A possible brain network for representation of cooperative behavior and its implications for the psychopathology of schizophrenia.

It has been shown that social deficits contribute to psychopathology in schizophrenia, such as the bleulerian autism. A possible dysfunction in the mirror neuron system may be the reason for these deficits in the disorder. We wanted to better characterize the neural networks involved in the perception of social behavior. Fifteen healthy participants were presented with video clips of 8 seconds' duration depicting either (1) one actor manipulating an object, (2) two actors with only one manipulating an object or (3) two actors cooperating in manipulating an object and 2 other control conditions. Functional magnetic resonance imaging data were acquired during watching these videos. We found the perception of social cooperation is supported by a neural network comprising the precuneus, the temporoparietal junction (supramarginal gyrus, angular gyrus, BA 39/40), the middle temporal gyrus (including superior temporal sulcus) and frontal regions (medial frontal gyrus, inferior frontal gyrus). These areas form a complex network also being activated during theory of mind and cooperative behavior tasks. Its nodes overlap with those of the mirror neuron system. Consequently, both theory of mind abilities and mirror mechanisms are relevant in the perception and understanding of social cooperative behavior. We outline the consequences of these results for a further understanding of schizophrenic psychopathology with respect to social deficits and ego disturbances.

The neural basis of disturbed efference copy mechanism in patients with schizophrenia.

Core psychopathological symptoms in patients with schizophrenia suggest that their sense of self may be disturbed. A disturbance in predictive motor mechanisms may be the cause of such symptoms. Ten patients with schizophrenia and ten healthy right-handed control subjects opened and closed their hand. This movement was filmed with an MRI compatible video camera and projected online onto a monitor. BOLD contrast was measured with fMRI. The temporal delay between movement and feedback was parametrically varied. Participants judged whether or not there was a delay. Patients were less sensitive to these delays than a matched control group. Comparing neural activation between the two groups showed a reduced attenuation of movement-sensitive perceptual areas in patients with increasing delay and a higher activation in the putamen in controls. The results provide further evidence that impaired efference copy mechanisms may contribute to the pathogenesis of schizophrenia and its first rank symptoms.

Misattributions of agency in schizophrenia are based on imprecise predictions about the sensory consequences of one's actions.

The experience of being the initiator of one's own actions seems to be infallible at first glance. Misattributions of agency of one's actions in certain neurological or psychiatric patients reveal, however, that the central mechanisms underlying this experience can go astray. In particular, delusions of influence in schizophrenia might result from deficits in an inferential mechanism that allows distinguishing whether or not a sensory event has been self-produced. This distinction is made by comparing the actual sensory information with the consequences of one's action as predicted on the basis of internal action-related signals such as efference copies. If this internal prediction matches the actual sensory event, an action is registered as self-caused; in case of a mismatch, the difference is interpreted as externally produced. We tested the hypothesis that delusions of influence are based on deficits in this comparator mechanism. In particular, we tested whether patients' impairments in action attribution tasks are caused by imprecise predictions about the sensory consequences of self-action. Schizophrenia patients and matched controls performed pointing movements in a virtual-reality setup in which the visual consequences of movements could be rotated with respect to the actual movement. Experiment 1 revealed higher thresholds for detecting experimental feedback rotations in the patient group. The size of these thresholds correlated positively with patients' delusions of influence. Experiment 2 required subjects to estimate their direction of pointing visually in the presence of constantly rotated visual feedback. When compared to controls, patients' estimates were significantly better adapted to the feedback rotation and exhibited an increased variability. In interleaved trials without visual feedback, i.e. when pointing estimates relied solely on internal action-related signals, this variability was likewise increased and correlated with both delusions of influence and the size of patients' detection thresholds as assessed in the first experiment. These findings support the notion that delusions of influence are based on imprecise internal predictions about the sensory consequences of one's actions. Moreover, we suggest that such imprecise predictions prompt patients to rely more strongly on (and thus adapt to) external agency cues, in this case vision. Such context-dependent weighted integration of imprecise internal predictions and alternative agency cues might thus reflect the common basis for the various misattributions of agency in schizophrenia patients.