급성 뇌경색에서 시간 경과에 따른 혈청 신경원 특이 에놀라제(neuron specific enolase)의 변화
Change of Serum Neuron Specific Enolase Level During Acute Stage of Cerebral Infarction
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Background: Neuron-specific enolase (NSE) is a useful indicator of neuronal injury in acute cerebral infarction. We investigated the changes in serial serum NSE levels in patients with acute cerebral infarction. Methods: We measured serial serum NSE levels at 24, 48, 72, and 96 hours, and 2 weeks after the onset of cerebral infarction in 30 patients (15 territorial and 15 lacunar infarctions). We also measured the NSE levels in age-matched controls (n=15) who had no evidence of acute stroke or other neurological disorders. The NSE level was measured using a radioimmunoassay. Results: The initial serum NSE level was significantly higher in the cerebral infarction group than in the control group (6.6±2 vs 4.7±1.6 ng/mL [mean±SD], p=0.006). This difference was also observed between the territorial and lacunar infarction groups until 72 hours after the cerebral infarction. The serum NSE level peaked at 72 hours after the infarction in both lacunar and territorial infarction groups. The correlation between the NSE level and the score on the NIH Stroke Scale was strongest at 48 hours after the cerebral infarction (r=0.469). Conclusions: Serum NSE level can be a good indicator for distinguishing lacunar from territorial infarction during the acute stage of cerebral infarction.
Abstract
Background: Neuron-specific enolase (NSE) is a useful indicator of neuronal injury in acute cerebral infarction. We investigated the changes in serial serum NSE levels in patients with acute cerebral infarction. Methods: We measured serial serum NSE levels at 24, 48, 72, and 96 hours, and 2 weeks after the onset of cerebral infarction in 30 patients (15 territorial and 15 lacunar infarctions). We also measured the NSE levels in age-matched controls (n=15) who had no evidence of acute stroke or other neurological disorders. The NSE level was measured using a radioimmunoassay. Results: The initial serum NSE level was significantly higher in the cerebral infarction group than in the control group (6.6±2 vs 4.7±1.6 ng/mL [mean±SD], p=0.006). This difference was also observed between the territorial and lacunar infarction groups until 72 hours after the cerebral infarction. The serum NSE level peaked at 72 hours after the infarction in both lacunar and territorial infarction groups. The correlation between the NSE level and the score on the NIH Stroke Scale was strongest at 48 hours after the cerebral infarction (r=0.469). Conclusions: Serum NSE level can be a good indicator for distinguishing lacunar from territorial infarction during the acute stage of cerebral infarction.
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