Mirror neuron system faulty in schizophrenia patients

By Eleanor McDermid, Senior medwireNews Reporter

An imaging study suggests that a faulty mirror neuron system could underlie the social dysfunction seen in patients with schizophrenia.

Researcher Sohee Park (Vanderbilt University, Nashville, Tennessee, USA) and colleagues found that the mirror neuron system, which is responsible for a person’s ability to perceive, understand and mimic biological movement, was “less fine-tuned” in schizophrenia patients than in mentally healthy controls.

“One route to understanding the minds of others is via internalized mimicking”, they write in The American Journal of Psychiatry. They therefore suggest that “disturbances in imitation could cascade into a failure to understand the minds of others and that poor social interactions could fuel social isolation, which in turn can worsen symptoms.”

In the study, participants had to respond to a video of a hand performing a movement, or a stationary hand with markers indicating which fingers to move, or a set of spatial markers indicating the same.

The 16 schizophrenia patients in the study performed the task with similar accuracy and speed to the 16 mentally healthy controls. However, functional magnetic resonance imaging showed differences between the groups in the activation of the mirror neuron system.

The control participants showed greater activation of this system when imitating the moving hand than when taking their cues from stationary markers, and they had a more differentiated response to imitative than nonimitative action, most notably for an area in the right inferior parietal lobe extending into the posterior superior temporal sulcus, which is responsible for the perception of biological movement.

However, the response of patients to imitative movements was less differentiated than that of controls, with significantly less activation in the right posterior superior temporal sulcus, as well as in another more anterior region of the right posterior superior temporal sulcus, and in the left inferior parietal lobe.

During nonimitative action, by contrast, they had greater activation than controls in the right and left posterior superior temporal sulcus and also in the inferior parietal lobe.

There were also differences when the study participants were simply observing action (ie, biological motion perception). Patients again had a less differentiated response than controls to animated versus nonanimated action, caused by less activation in the right inferior parietal lobe extending into the posterior superior temporal sulcus, and also in the left posterior superior temporal sulcus.

The researchers suggest that these activation changes may manifest as both enhanced sensitivity to social information and reduced sensitivity to the states of other people, as observed in schizophrenia patients.

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