Cited by 565Bipolar Disorder and TreatmentSchizophrenia research and treatmentNeural and Behavioral Psychology Studies

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

Bearden, Carrie E, Hoffman, Kathleen M, Cannon, Tyrone D·2001·Bipolar Disorders

Abstract

UNLABELLED: Bearden CE, Hoffman KM, Cannon TD. The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disord 2001: 3: 106 150. C Munksgaard, 2001 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.

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Crossref · 10.1034/j.1399-5618.2001.030302.x

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  • Clinical imaging studies have demonstrated robust structural and functional deficits in the PFC across a range of disorders including depression, bipolar disorder, anxiety, OCD, schizophrenia, PTSD, alcohol abuse disorder, and substance abuse disorder.

    “Clinical imaging studies have confirmed the results of these studies, demonstrating robust structural and functional deficits in the PFC across a range of disorders including depression, bipolar disorder, anxiety, obsessive compulsive disorder (OCD), schizophrenia, PTSD, alcohol abuse disorder, and substance abuse disorder (84–103).”
  • The neuroprogression hypothesis in bipolar disorder postulates that recurrent mood swings lead to growing damage in neurons and glia, impairing the integrity of neuronal circuits, reinforcing brain vulnerability to future mood episodes, and finally leading to neurodegeneration.

    “Once BD has manifested, the neuroprogression hypothesis in BD postulates that the recurrent mood swings might lead to growing damage in both neurons and glia, impairing the integrity of neuronal circuits and reinforce brain vulnerability to emerging mood episodes in the future (35), and finally leading to neurodegeneration (36).”

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Authors
Bearden, C. E., Hoffman, K. M., & Cannon, T. D.
Affiliations
  • University of Pennsylvania (US)
  • Children's Hospital of Philadelphia (US)
  • University of California, Los Angeles (US)
Corresponding author
Bearden, Carrie E
Venue
Bipolar Disorders
Publisher
Wiley
Published
2001-06
Volume
3
Issue
3
Pages
106-150
ISSN
  • 1398-5647 (ISSN-L)
  • 1399-5618
OpenAlex
W2009485462
Cited by
565
References
196
Citations by year
2026: 3 · 2025: 4 · 2024: 1 · 2023: 4 · 2022: 8 · 2021: 11 · 2020: 11 · 2019: 12 · 2018: 13 · 2017: 12 · 2016: 19 · 2015: 22 · 2014: 25 · 2013: 37 · 2012: 24
FWCI
3.97
Type
journal article
Language
en
Open access
closed
Locations
  • Bipolar Disorders (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
Keywords
bipolar disorder, neuropsychology, neuroanatomy, cognitive impairment, right hemisphere dysfunction, visuospatial impairment, white matter lesions, frontal lobe hypometabolism, basal ganglia, executive function, neurodevelopmental anomalies, disease progression, mania
MeSH terms
Adult, Basal Ganglia, Bipolar Disorder, Brain, Cognition Disorders, Female, Frontal Lobe, Humans, Functional Laterality, Magnetic Resonance Imaging, Male, Neuropsychological Tests, Severity of Illness Index, Mood Disorders

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