Neuroimaging and neurocognitive abnormalities associated with bipolar disorder in old age
Article first published online: 5 SEP 2013
Copyright © 2013 John Wiley & Sons, Ltd.
International Journal of Geriatric Psychiatry
Volume 29, Issue 4, pages 421–427, April 2014
How to Cite
Rej, S., Butters, M. A., Aizenstein, H. J., Begley, A., Tsay, J., Reynolds, C. F., Mulsant, B. H. and Gildengers, A. (2014), Neuroimaging and neurocognitive abnormalities associated with bipolar disorder in old age. Int. J. Geriat. Psychiatry, 29: 421–427. doi: 10.1002/gps.4021
- Issue published online: 6 MAR 2014
- Article first published online: 5 SEP 2013
- Manuscript Accepted: 30 JUL 2013
- Manuscript Revised: 29 JUL 2013
- Manuscript Received: 18 APR 2013
- Public Health Service. Grant Numbers: K23 MH 073772 (AGG), R01 MH 084921 (AGG), U01 MH68846 (BHM), R01 MH072947 (MAB), P30 MH71944 (CFR), K24 MH069430 (BHM)
- UPMC Endowment in Geriatric Psychiatry (CFR)
- John A. Hartford Center of Excellence in Geriatric Psychiatry (CFR)
- bipolar disorder;
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.
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.
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.
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.