Chapter 7 - Mechanisms underpinning neurocognitive dysfunction in bipolar disorder

Abstract

Bipolar disorder (BD) is associated with cognitive deficits that persist in remission in multiple domains. There is significant heterogeneity of cognitive function in BD. Cognitive impairment in BD is clinically relevant, but the etiology of cognitive dysfunction in BD is currently unknown. Brain imaging studies suggest that cognitive impairment in BD is related to frontostriatal and limbic functional abnormalities, which are at least partly mediated by structural dysconnectivity. Cognitive event-related potential (ERP) studies suggest that these functional changes are related to the early and late stages of information processing in BD. The studies investigating the relationship between volumetric, cortical thickness, and cognitive functions have reported less consistent findings. The shared genetic risk factors for BD and schizophrenia and abnormal neurodevelopment play an important role in cognitive dysfunction in BD. Medical comorbidities including metabolic syndrome and obesity and iatrogenic factors (i.e., antipsychotics) are also significant contributors of neurocognitive impairment in BD. There is an inconsistent and modest level of evidence regarding peripheral neurobiological markers of neurocognition, including inflammation, of BD, and the diagnostic specificity of these associations is unknown.