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遲發型缺氧性腦病變後之復健:病例報告

Rehabilitation in a Patient with Delayed Post-hypoxic Encephalopathy: A Case Report

摘要


遲發型缺氧性腦病變(delayed post-hypoxic encephalopathy)是指腦部急性缺氧的病人,在完全恢復正常一段時間之後,再度出現面部遲滯、混亂、躁動以及其他神經精神症狀。造成遲發型缺氧性腦病變的原因,以一氧化碳中毒的病人最多,不過其他會造成腦缺氧的事件,也可能造成遲發型缺氧性腦病變。遲發型缺氧性腦病變的病理發現,主要是大腦白質的去髓化(demyelination)。造成遲發型缺氧性腦病變的確切病理機轉,目前仍不清楚,因此也沒有明確的預防方法或是有效治療。遲發型缺氧性腦病變的診斷,以病史詢問最爲重要,但有一部分的病人需要接受腦部磁振造影以確定診斷。遲發型缺氧性腦病變病人的預後,大多數病人可恢復正常,但有一部分出現嚴重併發症,甚至死亡。針對嚴重程度的遲發型缺氧性腦病變病人,實施復健治療,可以減低缺乏活動所產生的併發症,並且使病人的日常生活功能獲得改善。本病例將報告一位中年男性,在一氧化碳中毒後一個月後,逐漸產生遲發型缺氧性腦病變,除了神經及精神症狀外,病人還出現雙側聲帶麻痺,並逐漸進展至接近植物人狀態。經過一年的復健後,病人的行動能力以及日常生活功能獲得一定程度的進展。

並列摘要


Carbon monoxide poisoning from accidents or suicide attempts often result in delayed post-hypoxic encephalopathy. Patients with delayed post-hypoxic encephalopathy typically present with recurrent apathy, confusion, agitation, and/or progressive neurological deficits, despite apparent transient recovery. Autopsy reports often reveal diffuse demyelination of subcortical white matter, but the exact pathogenesis is not clear. While comprehensive physical examination and history taking is necessary in diagnosing delayed post-hypoxic encephalopathy, magnetic resonance imaging can be very helpful in the diagnostic work-up. Rehabilitation for severe post-hypoxic encephalopathy can prevent complications such as immobilization and can improve patients' functional status. We report the history, diagnosis, and rehabilitative outcome of a 41-year-old man who developed delayed post-hypoxic encephalopathy one month after carbon monoxide poisoning. Severe neurological deficits were noted in this patient, including bilateral vocal cord paralysis and vegetative status. After about one year of intensive rehabilitation, the patient achieved significant improvements in his functional status and activities of daily living.

被引用紀錄


李瑞琦(2015)。一氧化碳中毒病人發生神經後遺症的獨立影響因子研究〔碩士論文,義守大學〕。華藝線上圖書館。https://doi.org/10.6343/ISU.2015.00207

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