Abstract
The deficit syndrome defines a subgroup of schizophrenia patients with prominent and enduring primary negative symptoms (1). Behavioral, structural, and functional neuroimaging studies have implicated mainly the dorsolateral prefrontal - thalamocortical circuit. Deficit syndrome patients seem to have larger ventricles in MRI studies (2). Neurological soft signs suggest parietal involvement with greater sensory integration impairment in deficit syndrome patients (3). On the contrary, some biological markers such as P50 gating have not shown any difference between deficit and non-deficit schizophrenia (4). Finally, no pharmacological treatment has so far proven effective for the treatment of primary enduring negative symptoms (5). In conclusion, deficit pathology in schizophrenia seems to involve the prefrontal and parietal lobes and have different neurobiological substrates than positive symptoms.
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