Department of Neurology, Royal Perth Hospital, Perth, Australia.
Western Australian Adult Epilepsy Service, Perth, Australia.
J Clin Neurophysiol. 2019 May;36(3):209-212. doi: 10.1097/WNP.0000000000000565.
Baclofen has been reported to cause both a metabolic encephalopathy and nonconvulsive status epilepticus. Baclofen is typically used in the management of muscle spasticity but is being increasingly used to manage alcohol withdrawal and opiate dependency. Given the increasing use of baclofen we describe the clinical and electrographical features of baclofen neurotoxicity seen at our institution.
The clinical and EEG features of patients with an encephalopathy in the setting of baclofen therapy were analyzed. Patients were identified via our hospital EEG database.
Fourteen patients were identified having presented with an acute confusional state without identifiable cause other than baclofen use. Five patients took a deliberate overdose, three of whom were baclofen naive, two patients presented after medication prescription error, and seven patients were on stable doses (30-140 mg daily). All patients presented with an encephalopathy, one patient was reported to have clinical seizures, and seven had multifocal myoclonus. EEGs were abnormal in all patients and showed moderate to severe generalized slowing. Generalized triphasic waves occurring at 1 to 2 Hz, sometimes with an anterior to posterior phase lag, were present in 10 patients (71%), and intermittent generalized suppression of the background was seen in three patients. Three patients received small doses of intravenous benzodiazepines, resulting in a marked depression of consciousness and respiration. All patients recovered within 48 hours of baclofen discontinuation.
Baclofen toxicity can produce an acute encephalopathy even at modest doses, with the EEG showing generalized slowing and triphasic waves consistent with a toxic encephalopathy. Management consists of supportive care and cessation of baclofen. Patients with baclofen neurotoxicity exhibit a marked vulnerability to the depressant effects of benzodiazepines.
巴氯芬已被报道可引起代谢性脑病和非惊厥性癫痫持续状态。巴氯芬通常用于治疗肌肉痉挛，但也越来越多地用于治疗酒精戒断和阿片类药物依赖。鉴于巴氯芬的使用越来越多，我们描述了在我们机构中看到的巴氯芬神经毒性的临床和脑电图特征。
分析了在巴氯芬治疗中出现脑病的患者的临床和脑电图特征。通过我们的医院脑电图数据库识别患者。
确定了 14 名患者，他们表现为急性意识混乱状态，除了使用巴氯芬外，没有可识别的其他原因。5 名患者故意过量服用，其中 3 名患者为巴氯芬初治，2 名患者在药物处方错误后出现，7 名患者服用稳定剂量（30-140 毫克/天）。所有患者均出现脑病，1 例患者报告有临床发作，7 例患者有多灶性肌阵挛。所有患者的脑电图均异常，显示中度至重度广泛减慢。10 名患者（71%）存在 1 至 2 Hz 出现的三相波，有时伴有前后相位滞后，3 名患者出现间歇性广泛背景抑制。3 名患者接受了小剂量静脉注射苯二氮䓬类药物，导致意识和呼吸明显抑制。所有患者在停止使用巴氯芬后 48 小时内恢复。
即使在适度剂量下，巴氯芬毒性也可引起急性脑病，脑电图显示广泛减慢和三相波，符合中毒性脑病。治疗包括支持性护理和停止巴氯芬。巴氯芬神经毒性的患者对苯二氮䓬类药物的抑制作用表现出明显的易感性。
