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Volume 181, Issue 3, Pages 237-240 (30 March 2010)


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High energy phosphate abnormalities normalize after antipsychotic treatment in schizophrenia: A longitudinal 31P MRS study of basal ganglia

Peruvumba N. Jayakumara, Bangalore N. GangadharbCorresponding Author Informationemail address, Ganesan Venkatasubramanianb, Sunali Desaia, Latha Velayudhanb, Dattathreya Subbakrishnac, Matcheri S. Keshavande

Received 19 April 2009; received in revised form 30 August 2009; accepted 16 October 2009.

Abstract 

We reported increased high-energy phosphate metabolism in the basal ganglia of antipsychotic-naïve schizophrenia patients using 31P Magnetic Resonance Spectroscopy (MRS). These patients were followed up for 1 year and and reassessed using 31P MRS. Fourteen (8 males) patients with DSM-IV schizophrenia and 14 (11 males) healthy controls underwent 31P MRS of sub-cortical structures (predominantly basal ganglia) twice (mean±S.D. interscan interval 1.15±0.17year) on a 1.5T scanner. Total scores on the Positive and Negative Syndrome Scale (PANSS) decreased significantly after treatment in schizophrenia patients. Patients had significantly lower mean PCr/ATP ratios than healthy controls at baseline but not during the follow-up. In patients, there was a significant positive correlation between the magnitude of improvement in PANSS total scores and the extent of change in the PCr/ATP ratio. Findings support the hypothesis that reduction of energy demand or induction of decreased energy-demanding processes might underlie the mechanism of action of antipsychotics in schizophrenia.

a Department of Neuroimaging & Interventional Radiology, National Institute of Mental Health and Neurosciences, Bangalore, India

b Department of Psychiatry, National Institute of Mental Health & Neurosciences, Bangalore, 560029, India

c Department of Biostatistics, National Institute of Mental Health and Neurosciences, Bangalore, India

d Department of Psychiatry & Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA

e Department of Psychiatry, Beth Israel Deaconess Medical Center Landmark Building, 401 Park Avenue, Boston, MA 02215, USA

Corresponding Author InformationCorresponding author. Tel.: +91 80 26995260; fax: +91 80 26564830.

PII: S0925-4927(09)00243-1

doi:10.1016/j.pscychresns.2009.10.010


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