Rakshathi Basavaraju

Association of intracortical inhibition with social cognition deficits in schizophrenia: Findings from a transcranial magnetic stimulation study

Abnormal cortical-inhibition has been hypothesized to underlie social-cognition deficits in schizophrenia. Studies using transcranial magnetic stimulation (TMS) as a neurophysiological probe have demonstrated cortical-inhibition deficits in this group. We compared TMS-measured short- and long-interval intracortical-inhibition (SICI & LICI) in antipsychotic-naïve (n=33) and medicated (n=21) schizophrenia patients and in healthy comparison subjects (n=45). We also studied the association between cortical-inhibition and social-cognition deficits in the patients. Antipsychotic-naïve patients had significant deficits in SICI (i.e., less inhibitory response). In this group, SICI had significant inverse correlations with emotion processing and a global social-cognition score. Impaired intracortical-inhibition may thus contribute to social-cognition deficits in schizophrenia.

Mirror Neuron Disinhibition may be Linked with Catatonic Echo-Phenomena: A Single Case TMS Study

Though computational models and animal studies are not explicitly linked, they inform each other. For example, the cellular mechanisms of stimulation are characterized in brain slice studies using uniform fields [8]. Conversely, the electric fields predicted by forward models are the input for animal studies [9]. Animal and computational studies will continue to inform clinical practice; in interpreting published studies and in ongoing research, the quasi-uniform assumption is ubiquitous.

Mirror neuron dysfunction and ego-boundary disturbances in schizophrenia: a transcranial magnetic stimulation study.

Background: Ego-boundary disturbance (EBD) is a unique symptom cluster characterized by passivity experiences (involving thoughts, actions, emotions and sensations) attributed by patients to some external agency. The neurobiology of these “first rank” symptoms is poorly understood. Aberrant mirror neuron activation may explain impaired self-monitoring and agency attribution underlying these symptoms. We aim to study mirror neuron activity (MNA) in schizophrenia patients with and without EBD using transcranial magnetic stimulation (TMS). Materials and Methods: 50 right-handed schizophrenia patients (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) were evaluated using the Mini-International Neuropsychiatric Interview and the Positive and Negative Syndrome Scale. They completed a TMS experiment to assess putative premotor MNA. Motor evoked potential (MEP) was recorded in the right first dorsal interosseous muscle (FDI) with (a) 120% of resting motor threshold (RMT), (b) stimulus intensity set to evoke MEP of motor threshold 1 mV amplitude (MT1), (c) two paired pulse paradigms (short- and long interval intra-cortical inhibition). These were done in three states: Actual observation of an action using the FDI, virtual-observation (video) of this action and resting state. The percent change of MEP from resting to action-observation states formed the measure of putative MNA. Results: MNA measured using MT1 and 120% RMT paradigms was significantly lower in the 18 patients with EBD (thought-broadcast/withdrawal/insertion, made-act/impulse/affect and somatic passivity) than the 32 patients without EBD (t = 2.431, P = 0.020; t = 2.051, P = 0.04 respectively for the two paradigms). The two groups did not differ on age, gender, education and total symptom scores. Conclusion: Schizophrenia patients with EBD have lower premotor MNA. This highlights the role of MNA dysfunction in the pathophysiology of this unique and intriguing symptom cluster in schizophrenia.