Neural Basis Of Social Cognition Research Articles

Specialized Networks for Social Cognition in the Primate Brain

Primates have evolved diverse cognitive capabilities to navigate their complex social world. To understand how the brain implements critical social cognitive abilities, we describe functional specialization in the domains of face processing, social interaction understanding, and mental state attribution. Systems for face processing are specialized from the level of single cells to populations of neurons within brain regions to hierarchically organized networks that extract and represent abstract social information. Such functional specialization is not confined to the sensorimotor periphery but appears to be a pervasive theme of primate brain organization all the way to the apex regions of cortical hierarchies. Circuits processing social information are juxtaposed with parallel systems involved in processing nonsocial information, suggesting common computations applied to different domains. The emerging picture of the neural basis of social cognition is a set of distinct but interacting subnetworks involved in component processes such as face perception and social reasoning, traversing large parts of the primate brain.

Effective connectivity of the human mirror neuron system during social cognition.

The human mirror neuron system (MNS) can be considered the neural basis of social cognition. Identifying the global network structure of this system can provide significant progress in the field. In this study, we use dynamic causal modeling (DCM) to determine the effective connectivity between central regions of the MNS for the first time during different social cognition tasks. Sixty-seven healthy participants completed fMRI scanning while performing social cognition tasks, including imitation, empathy and theory of mind. Superior temporal sulcus (STS), inferior parietal lobule (IPL) and Brodmann area 44 (BA44) formed the regions of interest for DCM. Varying connectivity patterns, 540 models were built and fitted for each participant. By applying group-level analysis, Bayesian model selection and Bayesian model averaging, the optimal family and model for all experimental tasks were found. For all social-cognitive processes, effective connectivity from STS to IPL and from STS to BA44 was found. For imitation, additional mutual connections occurred between STS and BA44, as well as BA44 and IPL. The results suggest inverse models in which the motor regions BA44 and IPL receive sensory information from the STS. In contrast, for imitation, a sensory loop with an exchange of motor-to-sensory and sensory-to-motor information seems to exist.

The Neural Basis of Social Cognition in Typically Developing Children and Its Relationship to Social Functioning.

Theory of mind (ToM), the ability to think about the perspectives, beliefs, and feelings of another, develops throughout childhood and adolescence and is an important skill for social interactions. This study examines neural activity in typically developing children during a novel ToM task – the Movie Mentalizing Task– and tests its relations to ToM behavioral performance and social functioning. In this fMRI task, children ages 8–13years (N=25) watched a brief movie clip and were asked to predict a character’s mental state after a social interaction. Engaging in the Movie Mentalizing Task activated the ToM neural network. Moreover, greater neural activity in the ToM network, including the superior temporal gyrus and inferior frontal gyrus, was associated with better behavioral performance on independent ToM tasks and was related to better social functioning, though these results do not survive correction for multiple comparisons. Results offer a new affective theory of mind task for children in the scanner that robustly recruits activity in theory of mind regions.

Neural network of social interaction observation in marmosets.

A crucial component of social cognition is to observe and understand the social interactions of other individuals. A promising nonhuman primate model for investigating the neural basis of social interaction observation is the common marmoset (Callithrix jacchus), a small New World primate that shares a rich social repertoire with humans. Here, we used functional magnetic resonance imaging acquired at 9.4 T to map the brain areas activated by social interaction observation in awake marmosets. We discovered a network of subcortical and cortical areas, predominately in the anterior lateral frontal and medial frontal cortex, that was specifically activated by social interaction observation. This network resembled that recently identified in Old World macaque monkeys. Our findings suggest that this network is largely conserved between New and Old World primates and support the use of marmosets for studying the neural basis of social cognition.

Prefrontal–amygdala circuits in social decision-making

An increasing amount of research effort is being directed toward investigating the neural bases of social cognition from a systems neuroscience perspective. Evidence from multiple animal species is beginning to provide a mechanistic understanding of the substrates of social behaviors at multiple levels of neurobiology, ranging from those underlying high-level social constructs in humans and their more rudimentary underpinnings in monkeys to circuit-level and cell-type-specific instantiations of social behaviors in rodents. Here we review literature examining the neural mechanisms of social decision-making in humans, non-human primates and rodents, focusing on the amygdala and the medial and orbital prefrontal cortical regions and their functional interactions. We also discuss how the neuropeptide oxytocin impacts these circuits and their downstream effects on social behaviors. Overall, we conclude that regulated interactions of neuronal activity in the prefrontal-amygdala pathways critically contribute to social decision-making in the brains of primates and rodents.

Social Cognition Deficits Are Pervasive across Both Classical and Overlap Frontotemporal Dementia Syndromes

Objectives: Frontotemporal dementia (FTD) syndromes are a complex group of disorders characterised by profound changes in behaviour and cognition. Many of the observed behavioural abnormalities are now recognised to be due to impaired social cognition. While deficits in emotion recognition and empathy are well-recognised in behavioural-variant (Bv)FTD, limited information exists about the nature of social cognitive impairment in the language variant primary progressive aphasia (PPA) that includes progressive non-fluent aphasia (PNFA) and semantic dementia (SD), and in the motor variants FTD amyotrophic lateral sclerosis (FTD-ALS) and FTD progressive supranuclear palsy (FTD-PSP). This prospective study sought to explore the nature and profile of social cognition deficits across the spectrum of FTD. Methods: Sixty patients on the FTD spectrum, i.e., classical (16 with BvFTD and 20 with PPA) and overlap FTD syndromes (13 with FTD-ALS and 11 with FTD-PSP) were evaluated by means of the social cognition tasks, the Interpersonal Reactivity Index (IRI) for empathy, and pictures of facial affect (POFA) for emotion recognition. General cognition and behaviour were also assessed. Results: A significant impairment in emotion recognition and empathy was detected in both the classical and overlap FTD syndromes. The recognition of positive emotions was relatively preserved compared to that of negative emotions. Among the FTD subtypes, maximal impairment of empathy was demonstrated in FTD-PSP. Conclusion: Social cognition impairment is pervasive across the spectrum of FTD disorders, and tests of emotion recognition and empathy are clinically useful to identify the nature of behavioural problems in both classical and overlap FTD. Our findings also have implications for understanding the neural basis of social cognition in FTD.

Social cognition in schizophrenia: Validation of an ecological fMRI task

Neuroimaging studies have revealed brain regions involved in social cognition, which reportedly show functional alterations in schizophrenia. However, the social neural network has not been investigated with regards to language perception and social interactions in daily life. Here we developed and validated an integrative fMRI task to explore the neural basis of social cognition with regards to language perception in schizophrenia. The task comprised listening to film extracts and inferring mental states to characters. We first identified the functional network activated during the task in 28 healthy controls (HC). Next, we evaluated the reproducibility of Blood-Oxygen-Level Dependent (BOLD) variations in 14 HC participants. Finally, we investigated network impairment in 20 patients with schizophrenia (SZ) compared to HC. The HC group exhibited bilateral activation in the superior and middle temporal gyri (including the poles and the temporo-parietal junction). Overall, our novel integrative task induced activation of a functional network with good reproducibility and involved in language conveying social information. Compared to the HC group, the SZ group showed decreased recruitment of the right temporo-parietal junction. These findings may be useful for testing the impact of remediation on the brain, particularly on the network of language conveying social information.

[The neural bases of social cognition in major depressive disorder: a review].

Major depressive disorder (MDD) is associated with a significant impairment of social and interpersonal functioning. Several neuroimaging studies have evaluated social cognition, i.e. how people with MDD process, store and analyze information about other people and social situations. We conducted a focused review and selected manuscript published until August 2016 indexed on PubMed and PsycINFO, searching for the following keywords: "major depressive disorder", "major depression", "unipolar depression", "clinical depression", "fMRI", "emotion comprehension", "emotion perception", "affect comprehension", "affect perception", "facial expression", "prosody", "theory of mind", "mentalizing", "empathy". During depressive episodes, patients with MDD show a difference pattern of neural response during emotion processing, compared to healthy controls. Many studies show that those alterations disappear once the acute episodes remit. However, other studies show that the alterations may persist during remission periods. Limits. The studies evaluate only one component of social cognition and not all studies include a control group. Neurobiological research supports a role of social cognition deficits in MDD, especially for what pertains interpersonal functioning, this suggesting the need for further research and the possibility for treatment implications.

[Neural basis of social cognition in bipolar disorder].

This article review studies social and interpersonal functioning in patients with bipolar disorder (BD), and reports on the neurobiological underpinnings of the dysfunctions in emotion recognition, i.e. one of the main domains of social cognition. A bibliographical research of controlled studies from 1967 to 2015 was completed in PubMed and PsycINFO using the keywords: "fMRI", "emotion comprehension", "emotion perception", "affect comprehension", "affect perception", "facial expression", "prosody", "theory of mind", "mentalizing", "attributional style", "social perception", "empathy" and "bipolar disorder" or "unipolar depression". Limbic hyperactivity, with a lack of appropriate cortical control, has been reported in subjects with BD during social interactions. This is particularly evident during the acute affective episodes but may persist during the euthymic phases. Deficits in emotion regulation, including neural systems implicated both in voluntary and automatic emotion regulatory subprocesses, are present in DB, particularly for what pertains to social interactions and interpersonal functioning. Patients with bipolar disorder may present a dysfunction in the cortical ability to modulate the limbic system, which may show hyperactivity during social interactions. More studies are needed, including studies to evaluate treatment implications.

Common and distinct neural mechanisms of the fundamental dimensions of social cognition

In the present study, we used a valence classification task to investigate the common and distinct neural basis of the two fundamental dimensions of social cognition (agency and communion) using functional magnetic resonance imaging (fMRI). The results showed that several brain areas associated with mentalizing, along with the inferior parietal gyrus in the mirror system, showed overlap in response to both agentic and communal words. These findings suggest that both content categories are related to the neural basis of social cognition; further, several areas in the default mode network (DMN) showed similar deactivations between agency and communion, reflecting task-induced deactivation (TID). In terms of distinct activations, the findings indicated greater deactivations for communal than agentic content in the ventral anterior cingulate (vACC) and medial orbitofrontal cortex (mOFC). Communion also showed greater activation in some visual areas compared to agentic content, including occipital gyrus, lingual gyrus, and fusiform gyrus. These activations may reflect greater allocation of attentional resources to visual areas when processing communal content, or inhibition of cognitive activity irrelevant to task performance. If so, this suggests greater attention and engagement with communion-related content. The present research thus suggests common and differential activations for agency- versus communion-related content.

Frontal alpha oscillations distinguish leaders from followers: Multivariate decoding of mutually interacting brains

Successful social interactions rely upon the abilities of two or more people to mutually exchange information in real-time, while simultaneously adapting to one another. The neural basis of social cognition has mostly been investigated in isolated individuals, and more recently using two-person paradigms to quantify the neuronal dynamics underlying social interaction. While several studies have shown the relevance of understanding complementary and mutually adaptive processes, the neural mechanisms underlying such coordinative behavioral patterns during joint action remain largely unknown. Here, we employed a synchronized finger-tapping task while measuring dual-EEG from pairs of human participants who either mutually adjusted to each other in an interactive task or followed a computer metronome. Neurophysiologically, the interactive condition was characterized by a stronger suppression of alpha and low-beta oscillations over motor and frontal areas in contrast to the non-interactive computer condition. A multivariate analysis of two-brain activity to classify interactive versus non-interactive trials revealed asymmetric patterns of the frontal alpha-suppression in each pair, during both task anticipation and execution, such that only one member showed the frontal component. Analysis of the behavioral data showed that this distinction coincided with the leader–follower relationship in 8/9 pairs, with the leaders characterized by the stronger frontal alpha-suppression. This suggests that leaders invest more resources in prospective planning and control. Hence our results show that the spontaneous emergence of leader–follower relationships in dyadic interactions can be predicted from EEG recordings of brain activity prior to and during interaction. Furthermore, this emphasizes the importance of investigating complementarity in joint action.

Brain games: Toward a neuroecology of social behavior

In the target article, Schilbach et al. defend a "second-person neuroscience" perspective that focuses on the neural basis of social cognition during live, ongoing interactions between individuals. We argue that a second-person neuroscience would benefit from formal approaches borrowed from economics and behavioral ecology and that it should be extended to social interactions in nonhuman animals.

Alzheimer's Disease and the Frontotemporal Dementias: Contributions to Clinico-Pathological Studies, Diagnosis, and Cognitive Neuroscience

This review focuses on six key papers published in the mid 2000 s based on work conducted in Cambridge. The first two relate to clinico-pathological studies which established that Alzheimer's disease (AD) is a relatively common cause of focal cortical syndromes, notably progressive aphasia (largely nonfluent), progressive apraxia, and posterior cortical atrophy with complex visual symptoms. Building on these findings, criteria for the progressive aphasias have been developed which define the variant associated with AD (progressive logopenic aphasia). Memory in the dementias has been a major area of interest and one paper discussed here explored the neural basis for episodic and semantic memory failure in AD and semantic dementia. Despite very different memory profiles, the two disorders both cause severe hippocampal hypometabolism and atrophy but differ in the degree of involvement of other memory related structures. This work drew attention to the role of pathology in non-hippocampal structures early in AD. The next two articles deal with the behavioral variant frontotemporal dementia (bvFTD) which we have shown is associated with breakdown in theory of mind, social reasoning, empathy, and emotion processing and contributed towork on the neural basis of social cognition. We also identified a subgroup of bvFTD who fail to progress over many years, termed phenocopy cases, who are differentiated by their lack of atrophy on MRI. The final paper described the application of the Addenbrooke's Cognitive Examination-Revised, which has proven a useful brief assessment tool for the early detection of a range of neurodegenerative disorders including AD and FTD. It also appears to be helpful in predicting those with mild cognitive impairment who will progress to frank dementia.

The representation of self and person knowledge in the medial prefrontal cortex

Nearly 40 years ago, social psychologists began applying the information processing framework of cognitive psychology to the question of how humans understand and represent knowledge about themselves and others. This approach gave rise to the immensely successful field of social cognition and fundamentally changed the way in which social psychological phenomena are studied. More recently, social scientists of many stripes have turned to the methods of cognitive neuroscience to understand the neural basis of social cognition. A pervasive finding from this research is that social knowledge, be it about one's self or of others, is represented in the medial prefrontal cortex (MPFC). This review focuses on the social cognitive neuroscience of self and person knowledge in the MPFC. We begin with a brief historical overview of social cognition, followed by a review of recent and influential research on the brain basis of self and person knowledge. In the latter half of this review, we discuss the role of familiarity and similarity in person perception and of spontaneous processes in self and other-referential cognition. Throughout, we discuss the myriad ways in which the social cognitive neuroscience approach has provided new insights into the nature and structure of self and person knowledge. WIREs Cogn Sci 2012, 3:451-470. doi: 10.1002/wcs.1183 This article is categorized under: Neuroscience > Cognition.

An fMRI task for exploring memory effects of significant-other activation in social cognition

A novel functional magnetic resonance imaging (fMRI) paradigm for exploring the neurobiologic basis of a key aspect of social cognition was developed, adapted from Andersen’s transference paradigm (Andersen & Chen, 2002). This paradigm captures the extent to which current memory in relation to a stranger is impacted by activated knowledge of a significant other (SO). Forty healthy young adult participants were seen for two separate sessions and misled to believe that the sessions were unrelated to one another. In the first, participants listed descriptive sentences for each of four different important people in their lives (SOs), chose 20 irrelevant adjectives about each from a list, and provided descriptive sentences about 80 famous individuals. In the second session, at least two months later, participants were shown 20 sentences about each of six different supposed strangers (“targets”). Unbeknownst to participants, two of the targets resembled SOs described by the participant in the initial session (“the experimental targets”), two resembled SOs described by a different participant (the yoked-control), and two were constructed from a random assortment of sentences the participant listed about famous individuals (the no-representation control). The participants were then shown 30 sentences about each target and asked to rate how likely it was that they were just exposed to each about that particular target. For targets resembling SOs, 10 of the 30 sentences (the “lures”) had, in fact, not been seen previously about the target, but were from the participant’s own description of the pertinent SO. Therefore, participants should incorrectly rate these lures higher when the target resembled their own SO, as compared to the comparable lures in either control condition. Functional MRI images were collected during the entire second session using a GE Signa 3T whole body scanner. Individual and group level fMRI analyses were conducted using SPM8. Replicating Andersen’s findings, the average memory recognition score was higher for the “lures” in the SO condition (M =2.69; SD = .61) than for those in the yoked-control condition (M = 2.55; SD = .65), paired t (39) = 2.01, p = .05). In fMRI analyses, betas reflected the tendency of neural activity to increase when SO-relevant targets were presented during the learning phase and these were used to produce a second-level contrast map which showed significant differences in activation during the presentation of SO-resembling targets, in comparison with the yoked-control condition. Findings were significant at the level of p < .05 after correction for multiple comparisons using the false discovery rate method. Neural activity in bilateral fusiform cortex and the superior frontal gyrus increased during SO activation, while neural activity in the subgenual ACC (sgACC) decreased. This paradigm is a powerful tool for exploring the neural basis of social cognition and may well prove useful in characterizing psychiatric disorders in a developmentally sophisticated way. METHOD ● Participants 40 Healthy Young Adults Ages 18-30, mean=21.9 15 male, 25 female ● Initial Session ● Experimental Session ● Learning Task ● Memory Recognition Task RESULTS Fig 1. Statistically significant recognition memory effect, n=40, p=.05 Fig 2. Healthy control schema-relevant activity (red= increasing, blue=decreasing), N=40, corrected p<.05.  Selects 4 Significant Others and provides 10 positive and 10 negative short sentences about each  Identifies 25 “irrelevant” adjectives about each Significant Other  Provides 40 positive and 40 negative short sentences about 80 well-known individuals

Systematic review of the neural basis of social cognition in patients with mood disorders

This review integrates neuroimaging studies of 2 domains of social cognition--emotion comprehension and theory of mind (ToM)--in patients with major depressive disorder and bipolar disorder. The influence of key clinical and method variables on patterns of neural activation during social cognitive processing is also examined. Studies were identified using PsycINFO and PubMed (January 1967 to May 2011). The search terms were "fMRI," "emotion comprehension," "emotion perception," "affect comprehension," "affect perception," "facial expression," "prosody," "theory of mind," "mentalizing" and "empathy" in combination with "major depressive disorder," "bipolar disorder," "major depression," "unipolar depression," "clinical depression" and "mania." Taken together, neuroimaging studies of social cognition in patients with mood disorders reveal enhanced activation in limbic and emotion-related structures and attenuated activity within frontal regions associated with emotion regulation and higher cognitive functions. These results reveal an overall lack of inhibition by higher-order cognitive structures on limbic and emotion-related structures during social cognitive processing in patients with mood disorders. Critically, key variables, including illness burden, symptom severity, comorbidity, medication status and cognitive load may moderate this pattern of neural activation. Studies that did not include control tasks or a comparator group were included in this review. Further work is needed to examine the contribution of key moderator variables and to further elucidate the neural networks underlying altered social cognition in patients with mood disorders. The neural networks under lying higher-order social cognitive processes, including empathy, remain unexplored in patients with mood disorders.

The Neural Bases of Social Cognition and Story Comprehension

A great deal of research exists on the neural basis of theory-of-mind (ToM) or mentalizing. Qualitative reviews on this topic have identified a mentalizing network composed of the medial prefrontal cortex, posterior cingulate/precuneus, and bilateral temporal parietal junction. These conclusions, however, are not based on a quantitative and systematic approach. The current review presents a quantitative meta-analysis of neuroimaging studies pertaining to ToM, using the activation-likelihood estimation (ALE) approach. Separate ALE meta-analyses are presented for story-based and nonstory-based studies of ToM. The conjunction of these two meta-analyses reveals a core mentalizing network that includes areas not typically noted by previous reviews. A third ALE meta-analysis was conducted with respect to story comprehension in order to examine the relation between ToM and stories. Story processing overlapped with many regions of the core mentalizing network, and these shared regions bear some resemblance to a network implicated by a number of other processes.

Mesmerising mirror neurons

Mirror neurons have been hailed as the key to understanding social cognition. I argue that three currents of thought—relating to evolution, atomism and telepathy—have magnified the perceived importance of mirror neurons. When they are understood to be a product of associative learning, rather than an adaptation for social cognition, mirror neurons are no longer mesmerising, but they continue to raise important questions about both the psychology of science and the neural bases of social cognition.

Mirror neurons

What are mirror neurons? Mirror neurons are multimodal association neurons that increase their activity during the execution of certain actions and while hearing or seeing corresponding actions being performed by others. Neurons responding to the sound or sight of some actions, but only to the execution of different actions, are not mirror neurons. Where are mirror neurons found? Three research groups have reported the existence of mirror neurons in three regions of the macaque cortex (Figure 1). Pending systematic explorations, we do not know whether mirror neurons exist elsewhere in the macaque brain. Recently, mirror neurons have also been reported in the song-bird. Do humans have mirror neurons? This issue has been highly contentious, with no individual piece of evidence generally accepted as definitive, but quite a lot of indirect evidence for human mirror neurons has been reported. First, if a subject moves, the power of the mu-rhythm in the electro-encephalogram (EEG) recorded from his or her brain decreases. Similarly, the EEG rhythm desynchronizes when the subject observes somebody else move. Second, behavioral experiments indicate that the execution of an action is facilitated by viewing someone else execute a similar action, but hindered by viewing an incompatible action. Moreover, transcranial magnetic stimulation (TMS) studies evidence that watching performance of an action facilitates the motor cortical representation of the muscles involved in doing the same action. This shows that some neurons involved in performing an action are indeed selectively activated by seeing a similar action — in other words, mirror neurons do exist somewhere in the human brain. If humans do have mirror neurons, where are they? Disrupting activity in the ventral premotor cortex using repetitive TMS reduces the effect of viewing other people perform an action. Functional magnetic resonance imaging (fMRI) has shown that a great number of locations in the brain that are active during the execution of an action are also active when the same action is seen or heard; these include the premotor and parietal regions in which mirror neurons are found in monkeys (Figure 1). Unless one abandons the concept of evolutionary continuity, the conclusion that mirror neurons akin to those found in monkeys (and birds) exist at least in these regions of the human brain is most parsimonious. The results of fMRI experiments, however, suggest that a number of additional brain regions have mirror properties in the human brain, including the dorsal premotor, supplementary motor, the primary and secondary somatosensory cortex, the posterior middle temporal gyrus and parts of the cerebellum (Figure 1). Whether these shared activations indeed reflect the activity of mirror neurons in each of these regions remains to be established: some could also contain distinct populations of neurons active during the perception and the execution of actions that just happen to share the same voxel. Pending further single cell recordings, it would seem best to refer to these human brain regions as parts of a putative mirror neuron system. Is there evidence against the existence of mirror neurons in humans? Not really: for each experiment that fails to find evidence for mirror neurons in humans there is at least one that succeeds. For example, recent experiments used fMRI to test the prediction that, for a brain region that is part of the mirror neuron system, repeated viewing of an action would lead to reduced activation during subsequent execution of the same action (and vice versa): three of the four experiments that tried found such an effect. Given statistics that limit false positives to <5%, this ratio of 3:4 is strong evidence for the existence of human mirror neurons. But if there are mirror neurons, shouldn't all experiments find evidence for them? A basic power analysis falsifies this intuition: using the typical voxelwise thresholds of p < 0.001 in fMRI, one would expect even large effect sizes to remain undetected over 50% of the time. Do mirror neurons help us perceive the actions of others? Experiments in which brain areas thought to contain mirror neurons were disrupted, either using repetitive TMS or as a result of localized brain damage, have demonstrated a drop in the accuracy with which participants can report what action another individual has performed — particularly for those actions they can no longer perform accurately themselves. Often, however, the accuracy remains above chance. These results indicate that brain areas thought to contain mirror neurons are indeed contributing to our perception of the actions of others, but that they are unlikely to be the only player. Can we develop new mirror neurons? Hebbian learning suggests that performing an action while seeing and hearing oneself perform it should be enough for neurons involved in performance to start responding to the sight and sound of the same action. The fact that five hours of piano lessons suffice for the premotor cortex to start responding to piano music supports this view. Is the mirror system broken in patients with social deficits? Given that the mirror neuron system is implicated in understanding the actions of others, it has been widely suggested that defects in the system may play a part in neurological disorders characterised by social deficits, in particular autism. While some studies do show that, in individuals with autism, the putative mirror neuron system is activated less than usual while they view the emotions or actions of others, other studies do not. We now need to find out when autistic individuals may activate this system less, and examine whether this can help us understand this disorder. Are mirror neurons the neural basis of mind reading, empathy and language? Activations in brain regions involved in executing actions have been measured while people try to read the minds of others, empathize with them or listen to spoken language. Examining how much of that activity really stems from mirror neurons, and in particular to what extent there is a causal link between this activity and these mental functions is a key challenge for future research and will require TMS and lesion studies. Do we have mirror neurons for emotions or sensations? A handful of experiments suggest that brain regions involved in the experience of emotions and sensations become reactivated while we view the emotions and sensations of others. These regions might therefore contain mirror-like neurons for emotions and sensations. Pending single cell recordings, this conclusion remains tentative, though it is an influential idea. Why is the mirror neuron system so controversial? About a dozen papers have reported direct evidence for mirror neuron activity in monkeys and birds. Approximately 100 times as many papers refer to mirror neurons without directly recording their activity, often implying a link between mirror neurons and higher cognitive functions. While the existence of mirror neurons in animals is beyond doubt, the causal relationship between these neurons and phenomena such as empathy, mind reading, language, autism, esthetics, morals and politics is so poorly established, that the frequency with which the term mirror neuron is encountered in the literature should trigger some unease. So what is next? After the initial enthusiasm for the discovery of mirror neurons, and the stimulating wave of speculation that followed, we now need to concentrate on developing methods that can: localize these neurons in the human brain; examine what information they convey about the actions of others; test for a causal relationship between putative mirror neurons in various nodes of the system and higher brain functions in humans; and try to understand the evolution of this system. Mirror neurons give us a fascinating glimpse into the neural basis of social cognition — let us use careful experimentation instead of wild speculations and controversies to transform this glimpse into solid scientific understanding.

Of brain and bone: The unusual case of Dr. A

Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease), who presented with a profound behavioral disturbance characterized by acquired sociopathy. We conducted a detailed genetic, pathological, neuroimaging and cognitive study, including a battery of tests designed to investigate Dr. A's abilities to understand emotional cues and to infer mental states and intentions to others (theory of mind). Dr. A's genetic profile suggests the possibility that a mutation causing hereditary multiple exostoses, Ext2, may play a role in the pattern of neurodegeneration in frontotemporal dementia since knockout mice deficient in the Ext gene family member, Ext1, show severe CNS defects including loss of olfactory bulbs and abnormally small cerebral cortex. Dr. A showed significant impairment in emotion comprehension, second order theory of mind, attribution of intentions, and empathy despite preserved general cognitive abilities. Voxel-based morphometry on structural MRI images showed significant atrophy in the medial and right orbital frontal and anterior temporal regions with sparing of dorsolateral frontal cortex. This case demonstrates that social and emotional dysfunction in FTD can be dissociated from preserved performance on classic executive functioning tasks. The specific pattern of anatomical damage shown by VBM emphasizes the importance of the network including the superior medial frontal gyrus as well as temporal polar areas, in regulation of social cognition and theory of mind. This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.