April 3, 2014. Brain activation during the imitation and observation of others’ actions—an important component of social cognition—is altered in schizophrenia, reports a new study published online March 14 in the American Journal of Psychiatry. The functional magnetic resonance imaging (fMRI) study, led by Sohee Park of Vanderbilt University, Nashville, Tennessee, found that in people with schizophrenia, imitation as well as observation resulted in less specific activation of a network of brain regions involved in imitation—the hypothesized mirror neuron system—a finding that may provide a better understanding of social cognition deficits in schizophrenia.
People with schizophrenia show impairments in a number of social cognitive domains such as emotion processing and theory of mind (Green and Horan, 2010). A challenge of measuring social functioning in the illness is that many tasks rely on cognitive and perceptual abilities that may also be impaired. In the new study, Park and colleagues took a bottom-up approach by examining imitation, one of the building blocks of higher-level social functioning.
Monkey see, monkey do
Imitation of the actions of others is critical to the nonverbal type of learning that predominates in social cognition and is hypothesized to be a mechanism of understanding the feelings and intentions of others. The putative neural basis of imitation—the mirror neuron system—has been well characterized in nonhuman primates. Located in the parietal and premotor cortices, mirror neurons increase their firing rate when a monkey performs an action or watches another perform the same action.
Without electrophysiological analyses of individual neurons, the existence of mirror neurons in humans remains to be proven, although increasing evidence supports it (Oztop et al., 2013).
Impaired imitation could lead to difficulties understanding the thoughts and actions of others, which in turn could manifest as social difficulties. The few studies that have explored imitation in schizophrenia have found deficits, and though none have looked at brain activation during such tasks, Park’s group found abnormal activation of the posterior superior temporal activity in response to the perception of biological movement in the illness, a component of imitation (Kim et al., 2011). Deficits in social cognition are also present in children who have early psychotic experiences, who are more likely to later develop psychosis (see SRF related news report).
Looking in the mirror
In the current study, first author Katharine Thakkar and colleagues used functional magnetic resonance imaging (fMRI) to evaluate activation of the hypothesized human parietal-frontal-temporal mirror neuron system during action imitation in 16 subjects with schizophrenia (all taking antipsychotic medication) and 16 healthy controls.
During the task, stimuli were presented in two different forms: animated (a video of a hand pressing buttons on a three-button box in a sequence) or non-animated (an image of a hand pressing one of the three buttons or of X’s that were used to represent the buttons). Each trial consisted of three finger movements. Prior to each stimulus presentation, subjects were first visually cued to either imitate the upcoming stimulus presentation or simply watch it.
Healthy controls were more accurate than schizophrenia subjects when imitating the movements, but there were no differences between groups in the non-imitative condition. The groups also did not differ in the latency to initiate the first movement in a sequence, or in the time required to complete the three-movement sequence. Similar to prior reports, healthy subjects had greater activation in the posterior superior temporal sulcus, inferior parietal lobe, and inferior frontal gyrus during imitative compared to non-imitative activation, though significance was only achieved in the right hemisphere.
Consistent with the authors’ hypothesis, the parietal-frontal-temporal network was abnormally activated in schizophrenia. Healthy subjects exhibited a more differentiated response between the imitation and non-imitative action than the schizophrenia subjects did, with the greatest difference between the two subject groups occurring in the right inferior parietal lobe and extending into the posterior superior temporal sulcus. This maximal difference was due not only to greater activity in the posterior superior temporal sulcus during imitation in healthy subjects, but also because of patients’ greater activity in the right inferior parietal lobe and posterior superior temporal sulcus for non-imitative action.
Similar to the findings on imitation action, healthy controls showed more of a differentiation between the animated and non-animated action conditions than schizophrenia subjects did in the right inferior parietal lobe. Healthy subjects also showed greater activation than schizophrenia subjects in the left posterior superior temporal sulcus.
Linking these activity changes and imitation deficits to disease-associated social deficits is challenging. Greater activity in the right posterior superior temporal sulcus during action imitation was correlated with a better Brief Psychiatric Rating Scale (BPRS) score, and greater activity in the right inferior parietal lobe during non-imitative action corresponded to better negative symptoms, although both relationships only reached trend-level significance.
The most significant correlation (p = 0.02), however, contradicted the expected relationship between activation and social functioning: For animated over non-animated observation, greater activation of the right inferior parietal lobe was correlated with a worse score on the Social Functioning Scale. Interestingly, antipsychotic drugs appeared to have a beneficial effect for the same comparison—the higher a patient’s dose, the more his or her inferior parietal lobe activation resembled that of a healthy subject.—Allison A. Curley.
Thakkar KN, Peterman JS, Park S. Altered Brain Activation During Action Imitation and Observation in Schizophrenia: A Translational Approach to Investigating Social Dysfunction in Schizophrenia. Am J Psychiatry . 2014 Mar 14. Abstract