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Neuroimaging and neurocognitive abnormalities associated with bipolar disorder in old age
Author(s) -
Rej Soham,
Butters Meryl A.,
Aizenstein Howard J.,
Begley Amy,
Tsay Jawad,
Reynolds Charles F.,
Mulsant Benoit H.,
Gildengers Ariel
Publication year - 2014
Publication title -
international journal of geriatric psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.28
H-Index - 129
eISSN - 1099-1166
pISSN - 0885-6230
DOI - 10.1002/gps.4021
Subject(s) - neurocognitive , bipolar disorder , hyperintensity , dementia , psychology , cognition , neuropsychology , neuroimaging , effects of sleep deprivation on cognitive performance , cognitive decline , magnetic resonance imaging , atrophy , trail making test , white matter , medicine , audiology , psychiatry , disease , radiology
Objectives Cognitive dysfunction is prevalent in older adults with bipolar disorder (BD). High white matter hyperintensity (WMH) burden, a marker of white matter disease, detected on T2/fluid‐attenuated inversion recovery brain magnetic resonance imaging (MRI) has been consistently reported in BD across all age ranges, including older adults. Yet, whether high WMH burden is related to the excess cognitive impairment present in older adults with BD is unknown. Therefore, we examine whether higher WMH burden is related to worse cognitive function in older adults with BD. Methods This is a cross‐sectional study of 27 non‐demented BD patients aged ≥50 years and 12 similarly aged mentally healthy comparators (controls). Subjects underwent both brain MRI and comprehensive neurocognitive assessment. We employed correlational analyses to evaluate the burden of WMH and the relationship between WMH and cognitive function. Results Although BD subjects had worse performance in all cognitive domains, BD subjects had less total WMH burden ( t [13.4] = −3.57, p = 0.003). In control subjects, higher WMH was related to lower global cognitive function ( ρ = −0.57, n = 12, p = 0.05). However, WMH did not correlate with neuropsychological performance in BD subjects. Further, BD and control subjects did not differ with respect to total gray and hippocampal volumes. Conclusions Cognitive dysfunction in late‐life BD does not appear to be due primarily to processes related to increased WMH or reduced gray matter volume. Future longitudinal studies should examine other potential neuroprogressive pathways such as inflammation, mitochondrial dysfunction, serum anticholinergic burden, and altered neurogenesis. Copyright © 2013 John Wiley & Sons, Ltd.