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作 者:厉含之[1] 李国良[1] 李琛[1] 杨欢[1] 李静[1] 刘宝琼[1]
出 处:《中华神经科杂志》2013年第3期159-163,共5页Chinese Journal of Neurology
摘 要:目的探讨阵发性交感神经过度兴奋(paroxysmal sympathetic hyperactivity,PSH)的临床特征,提高临床医生对本病的诊断及治疗水平。方法对10例PSH患者的年龄、性别、病程、临床表现及辅助检查等资料进行分析。结果10例患者中男性9例,女性1例,年龄15~78(37.6±19.1)岁。其中严重脑外伤5例,脑出血、反复脑梗死、缺血缺氧性脑病、蛛网膜囊肿脑脊液腹腔分流术后、隐球菌脑膜脑炎各1例。10例患者均以阵发性躁动、高热、大汗、血压升高、心动过速、呼吸急促及肌张力障碍等症状为主要临床表现。PSH首次发作在脑损伤后24h内者3例,24h至3周者5例,第5个月及第9年者各1例。发作频率不等,可数天1次至1d数次。发作持续时间最短在1min以内,最长达3h。好发于夜间者4例,好发于觉醒时1例,昼夜发作无明显差别者5例。发作期意识清楚2例,意识状态改变难以判断8例。发作间期格拉斯哥昏迷评分3~8分8例,15分2例。10例行脑电图检查,均未见癫痫波。神经影像学检查提示额叶、颞叶、顶叶、枕叶、脑桥、基底节、侧脑室旁等不同部位损伤。9例患者曾用抗癫痫药物治疗无效;β受体阻滞剂和多巴胺受体激动剂联合应用对PSH有较好疗效。完全控制2例,有效6例,无效1例,失访1例。结论不同病因、不同程度脑损伤均可致PSH。PSH易被误诊为癫痫,抗癫痫治疗无效。β受体阻滞剂和多巴胺受体激动剂联合治疗有效。Objective To study the clinical features of paroxysmal sympathetic hyperactivity (PSH). Methods The clinical data, imaging and electroencephalography (EEG) of 10 patients with PSH was analyzed retrospectively. Results Of the 10 patients with PSH, 9 were males and 1 was a female. The overall age of all the patients was (37.6 ±19. 1 ) years, ranging from 15 to 78 years. The primary diseases included traumatic brain injury 5 cases, intracranial hemorrhage 1 case, cerebral infarction 1 case, hypoxic isehemic encephalopathy 1 case, arachnoid cyst 1 case and cryptococcal meningoencephalitis 1 case. All patients developed at least 5 of 7 features which contained paroxysmal agitation, hyperthemia, diaphoresis, tachypnea, tachycardia, hypertension and dystonia. PSH occurred within 24 hours after brain injury in 3 patients; 24 hours to 3 weeks in 5 patients; 5 months in 1 patient; 9 years in 1 patient. The frequency varied from one time in several days to several times in one day. The duration varied from 1 minute to 3 hours. The episodes in 4 patients occurred more often at night, 1 around palinesthesia and the frequency of other 5 patients showed no differences between day and night. There were 2 cases appeared sober-minded, and the states of consciousness of the other 8 cases were hard to judge during PSH. The Glasgow Coma Scale scores of 8 cases were 3 to 8 points and the other 2 cases were 15 points. No epileptic-form activity was detected by EEG and no particular lesions were responsible. Neuro-imaging examinations suggested frontal lobe, temporal lobe, parietal lobe, occipital lobe, basal ganglion, pons and lateral ventricle were damaged. And 9 patients received an ineffective antiepileptic drug treatment. The efficacy in the management of PSH with dopamine agonists combining with β-blockers was observed. Two patients achieved complete remission, 6 patients had a reduction in episode frequency, 1 patient showed no response to the therapy and I patient discharged and could not be connected. Conclusions
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