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J Neurol Neurosurg Psychiatry 2004;75:221-225 doi:10.1136/jnnp.2002.002014
  • Paper

Corpus callosum signal intensity in patients with bipolar and unipolar disorder

  1. P Brambilla2,
  2. M Nicoletti3,
  3. R B Sassi1,
  4. A G Mallinger4,
  5. E Frank5,
  6. M S Keshavan1,
  7. J C Soares3
  1. 1Department of Psychiatry, Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, Pennsylvania, USA
  2. 2Department of Psychiatry, IRCCS S Matteo, University of Pavia School of Medicine, Italy
  3. 3Division of Mood and Anxiety Disorders, Department of Psychiatry, University of Texas Health Science Center, San Antonio, Texas, USA
  4. 4Department of Psychiatry, University of Pittsburgh School of Medicine
  5. 5Department of Psychiatry, University of Pittsburgh
  1. Correspondence to:
 Dr Jair C Soares
 Department of Psychiatry, Division of Mood and Anxiety Disorders, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA; soaresuthscsa.edu
  • Received 19 August 2002
  • Accepted 7 May 2003
  • Revised 14 March 2003

Abstract

Background: Anatomical abnormalities in the corpus callosum have been reported in magnetic resonance imaging (MRI) studies in patients with bipolar but not unipolar disorder. MRI signal intensity can be used as a putative index of corpus callosum myelination.

Objectives: To measure MRI signal intensity in patients with bipolar and unipolar disorder to investigate abnormalities of corpus callosum myelination.

Methods: The study involved 29 DSM-IV bipolar patients (mean (SD) age, 35 (11) years; 16 male, 13 female), 23 DSM-IV unipolar patients (41 (10) years; 4 male, 19 female), and 36 healthy controls (37 (10) years; 23 male, 13 female). A 1.5T GE Signa magnet was employed, with a fast spin echo sequence. Corpus callosum signal intensity was obtained blindly using the semiautomated software NIH Image 1.62.

Results: Bipolar patients had lower corpus callosum signal intensity for all callosal subregions (genu, anterior and posterior body, isthmus, splenium) than healthy controls (ANCOVA, age and sex as covariates, p<0.05). No significant differences were found between unipolar and healthy subjects (ANCOVA, age and sex as covariates, p>0.05).

Conclusions: The findings suggest abnormalities in corpus callosum white matter in bipolar but not unipolar patients, possibly because of altered myelination. Such abnormalities could lead to impaired interhemispheric communication in bipolar disorder. Longitudinal MRI studies involving first episode and early onset bipolar patients will be necessary for a better understanding of the potential role of abnormalities of corpus callosum myelination in the pathophysiology of bipolar disorder.

Footnotes

  • Competing interests: none declared

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