to boost bass & treble, but if you’re more the piano concerto type, you’d want a touch more mid-range; then again, if your tastes are more varied, it might make sense to emphasize all three frequency bands equally so as not to aurally marginalize any particular genre. Another for instance more relevant to motor output: when you drive in the city, you rarely ever get out of 2nd gear, but on the highway, you’re almost always in the upper gears. In the same sense, the brain attempts to use the Hebbian rule to optimize its (sensory) inputs and (motor) outputs to the sensory stimuli impinging on it and the motor programs it generates.

You may have noticed in all this that I’ve skipped over one important point: how (genetic wiring notwithstanding), do mirror neurons extract the information about a movement being performed by another agent? It is not at all understood how this occurs in the adult, so how it could be happening in babies is even more mysterious, especially in light of the messiness of infant brains that I’ve spoken of. It simply must be the case that visual stimuli are translated into data concerning the movement of bodies. It is possible that specialized structures for recognizing arms and hands, faces and feet, become sophisticated very early on, but nothing like this has been observed to-date. The needed course of research is clear, but developing experiments to elucidate what might be at work is not. We can only wait and watch from the wings while the scientific players act, and perhaps deliver soto voce direction from time to time.


1. James, W. The Principles of Psychology Vol. 1. Henry Holt & Company (1890)
2. Lepage JF, Théoret H. (2007) The mirror neuron system: grasping others’ actions from birth? Dev Sci. 10(5):513-23.
3. Rizzolatti, G., & Craighero, L., (2004) The Mirror Neuron System. Annu. Rev. Neurosci. 27, 169-192.
4. Hebb, D.O. The Organization of Behavior. John H. Wiley & Sons (1967)
5. Edelman, G.M. Neural Darwinism. Oxford Paperbacks (1990)

Mirror Neurons & Autism

The Mirror Neuron system (MNS) is thought to underlie imitation in primates, and has been implicated in Autism Spectrum disorder in humans(1, 2). First observed in Macaques, mirror neurons are classified as units that selectively increase their firing rate both during the execution of a motor action by an individual and while that individual observes the same action performed by another . The interest in the MNS in relation to autism was sparked by the fact that two of its major symptoms are generalized social interaction & communication deficits which would seem to rely on something like the MNS. In order to explore how MNS properties might differ in normal vs. autistic patients, Hugo Théoret has been performing experiments in human subjects. His results suggest that a general deficit of something akin to the mirror neuron system is present in autistic individuals.

(EMG stuff)

Dr. Théoret uses two techniques in his research on the mirror neuron system. These are electromyography (EMG) and transcranial magnetic stimulation (TCMS or TMS). EMG measures the voltage difference between ground and the skin nearby a muscle group. Muscle contraction is accompanied by currents which cause a change in voltage or potential. The is sensitive enough to detect voltage changes when an individual even considers a movement involving the measured muscle group. TMS is a coarse method of selectively activating cortical regions(3). The combined use of these tools has allowed Dr. Théoret to use simple experiments to draw interesting conclusions about individuals with Autism.


Dr. Théoret’s main finding can be summarized by describing two experimental outcomes. First, in normal (non-autistic) individuals, there is a reliable deflection of the electromyogram produced by having the subjects watch a video of an action being performed which involves the measured muscle. For instance, if the right bicep is being measured, there will be an observable deflection of the potential in that muscle when the subject watches a video of an arm lifting an apple. There is also a measurable potential-deflection in that muscle when the proper area of motor cortex is stimulated via TMS. Beyond these individual effects, there is a summation effect such that the deflection is even larger when the subject both observes the video and receives the TMS.

Second, in autistic subjects, there is no deflection of the electromyogram upon a subject’s observation of the above described video. There is in these subjects a potential produced by TMS of the appropriate area, implying that there is no defect in the circuitry to produce such sub-threshold muscle activation. Needless to say there is no summation effect in these subjects.

Dr. Théoret feels that this work implies that understanding of others’ actions is achieved by an individual mapping actions onto their own motor cortex(4). This is an intriguing hypothesis, but there are really two possibilities which both fit with the data. One is as suggested by Dr. Théoret, the other would be that the mirror neuron system alone interprets the intention of the action, and (when possible) maps the action onto the motor cortex. The former possibility would require, for instance, that anybody receiving sufficiently strong TMS would necessarily experience the feeling that they were either observing somebody perform an action or that they were performing the action themselves. This is in keeping with the theory will laid out by Daniel M. Wegner in his book The Illusion of Conscious Will. Without getting too far afield, Dr. Wegner believes that we have a general ability to ascribe agency to observed acts, attributing them to either to ourselves or to others.

The implications of this work are that a defect in the mirror neuron system is responsible for social-interaction pathology in patients with autism. In fact, some researchers believe that defects in the mirror neuron system could lead to all the deficits associated with autism(5). Of course, others feel that such dysfunction cannot be responsible for all the symptoms of autism(6). It remains to be seen whether any definitive explanation of the role of the mirror neuron system in autism will arise, but it is clear that it plays some role in the interpretation of actions.


1. Rizzolatti, G., & Craighero, L., (2004) The Mirror Neuron System, Annu. Rev. Neurosci. 27, 169-192.
2. Oberman, L.M., & Ramachandran, V.S., (2007) The simulating social mind: the role of the mirror neuron system and simulation in the social and communicative deficits of autism spectrum disorders. Psychol. Bull., 133, 310-327.
3. Fitzgerald, P.B., Fountain, S. & Daskalakis, Z.J. (2006). A comprehensive review of the effects of rTMS on motor cortical excitability and inhibition. Clinical Neurophysiology 117, 2584-2596
4. Théoret, H., Halligan, E., Kobayashi, M., Fregni, F., Tager-Flusberg, H. & Pascual-Leone, A. (2005) Impaired motor facilitation during action observation in individuals with autism spectrum disorder. Curr Biol. 2005 15, R84-R85.
5. Iacoboni, M., Dapretto, M. (2006) The mirror neuron system and the consequences of its dysfunction. Nat Rev Neurosci. 7, 942-951.
6. Hadjikhani, N., Joseph, R.M., Snyder, J. & Tager-Flusberg, H. (2006) Anatomical differences in the mirror neuron system and social cognition network in autism. Cereb. Cortex. 16, 1276-1282.