NEGATIVE MYOCLONUS DURING VALPROATE-RELATED STUPOR - NEUROPHYSIOLOGICAL EVIDENCE OF A CORTICAL NONEPILEPTIC ORIGIN
NEGATIVE MYOCLONUS DURING VALPROATE-RELATED STUPOR - NEUROPHYSIOLOGICAL EVIDENCE OF A CORTICAL NONEPILEPTIC ORIGIN
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DOI：
10.1016/0013-4694(94)00268-p
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发表时间：
1995-02-01
期刊：
影响因子：
--
通讯作者：
QUATTRONE, A
中科院分区：
文献类型：
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作者：
AGUGLIA, U;GAMBARDELLA, A;QUATTRONE, A
我们回顾性分析了6例癫痫患者的临床和神经生理学资料，这些患者在服用丙戊酸钠（VPA）后几天出现了肌克隆阴性和昏迷。丙戊酸停药后临床体征和症状迅速缓解。我们试图阐明vpa诱导的昏迷的病理生理机制，并进一步提供肌阵挛阴性的多导图和反向平均脑电图记录。在vpa诱导的昏迷期间，脑电图显示患者的后背景减慢。3例患者间期出现癫痫样放电。在所有6例患者中，同时使用视频多波记录的密切检查显示肌阵挛阴性，与侧侧尖峰放电无关。在3例常规脑电图无峰的患者中，有2例进行了反向平均脑电图记录，我们检测到一个大的（5 μ V）皮质正负波时间锁定（30-40 msec），并伴有对侧手腕的姿势改变。这种皮质电位与代谢性或中毒性脑病继发星形肌的患者相似。在一名患者中，静脉注射10mg地西泮并没有改变这种皮质电位，也没有逆转临床表现。在所有患者中，唯一异常的实验室发现是静脉氨血症水平升高。我们的研究结果反对癫痫性VPA脑病的起源，并进一步支持皮层非癫痫性机制介导负性肌阵挛。在处理这种情况时应避免使用苯二氮卓类药物。
We retrospectively reviewed clinical and neurophysiological data of 6 epileptic patients who developed negative myoclonus and stupor a few days after introduction of valproate (VPA). Prompt remission of clinical signs and symptoms followed valproate withdrawal. We attempted to elucidate the pathophysiological mechanism of VPA-induced stupor and provide further polygraphic and backaveraging EEG documentation of negative myoclonus. During VPA-induced stupor electroencephalograms revealed posterior background slowing in an patients. Interictal epileptiform discharges were present in 3 patients. In all 6 patients close examination using simultaneous video-polygraphic recording showed negative myoclonus which was not time-related to lateralized spike discharges. In 2 of 3 patients with no spikes on conventional EEG who underwent backaveraged EEG recordings we detected a large (5 mu V) cortical positive-negative wave time-locked (30-40 msec) with the postural modification of the contralateral wrist. This cortical potential was similar to that observed in patients with asterixis secondary to metabolic or toxic encephalopathies. In one patient i.v. administration of 10 mg diazepam did not modify this cortical potential and did not reverse the clinical manifestations. In all patients the only abnormal laboratory finding was an increased level of venous ammonemia.Our findings are against an epileptic origin of VPA encephalopathy and provide further argument in favour of a cortical non-epileptic mechanism mediating negative myoclonus. Benzodiazepines should be avoided in the management of this condition.