Neural Engineering
Nabil Othman
Undergraduate Researcher
Marquette University
Frankfort, Illinois, United States
Kyle Kern
Assistant Professor of Neurology
University of California, Los Angeles, United States
Clinton B. Wright, M.D., M.S.
Director of the Division of Clinical Research
National Institute of Neurological Disorders and Strkoe, United States
Richard Leigh, M.D.
Associate Professor of Neurology
Johns Hopkins University, United States
81 participants were enrolled in the study, 68 received a baseline examination, with 1 scan of insufficient quality, leaving 67 for analysis. The mean age was 70±10 years old, and 44% were female. Index stroke was in the left hemisphere for 25 participants, the right hemisphere for 31 participants, bilateral for 8 participants. An additional 3 participants had no visible acute index ischemic lesion, 2 of which were diagnosed with a TIA and 1 CRAO. Median time from index stroke to baseline imaging was 3±2 months. Of those included in the baseline analysis, 43 participants had at least one year of follow-up MRI and were included in the longitudinal and trajectory analyses, of whom the mean age was 69±9 years old and 43% were female. In the baseline analysis, no significant relationship was identified between hippocampal volume and cognitive function. Age, race, hospital site, and acute stroke severity were all associated with lower MoCA scores at baseline. In the longitudinal analysis, hippocampal volumes significantly decreased over time (B=-1.543 mm3/month; 95% CI: [-2.772 -0.313]; p< 0.05). The hippocampi ipsilateral (n=164) to the stroke hemisphere decreased at a slower rate relative to the hippocampi contralateral (n=180) to the stroke hemisphere (B= -6.5336 mm3/month; 95% CI: [-11.623 -1.045]; p < 0.05). No other covariates were significantly associated with decline in hippocampal volume. In the trajectory analysis, residual hippocampal fraction was a significant predictor of both increasing MoCA scores (B=0.504 MoCA point/month; 95% CI: [0.277 0.732]; p< 0.0001) and memory subscores (B=0.619 MoCA point/month; 95% CI: [0.342 0.896]; p< 0.0001).
We found that in patients with cerebrovascular disease who have suffered a stroke, hippocampal volumes decrease with greater loss of volume in the hemisphere contralateral to the prior stroke. We also identified an association between change in hippocampal volume and change in MoCA score and memory subscore. These findings suggest a decrease in hippocampal volume occurs after stroke and may be contributing to post-stroke cognitive decline.
Future studies will explore predictors of hippocampal volume post-stroke as well as
if longitudinal changes in hippocampal volume are related to cognition in both stroke and non-stroke patients.
This work was supported by the National Institute of Neurological Disorders and Stroke (NINDS) Intramural Research Program