뇌미세혈관병증 3가지 표식과 열공뇌경색 초기 신경학적 악화와의 관련성
Association of 3 Stigmas of Cerebral Microangiopathy With Early Neurological Deterioration in Lacunar Infarction
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Background: Neurological deterioration following acute lacunar infarction is not uncommon. Its association with poor clinical outcome is well-known, but little is known about what causes it. This study aimed to elucidate whether 3 stigmas of cerebral microangiopathy, a pathogenesis of lacunar infarction, are associated with neurological deterioration in patients with acute lacunar infarction. Methods: Patients with acute lacunar infarction who were admitted within 24 hours of onset were identified using a prospective stroke registry. Patients who presented neurological deterioration within 7 days of hospitalization (progressive lacune group) were matched to 4 controls (non-progressive lacune group) for ‘onset to arrival time’. Three stigmas of cerebral microangiopathy (leukoaraiosis, cerebral microbleeds, and silent lacunes) were measured using initial brain MRI, and their associations with neurological deterioration were analyzed. Results: During 45 months, a total of 23 patients were identified and matched to 80 controls. Simple comparison of 2groups showed that those 3 stigmas of cerebral microangiopathy were not significantly associated with neurological deterioration. Hyperlipidemia (p=0.18), history of transient ischemic attack or stroke (p=0.01), initial NIH stroke scale (p=0.07), white blood cell counts (p=0.16), and lesion volume (p=0.03) were possibly different (p’s<0.2) between 2 groups. Multivariable logistic regression analysis did not reveal any significant association of those 3 stigmas with neurological deterioration, too (all p values>0.5). Conclusions: This study did not find a relationship between cerebral microangiopathy and neurological deterioration following acute lacunar infarction. The possibility of inadequate power should be noted.
Abstract
Background: Neurological deterioration following acute lacunar infarction is not uncommon. Its association with poor clinical outcome is well-known, but little is known about what causes it. This study aimed to elucidate whether 3 stigmas of cerebral microangiopathy, a pathogenesis of lacunar infarction, are associated with neurological deterioration in patients with acute lacunar infarction. Methods: Patients with acute lacunar infarction who were admitted within 24 hours of onset were identified using a prospective stroke registry. Patients who presented neurological deterioration within 7 days of hospitalization (progressive lacune group) were matched to 4 controls (non-progressive lacune group) for ‘onset to arrival time’. Three stigmas of cerebral microangiopathy (leukoaraiosis, cerebral microbleeds, and silent lacunes) were measured using initial brain MRI, and their associations with neurological deterioration were analyzed. Results: During 45 months, a total of 23 patients were identified and matched to 80 controls. Simple comparison of 2groups showed that those 3 stigmas of cerebral microangiopathy were not significantly associated with neurological deterioration. Hyperlipidemia (p=0.18), history of transient ischemic attack or stroke (p=0.01), initial NIH stroke scale (p=0.07), white blood cell counts (p=0.16), and lesion volume (p=0.03) were possibly different (p’s<0.2) between 2 groups. Multivariable logistic regression analysis did not reveal any significant association of those 3 stigmas with neurological deterioration, too (all p values>0.5). Conclusions: This study did not find a relationship between cerebral microangiopathy and neurological deterioration following acute lacunar infarction. The possibility of inadequate power should be noted.
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