Neuroimaging in bipolar disorder: What have we learned?

Citation
Al. Stoll et al., Neuroimaging in bipolar disorder: What have we learned?, BIOL PSYCHI, 48(6), 2000, pp. 505-517
Citations number
103
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BIOLOGICAL PSYCHIATRY
ISSN journal
00063223 → ACNP
Volume
48
Issue
6
Year of publication
2000
Pages
505 - 517
Database
ISI
SICI code
0006-3223(20000915)48:6<505:NIBDWH>2.0.ZU;2-W
Abstract
New technologies are offering increasingly powerful means to obtain structu ral, chemical, and functional images of the brain during life, often withou t the use of ionizing radiation. Bipolar disorder, with ifs clear physiolog ic features, would appear to be a prime candidate for the application of cu rrent brain imaging; however, only a modest number of studies have been rep orted to date, and most studies have small sample sizes and heterogeneous s ubject groups. Nonetheless, there are a few consistent findings among these studies, including the following: I) Structural imaging studies suggest an increased number of white matter hyperintensities in patients with bipolar disorder. These may be lesions unique to bipolar disorder and its treatmen t, or related to cardiovascular risk factors, which are more common in bipo lar patients. Decreased cerebellar size and anomalies of cerebellar blood v olume have also been reported. Increased sulcal prominence and enlargement of the lateral and third ventricles are less consistently observed findings . 2) Spectroscopic imaging suggests abnormalities of metabolism of choline- containing compounds in symptomatically ill bipolar patients and, possibly treatment-induced changes in choline- and myoinositol-containing compounds. Each of these groups of metabolites serves as a component of membrane phos pholipids and cellular second-messenger cycles. 3) Metabolic and blood flow studies provide evidence for decreased activity of the prefrontal cortex ( PFC) in bipolar patients during depression. It is not clear if these change s are restricted to particular subregions of the PFC, nor if they are rever sed with mania. No single pathophysiologic mechanism yet explains these findings, although all might be due to regional alterations in cellular activity and metabolis m or changes in cell membrane composition and turnover. The development of imaging technologies has far outpaced their use in bipol ar disorder. The promise of future studies is great, with more powerful mag netic resonance scanners, additional ligands for positron emission tomograp hy and single photon emission computed tomography imaging, and improved ima ge generation and processing already available. (C) 2000 Society of Biologi cal Psychiatry.