Abstract TMP38: Dysregulated Post-Stroke Immune Response is Associated With Cerebral Volume Loss in the Contralateral Non-Ischemic Hemisphere

Abstract

Background: There is delicate homeostatic balance between the central nervous system and immune system. Cerebral insults, like ischemia, trigger an immune-depressive state to suppress a potential immune response directed against the neuroglial tissue; however, this supposedly protective reaction inadvertently creates an infection-prone state in the peri-stroke setting. In this study, we assessed the magnitude of cerebral volume loss in the unaffected contralateral hemisphere following stroke, and determined its relationship with the intimate cascades of inflammation, immune-depression and infection. Methods: The change in contralateral hemisphere volume was determined by voxel-based morphometry on admission and follow-up MRI’s in a consecutive series of 50 patients with ischemic stroke involving the MCA territory. Information related to clinical features, infectious complications, and markers of inflammation (erythrocyte sedimentation rate, neutrophil/lymphocyte ratio, C-reactive protein) and immunodepression (plasma high mobility group box 1 protein level; HMGB-1) were prospectively collected. Results: The contralateral hemisphere volume decreased by a median (interquartile range) of 2.80% (0.70-5.64) after a follow-up duration of 101 (63-123) days (p<0.001); the monthly volume reduction was 0.82% (0.18-1.79). Old age, stroke severity, neutrophil/lymphocyte ratio, and development of infections during hospitalization were significantly associated with monthly volume loss (p<0.05). Stroke severity (NIHSS score or infarct volume) and inflammation related parameters (neutrophil/lymphocyte ratio or systemic infections) remained independently and positively associated with monthly volume loss when assessed in multivariate regression models, while plasma HMGB-1 levels were inversely related to this loss. Conclusions: Cerebral tissue damage following stroke is not limited to the ischemic hemisphere. Apart from stroke severity, a pro-inflammatory state and an impaired immune-depressive response contribute to cerebral volume loss in the non-ischemic hemisphere.