The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review

• Published in: Bipolar disorders 2001-06, Vol.3 (3), p.106-150
• Main Authors: Bearden, Carrie E, Hoffman, Kathleen M, Cannon, Tyrone D
• Format: Article
• Language: English
• Subjects: Adult; affective disorders; Basal Ganglia - abnormalities; Basal Ganglia - physiopathology; bipolar disorder; Bipolar Disorder - physiopathology; Bipolar Disorder - psychology; Brain - abnormalities; Brain - physiopathology; cognition; Cognition Disorders - diagnosis; Cognition Disorders - etiology; depression; Female; Frontal Lobe - abnormalities; Frontal Lobe - physiopathology; Functional Laterality - physiology; Humans; Magnetic Resonance Imaging; Male; mania; Mood Disorders - psychology; neuroanatomy; neuroimaging; Neuropsychological Tests; neuropsychology; Severity of Illness Index
• ISSN: 1398-5647; 1399-5618
• DOI: 10.1034/j.1399-5618.2001.030302.x

Objectives: To present a comprehensive review of the existing neuropsychological and neuroimaging literature on bipolar affective disorder. This review critically evaluates two common conceptions regarding the neuropsychology of bipolar disorder: 1) that, in contrast to schizophrenia, bipolar affective disorder is not associated with general cognitive impairment independent of illness episodes, and 2) relative right hemisphere (RH) dysfunction is implicated in bipolar illness patients, supported by reports of relatively greater impairment in visuospatial functioning, lateralization abnormalities, and mania secondary to RH lesions.

Methods: The major computerized databases (Medline and PSYCInfo) were consulted in order to conduct a comprehensive, integrated review of the literature on the neuropsychology and neuroanatomy of bipolar disorder. Articles meeting specified criteria were included in this review.

Results: In a critical evaluation of the above notions, this paper determines that: 1) while there is little evidence for selective RH dysfunction, significant cognitive impairment may be present in bipolar illness, particularly in a subgroup of chronic, elderly or multiple‐episode patients, suggesting a possible toxic disease process, and 2) the underlying functional correlate of these cognitive deficits may be white matter lesions (‘signal hyperintensities’) in the frontal lobes and basal ganglia, regions critical for executive function, attention, speeded information processing, learning and memory, and affect regulation. While this hypothesized neural correlate of cognitive impairment in bipolar disorder is speculative, preliminary functional neuroimaging evidence supports the notion of frontal and subcortical hypometabolism in bipolar illness.

Conclusions: The etiology of the structural brain abnormalities commonly seen in bipolar illness, and their corresponding functional deficits, remains unknown. It is possible that neurodevelopmental anomalies may play a role, and it remains to be determined whether there is also some pathophysiological progression that occurs with repeated illness episodes. More research is needed on first‐episode patients, relatives of bipolar probands, and within prospective longitudinal paradigms in order to isolate disease‐specific impairments and genetic markers of neurocognitive function in bipolar disorder.