Schmidley J W, Simon R P
Ann Neurol. 1981 Jan;9(1):81-4. doi: 10.1002/ana.410090116.
Six patients showed a transient and otherwise unexplained cerebrospinal fluid (CSF) pleocytosis following a flurry of generalized convulsions. Each had an obvious cause for repeated seizures. No evidence was found for an infectious, inflammatory, neoplastic, or other cause for the pleocytosis. All CSF specimens were clear and colorless, under normal pressure, and bacteriologically sterile. The maximal leukocyte count ranged from 9 to 80 per cubic millimeter and reached a maximum on the day after cessation of convulsions. No specimen contained more than 650 erythrocytes. Two patients initially had a mildly increased CSF protein; glucose values were unremarkable. We propose that the pleocytosis in these patients was a result of frequently repeated generalized convulsions. The mechanism of postictal pleocytosis is uncertain. It may result from transient breakdown of the blood-brain barrier, which has been demonstrated after seizures in experimental animals. Although infectious causes must first be considered and rigorously searched for, it appears that seizures alone may cause a transient CSF pleocytosis.
6例患者在一阵全身性惊厥后出现短暂且原因不明的脑脊液(CSF)细胞增多。每位患者都有反复癫痫发作的明显病因。未发现细胞增多的感染性、炎症性、肿瘤性或其他病因。所有脑脊液标本均清澈无色,压力正常,细菌学检查无菌。白细胞计数最高范围为每立方毫米9至80个,在惊厥停止后的第二天达到最高值。没有标本中的红细胞超过650个。2例患者最初脑脊液蛋白轻度升高;葡萄糖值无异常。我们认为这些患者的细胞增多是频繁反复全身性惊厥的结果。发作后细胞增多的机制尚不确定。它可能是由于血脑屏障的短暂破坏,这在实验动物癫痫发作后已得到证实。虽然必须首先考虑并严格寻找感染性病因,但似乎仅癫痫发作就可能导致短暂的脑脊液细胞增多。