Imamura T, Ejima A, Sahara M, Saito H, Tsuburaya K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
No To Shinkei. 1992 Feb;44(2):149-53.
Chronic intoxication of phenytoin (PHT) is a well known cause of cerebellar atrophy or irreversible cerebellar ataxia. Little attention, on the other hand, is paid for acute PHT intoxication because its clinical signs are believed to be reversible. We here report a patient with acute PHT intoxication, which resulted in irreversible cerebellar ataxia with radiologically definite cerebellar atrophy. A 39-year-old man admitted to our hospital because of cerebellar ataxia and confusional state. He had been treated with PHT for convulsive seizures after receiving craniotomy for left parietal brain abscess 9 years before. The concentration of his serum PHT had been 4 to 7 micrograms/ml because he had frequently omitted taking drug, and the dose of PHT had been increased to 600 mg/day one year before. He had admitted to another hospital 2 months before for left Bell's palsy and had been obliged to take drug regularly. Cerebellar signs and confusion had gradually developed for 7 weeks. On admission to our hospital, he was awake but in severe confusional state with slurred speech and nystagmus. His serum PHT was 86 micrograms/ml, which returned to therapeutic range 2 weeks after the discontinuation of PHT. His consciousness normalized and nystagmus disappeared. However, slurred speech continued and neurological examination revealed postural tremor and severe limb ataxia. During the subsequent 10 months, his cerebellar signs showed minimal improvement. Computed tomographies of his brain on 3rd and 5th month after the onset of his cerebellar dysfunction showed the definite cerebellar atrophy which had not been noted on the CTs 7 months before and 7 weeks after the onset.(ABSTRACT TRUNCATED AT 250 WORDS)
苯妥英(PHT)慢性中毒是小脑萎缩或不可逆性小脑共济失调的常见病因。另一方面,急性PHT中毒却很少受到关注,因为其临床症状被认为是可逆的。我们在此报告一例急性PHT中毒患者,该患者出现了不可逆性小脑共济失调,影像学检查显示有明确的小脑萎缩。一名39岁男性因小脑共济失调和意识模糊状态入院。9年前他因左顶叶脑脓肿接受开颅手术后,一直用PHT治疗惊厥性癫痫。由于他经常漏服药物,其血清PHT浓度一直维持在4至7微克/毫升,且在1年前PHT剂量已增加至600毫克/天。2个月前他因左侧贝尔面瘫入住另一家医院,并被迫规律服药。小脑体征和意识模糊逐渐发展了7周。入院时,他意识清醒,但处于严重意识模糊状态,言语不清且有眼球震颤。他的血清PHT为86微克/毫升,停用PHT 2周后恢复到治疗范围。他的意识恢复正常,眼球震颤消失。然而,言语不清仍持续存在,神经系统检查发现有姿势性震颤和严重的肢体共济失调。在随后的10个月里,他的小脑体征仅有轻微改善。小脑功能障碍发作后第3个月和第5个月的脑部计算机断层扫描显示有明确的小脑萎缩,而在发病前7个月和发病后7周的CT检查中均未发现。(摘要截选至250字)