Hostname: page-component-5c6d5d7d68-sv6ng Total loading time: 0 Render date: 2024-08-16T17:31:29.979Z Has data issue: false hasContentIssue false

Question-and-Answer Session

Published online by Cambridge University Press:  07 November 2014

Abstract

Bipolar disorder is a prevalent psychiatric disorder with a high rate of misdiagnosis and evidence of degenerative progression. Research indicates that the interval between bipolar episodes decreases steadily until the patient settles into a relatively frequent course of mania and depression. Various imaging techniques have been used in the understanding of the brain pathology underlying bipolar disorder through identification of patterns consistent with disruption of the normal brain activity in bipolar patients. These techniques have demonstrated evidence of abnormalities in the structure and function of the prefrontal cortex. In addition, the cerebellar vermis, which serves as an error-detection function to modulate the iterative network, appears to shrink with recurrent episodes. Functional imaging demonstrates that the anterior limbic network is overactivated and overresponsive in patients with bipolar disorder. In many patients, those deficits are often compensated for by activation of other brain areas. Ultimately, when the compensation fails, expression of bipolar symptoms arise. Using magnetic resonance spectroscopy, simple models can be constructed based on the hypothesis that mitochondrial function may be impaired in bipolar disorder. There is also increasing evidence that psychotropic medications can affect specific brain regions that are thought to be involved in the pathogenesis of psychiatric disorders. Glutamate levels appear to be elevated in untreated patients with bipolar disorder, which may cause glutamatergic neurotoxicity and negative therapeutic implications. Further advances in brain imaging may contribute to the improvement of available therapies and the understanding which treatments will be most suitable for specific patients.

Type
Other
Copyright
Copyright © Cambridge University Press 2007

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Harvey, AG, Mullin, BC, Hinshaw, SP. Sleep and circadian rhythms in children and adolescents with bipolar disorder. Dev Psychopathol. 2006;18:11471168.Google Scholar
2.Frank, E. Treating Bipolar Disorder: A Clinician's Guide to Interpersonal and Social Rhythm Therapy. New York, NY: Guilford Press, Inc; 2005.Google Scholar
3.Frank, E. Interpersonal and social rhythm therapy: a means of improving depression and preventing relapse in bipolar disorder. J Clin Psychol. 2007;63(5):463473.CrossRefGoogle ScholarPubMed
4.Frank, E, Kupfer, DJ, Thase, ME, et al.Two-year outcomes for interpersonal and social rhythm therapy in individuals with bipolar I disorder. Arch Gen Psychiatry. 2005;62:9961004.Google Scholar
5.Yildiz-Yesiloglu, A, Guleryuz, S, Ankert, DP. Is protein kinase C inhibition a keystone in treatment of mania? An optimum power, double-blind, placebo-controlled trial of tamaxifen. Under review.Google Scholar
6.Jensen, JE, Hirashima, F, Cohen, BM, et al.Brain 31P-MRS at 4.0 Tesla: effects of triacetyluridine (TAU) in the treatment of mood disorders. Proceedings of the International Society of Magnetic Resonance in Medicine. 2004;1482.Google Scholar