[ARTICLE] White Matter Neurometabolic Signatures Support the Deficit and Nondeficit Distinction in Antipsychotic-Naïve First-Episode Psychosis Patients

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White Matter Neurometabolic Signatures & Schizophrenia
White Matter Neurometabolic Signatures & Schizophrenia

le 23 mars 2021

Published in Schizophr Bull

Collaborative research project led by Prof. Kraguljac (Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, SC 501, Birmingham, AL, USA) in which in Dr. Briend participated


The deficit syndrome is thought to be a more homogenous clinical subgroup within the syndrome of schizophrenia that is characterized by enduring negative symptoms. It is hypothesized that distinct pathophysiological processes underlie the subtypes, where the deficit syndrome reflects an early onset nonprogressive developmental process, and the nondeficit form of the illness is characterized by attenuated neuroplasticity secondary to elevated glutamate levels. We used single-voxel magnetic resonance spectroscopy (PRESS; TE: 30 ms) to measure left frontal white matter neurometabolite levels in 61 antipsychotic-naïve first-episode psychosis patients (39 who did not display deficit features, 22 who did display deficit features, assessed with the Schedule for the Deficit Syndrome) and 59 healthy controls. Metabolite levels were quantified with the LCModel. We used a MANCOVA to determine neurometabolite differences between healthy controls, deficit syndrome patients, and nondeficit patients. We report a significant group difference when all metabolites were considered jointly (F[10,208] = 2.16; P = .02). Post hoc analyses showed that patients presenting without deficit features had higher glutamate levels than patients with deficit features and controls. Patients presenting without deficit features also had significantly higher myoinositol levels than controls; myoinositol levels were trend-level higher in patients presenting with deficit features compared to controls. Our data support the idea that the pathophysiology of patients presenting without deficit features may differ from those presenting with deficit features.


N-acetyl- aspartate; antipsychotic naïve; deficit syndrome; glutamate; magnetic resonance spectroscopy; myoinositol.

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