Adachi T, Kobayashi S, Yamaguchi S, Okada K
Department of Internal Medicine III, Shimane Medical University, Izumo, Japan.
J Neurol. 2000 Apr;247(4):280-5. doi: 10.1007/s004150050584.
Small subcortical infarctions resulting from large-vessel disease are often observed. It is important to distinguish these from pure lacunar infarction resulting from small-vessel disease because the investigations and examinations differ. We investigated the differences on brain magnetic resonance imaging (MRI) between small subcortical "lacunar-like" infarcts resulting from large-vessel disease and pure lacunar infarcts. Thirteen subjects with small lacunar-like infarcts (size < 2 cm), resulting from large-vessel disease, and 30 subjects with lacunar infarcts (< 2 cm), without large-vessel disease were studied. We measured infarction size using a 1.5-T MRI device and evaluated silent subcortical hyperintensity lesions using the modified Scheltens' score. Large-vessel lesion was confirmed by conventional angiography, duplex carotid scan, and magnetic resonance angiography. There was no difference in the mean age of the two groups. Cerebrovascular risk factors and atherosclerotic complications were also comparable for the two groups. Progressive stroke was more common in the lacunar-like infarction group than in the lacunar infarction group (P = 0.004). Scores for periventricular hyperintensity, white matter hyperintensity, basal ganglia hyperintensity, and total subcortical hyperintensity scores were significantly higher in the lacunar infarction group than in the lacunar-like infarction group. The difference in basal ganglia hyperintensity scores was remarkable (P = 0.001). The enlargement of the perivascular space was also significantly greater in the lacunar infarction group than in the lacunar-like infarction group. These findings seem to reflect differences in the pathogenesis of infarction between the two groups. Silent subcortical hyperintensity lesions and enlargement of perivascular space are useful for between distinguishing small lacunar-like infarct resulting from large-vessel disease and pure lacunar infarction. This may have significant implications for the management of patients with lacunar-sized infarctions. It suggests that the pathogenesis of lacunar-sized infarction is variable.
常可见由大血管疾病导致的小皮质下梗死。将这些梗死与小血管疾病引起的纯腔隙性梗死区分开来很重要，因为两者的检查方法有所不同。我们研究了大血管疾病导致的小皮质下“类腔隙性”梗死与纯腔隙性梗死在脑磁共振成像（MRI）上的差异。研究了13例由大血管疾病导致小类腔隙性梗死（大小<2 cm）的受试者以及30例无大血管疾病的腔隙性梗死（<2 cm）受试者。我们使用1.5-T MRI设备测量梗死大小，并使用改良的Scheltens评分评估无症状皮质下高信号病变。通过传统血管造影、双功能颈动脉扫描和磁共振血管造影确认大血管病变。两组的平均年龄无差异。两组的脑血管危险因素和动脉粥样硬化并发症也具有可比性。进展性卒中在类腔隙性梗死组比腔隙性梗死组更常见（P = 0.004）。腔隙性梗死组的脑室周围高信号、白质高信号、基底节高信号评分及皮质下高信号总分均显著高于类腔隙性梗死组。基底节高信号评分差异显著（P = 0.001）。腔隙性梗死组的血管周围间隙扩大也明显大于类腔隙性梗死组。这些发现似乎反映了两组梗死发病机制的差异。无症状皮质下高信号病变和血管周围间隙扩大有助于区分大血管疾病导致的小类腔隙性梗死和纯腔隙性梗死。这可能对腔隙性梗死大小的患者管理具有重要意义。这表明腔隙性梗死大小的发病机制是可变的。
