Neuroimaging and neurocognitive abnormalities associated with bipolar disorder in old age

International Journal of Geriatric Psychiatry - Tập 29 Số 4 - Trang 421-427 - 2014
Soham Rej1, Meryl A. Butters2, Howard Aizenstein2, Amy Begley2, Jawad Tsay3, Charles F. Reynolds2, Benoit H. Mulsant4, Ariel Gildengers2
1Department of Psychiatry, McGill University, Montreal, QC, Canada
2Department of Psychiatry, University of Pittsburgh School of Medicine; Pittsburgh, PA USA
3Department of Radiology, Cleveland Clinic, Cleveland, OH, USA
4Department of Psychiatry; Centre for Addiction and Mental Health and the University of Toronto; Toronto ON Canada

Tóm tắt

ObjectivesCognitive 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.MethodsThis 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.ResultsAlthough 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.ConclusionsCognitive 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.

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