Amantadine Enhances Recovery from Delayed Neuropsychiatric Effects Caused by Carbon Monoxide Poisoning: A Case Report

S. T. Eddine, A. Oumoussa, I. Adali, F. Manoudi
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Abstract

Carbon monoxide (CO) poisoning causes severe brain damage, including delayed neuropsychiatric sequelae (DNS), which occur after a lucid interval following recovery from the insult of acute CO poisoning. Delayed neuropsychiatric syndrome (DNS) is a well-known complication following carbon monoxide (CO) poisoning and develops in up to 50 % of adult survivors. The syndrome is probably immunologically mediated. We describe a 19-year-old female who developed DNS, including slowness, Parkinsonism; irritability and cognitive impairment. All symptoms, including cognitive impairment, were dramatically improved by amantadine monotherapy. The present case illustrates the possibility of amantadine treatment for cognitive impairment and parkinsonism induced by CO poisoning.
金刚烷胺可促进一氧化碳中毒所致迟发性神经精神影响的恢复:病例报告
一氧化碳(CO)中毒会造成严重的脑损伤,包括迟发性神经精神后遗症(DNS),这种后遗症是在急性一氧化碳(CO)中毒恢复后的一段清醒期后出现的。迟发性神经精神综合征(DNS)是众所周知的一氧化碳(CO)中毒后并发症,高达 50% 的成年幸存者会出现这种症状。该综合征可能是由免疫介导的。我们描述了一名出现 DNS 的 19 岁女性,她的症状包括行动迟缓、帕金森症、易怒和认知障碍。金刚烷胺单药治疗后,包括认知障碍在内的所有症状均得到显著改善。本病例说明了金刚烷胺治疗一氧化碳中毒引起的认知障碍和帕金森氏症的可能性。
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