The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.
Striatal structure and function in mood disorders: a comprehensive review
Article first published online: 22 DEC 2010
© 2010 John Wiley and Sons A/S
Volume 12, Issue 8, pages 764–785, December 2010
How to Cite
Marchand, W. R. and Yurgelun-Todd, D. (2010), Striatal structure and function in mood disorders: a comprehensive review. Bipolar Disorders, 12: 764–785. doi: 10.1111/j.1399-5618.2010.00874.x
- Issue published online: 22 DEC 2010
- Article first published online: 22 DEC 2010
- Received 4 December 2009, revised and accepted for publication 31 August 2010
- basal ganglia;
- bipolar disorder;
- major depression;
Marchand WR, Yurgelun-Todd D. Striatal structure and function in mood disorders: a comprehensive review. Bipolar Disord 2010: 12: 764–785. © 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S.
Objectives: A large and diverse literature has implicated abnormalities of striatal structure and function in both unipolar and bipolar disorder. Recent functional imaging studies have greatly expanded this body of research. The aim of this review is to provide a comprehensive and critical appraisal of the relevant literature.
Methods: A total of 331 relevant articles were reviewed to develop an integrated overview of striatal function in mood disorders.
Results: There is compelling evidence from multiple studies that functional abnormalities of the striatum and greater corticostriatal circuitry exist in at least some forms of affective illness. The literature does not yet provide data to determine whether these aberrations represent primary pathology or they contribute directly to symptom expression. Finally, there is considerable evidence that bipolar disorder may be associated with striatal hyperactivity and some suggestion that unipolar illness may be associated with hypoactivation.
Conclusions: Additional research investigating striatal function in affective disorders will be critical to the development of comprehensive models of the neurobiology of these conditions.