Striatal and cortical midline activation and connectivity associated with suicidal ideation and depression in bipolar II disorder.

Autor: Marchand WR; George E. Wahlen Veterans Affairs Medical Center, Salt Lake City, UT, USA. wmarchand@me.com, Lee JN, Garn C, Thatcher J, Gale P, Kreitschitz S, Johnson S, Wood N
Jazyk: angličtina
Zdroj: Journal of affective disorders [J Affect Disord] 2011 Oct; Vol. 133 (3), pp. 638-45. Date of Electronic Publication: 2011 May 28.
DOI: 10.1016/j.jad.2011.04.039
Abstrakt: Background: Considerable evidence implicates dysfunction of striatal and cortical midline structure (CMS) circuitry in mood disorders. Whether such aberrations exist in bipolar II depression is unknown.
Methods: Sixteen unmedicated subjects with bipolar II depression and 19 healthy controls were studied using functional MRI and a motor activation paradigm. Analyses of both activation and functional connectivity were conducted.
Results: A history of suicidal ideation (SI) was negatively correlated with activation of the left putamen while depression severity was positively correlated with activation of the left thalamus. The superior bilateral putamen was simultaneously correlated with depression severity and anti-correlated with SI. Striatal functional connectivity was altered with the bilateral CMS and right inferior parietal lobule. Depression severity was correlated with strength of connectivity between the bilateral striatum and the right lingual gyrus and left cerebellum.
Limitations: Only males experiencing an episode of major depression were studied.
Conclusions: Striatal and CMS circuit abnormalities likely contribute to the neurobiology of bipolar II depression. Altered connectivity of the striatum may directly impact depression severity. Further, dissociable components of activation associated with depression severity and suicidal ideation may exist. Finally, the motor activation paradigm used in this study appears to be a useful probe of some neural processes underlying bipolar II depression.
(Published by Elsevier B.V.)
Databáze: MEDLINE
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