İskemik İnme Hastalarında İskemik Lezyonun Karşı Hemisferinde Oluşan Serebral Hacim Kaybının İnme İlişkili İnflamasyon ile İlişkisi

Abstract

Central nervous system (CNS) and immune system are in a two-way relationship with a delicate homeostatic balance. This relationship is disrupted following CNS insults, such as ischemic stroke. The introduction of cerebral parenchyma-specific antigens into the systemic circulation after stroke, triggers a natural and adaptive immune response directed towards the focal ischemic tissue. As a protective reaction, mechanisms involving the hypopituitary adrenal axis, the sympathetic nervous system, the parasympathetic nervous system induce an immune-depressive response in the peripheral immune system; however, this leads to an infection prone state in stroke patients. It is considered that these intimate cascades of inflammation, immune-depression and infection are associated with neuro-glial loss in cerebral tissue in the long term. In this study, our aim was to determine whether cerebral volume loss occurs in the unaffected hemisphere contralateral to the ischemic hemisphere, and identify factors associated with this possible volume loss. A total of 31 patients with ischemic stroke were enrolled into the study; parameters including clinical features, laboratory values (complete blood count, erythrocyte sedimentation rate, C-reactive protein, procalcitonin), heart rate variability, and development of infections following stroke were collected in all patients. Contralateral hemisphere volume was determined by voxel-based morphometry on admission and follow-up magnetic resonance imaging (MRI). The contralateral hemisphere volume decreased by a median (IQR) of 2.53% (0.63-5.72) on images obtained after a median follow-up of 73 (52-114) days (p <0.001). The monthly volume reduction was 1.26% (0.00-2,53). Baseline NIH stroke scale score, infarct volume, neutrophil count, neutrophil / lymphocyte ratio, SAPS II score and pneumonia or urinary tract infection during admission constituted factors significantly associated with monthly volume loss in the contralateral hemisphere (p <0.05). When various combinations of variables related to stroke severity (NIH stroke scale score, infarct volume, SAPS II score) and inflammatory response (neutrophil/lymphocyte ratio, development of infections) were assessed in multivariate regression models, both variable groups remained independently associated with monthly volume loss. These findings suggest that cerebral volume loss is not limited to the symptomatic hemisphere in ischemic stroke patients and this volume loss is related to stroke severity and impaired CNS-immune system homeostasis.