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金刚烷胺治疗迟发性缺氧性脑病后的神经行为缺陷

Amantadine for neurobehavioural deficits following delayed post-hypoxic encephalopathy.

作者信息

Arciniegas David B, Frey Kimberly L, Anderson C Alan, Brousseau Kristin M, Harris Susie N

机构信息

Brain Injury Rehabilitation Unit, Spalding Rehabilitation Hospital, Aurora, CO, USA.

出版信息

Brain Inj. 2004 Dec;18(12):1309-18. doi: 10.1080/02699050410001720130.

Abstract

Delayed post-hypoxic encephalopathy is an uncommon but potentially debilitating consequence of hypoxic-ischemic brain injury. This condition is characterized by delayed neurological deterioration days-to-weeks after an initial partial or complete recovery from hypoxic-ischemic brain injury. The course of recovery from this condition is highly variable, ranging from rapid and fatal progression over several weeks to delayed but occasionally complete recovery. There are no reports describing neurorehabilitative, including neuropharmacologic, interventions for persons with persistent neurological and/or neurobehavioural deficits following delayed post-hypoxic encephalopathy. This study describes the case of a 24-year old male who developed delayed post-hypoxic encephalopathy following an unintentional methadone and diazepam overdose and who demonstrated cognitive and neurobehavioural improvements during treatment with amantadine HCl hydrochloride in a single-case, open-label design. A brief review of the literature regarding this condition, its treatment and suggestions for further study are presented.

摘要

迟发性缺氧性脑病是缺氧缺血性脑损伤一种罕见但可能使人衰弱的后果。这种病症的特点是在缺氧缺血性脑损伤最初部分或完全恢复后的数天至数周出现延迟性神经功能恶化。从这种病症恢复的过程差异很大,从数周内迅速致命进展到延迟但偶尔完全恢复。尚无报告描述针对迟发性缺氧性脑病后持续存在神经和/或神经行为缺陷者的神经康复干预措施,包括神经药理学干预。本研究描述了一名24岁男性病例,该患者在意外过量服用美沙酮和地西泮后发生迟发性缺氧性脑病,在一项单病例、开放标签设计中,其在接受盐酸金刚烷胺治疗期间认知和神经行为有改善。本文还简要回顾了关于这种病症、其治疗方法及进一步研究建议的文献。

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