Cherian Koshi A, Legatt Alan D
Montefiore Medical Center/Albert Einstein College of Medicine, Bronx, New York.
Montefiore Medical Center/Albert Einstein College of Medicine, Bronx, New York.
Pediatr Neurol. 2017 Aug;73:88-91. doi: 10.1016/j.pediatrneurol.2016.12.011. Epub 2017 Jan 4.
Valproic acid may induce hyperammonemic encephalopathy. Various electroencephalogram (EEG) abnormalities have been documented in association with this condition, but not burst suppression, an abnormal EEG pattern that is associated with severe encephalopathy.
Serial EEGs, clinical observations, and laboratory findings were analyzed.
This 13-year-old girl with autism and intractable epilepsy experienced increased seizures; her valproic acid dose was increased and other antiepileptic drugs were administered. She became lethargic, and her EEG showed a burst suppression pattern. Her ammonia concentration was increased to 101 μmol/L and her valproic acid level was increased to 269.9 mg/L. Valproic acid was discontinued and carnitine was administered. Subsequently she became more alert, her ammonia concentration decreased, and her EEG changed from a burst suppression pattern to a continuous pattern. Within three days, she was back to her baseline level of functioning.
Valproic acid-induced hyperammonemic encephalopathy can produce a burst suppression EEG patternin the patient's.
丙戊酸可能诱发高氨血症性脑病。已有多种脑电图（EEG）异常与该病症相关的记录，但与严重脑病相关的异常EEG模式——爆发抑制却未见相关记录。
对系列脑电图、临床观察结果及实验室检查结果进行分析。
这名13岁患有自闭症和难治性癫痫的女孩癫痫发作增多；增加了丙戊酸剂量并加用了其他抗癫痫药物。她变得嗜睡，脑电图显示为爆发抑制模式。她的氨浓度升至101μmol/L，丙戊酸水平升至269.9mg/L。停用丙戊酸并给予肉碱。随后她变得更加清醒，氨浓度降低，脑电图从爆发抑制模式转变为连续模式。三天内，她恢复到了基线功能水平。
丙戊酸诱发的高氨血症性脑病可使患者脑电图呈现爆发抑制模式。
