P.552 Acylcarnitine levels in paranoid schizophrenia with metabolic syndrome during treatment of second-generation antipsychotics

Abstract

Individuals with schizophrenia have been found to display neurocognitive deficits on the order of 1 standard deviation below the mean of healthy controls on a range of cognitive domains, with no clear pattern of deficits that characterizes the majority of individuals with schizophrenia. Such findings have led some to suggest that schizophrenia is characterized by a “generalized” neurocognitive deficit, implying that a common underlying etiology impacts all cognitive domains. Central nervous system accounts of the generalized deficit have been proposed (e.g., NMDA and GABA interneuron receptor dysfunction); however, there may also be more diffuse “general systems” abnormalities that affect brain function. The current study evaluated the role of one type of general systems abnormality, metabolic dysfunction, on global cognitive functioning in a sample of outpatients with schizophrenia (n = 27) and demographically matched healthy controls (n = 33). Participants completed a battery of neuropsychological tests, as well as metabolic measurements to assess blood glucose, blood pressure, and abdominal obesity. Results indicated that higher pulse pressure predicted the generalized neurocognitive deficit in schizophrenia, but not healthy controls; however, blood glucose and abdominal obesity did not predict cognitive performance in either group. These findings provide support for the role of metabolic abnormalities in the generalized neurocognitive deficit in schizophrenia, and suggest that treatment of hypertension may be a novel adjunctive treatment target for remediating cognitive deficits in schizophrenia.