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Magnetic resonance spectroscopic measurement of cerebral gamma-aminobutyric acid concentrations in patients with bipolar disorders

Published online by Cambridge University Press:  24 June 2014

Po W. Wang*
Affiliation:
Department of Psychiatry and Behavioral Sciences, Bipolar Disorders Clinic, Stanford University School of Medicine, Stanford, CA, USA
Napapon Sailasuta
Affiliation:
Department of Medicine, University of Hawaii, Honolulu, HI ,USA
Rebecca A. Chandler
Affiliation:
Department of Psychiatry, Oxford University, Oxford, UK
Terence A. Ketter
Affiliation:
Department of Psychiatry and Behavioral Sciences, Bipolar Disorders Clinic, Stanford University School of Medicine, Stanford, CA, USA
*
Po W. Wang, MD, Acting Assistant Professor, Department of Psychiatry and Behavioral Sciences, Bipolar Disorders Clinic, Stanford University School of Medicine, 401 Quarry Road, Suite 2117, Stanford, CA 94305-5723, USA. Tel: +1 650 723 2483; Fax: +1 650 723 2507; E-mail: wangp0@stanford.edu

Abstract

Background:

Animal models of depression and psychopharmacological mechanisms of action suggest the importance of the gamma-amino butyric acid (GABA) system in the pathophysiology of mood disorders. Mood stabilizers have overlapping effects on GABAergic neurotransmission, and antidepressant use has been associated with alterations in GABAB receptor function. Magnetic resonance spectroscopy (MRS) provides an opportunity to noninvasively assess cerebral GABA concentrations in anterior paralimbic circuits that have been implicated in mood disorders.

Methods:

In bipolar disorder patients and healthy control subjects, we used MRS with a modified GABA-edited point resolved spectroscopy sequence (TE 68 ms, TR 1500 ms, 512 averages, total scan time 26 min) to assess GABA in an 18-cm3 occipital voxel. In addition, in another cohort of bipolar disorder patients and healthy control subjects, we similarly assessed GABA in a 12.5-cm3 medial prefrontal/anterior cingulate (MPF/AC) voxel. The concentration of GABA was referenced to creatine (Cr) from unedited spectra.

Results:

In bipolar patients and controls, we consistently detected 3.0 p.p.m. GABA peaks in occipital lobe and MPF/AC. In 16 bipolar (nine bipolar I and seven bipolar II) disorder patients, compared with six healthy control subjects, mean occipital GABA/Cr concentration was 61% higher. In addition, in 15 bipolar (five bipolar I, nine bipolar II, and one bipolar not otherwise specified) disorder patients, compared with six healthy control subjects, mean MPF/AC GABA/Cr concentration tended to be 41% higher.

Conclusions:

Patients with bipolar disorders may have increased cerebral GABA concentrations. Although this was more evident in the occipital lobe, MPC/AC GABA disturbance may be of greater potential interest in view the more established role of MPF/AC in affective processing. Additional studies are warranted to assess changes in GABAergic neurotransmission and the influences of diagnosis, mood state, and medication status in bipolar disorder patients.

Type
Case Report
Copyright
Copyright © 2006 Blackwell Munksgaard

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