Okuda Shiho, Ueno Masao, Hayakawa Michiko, Araki Manabu, Kanda Fumio, Takano Shin
Department of Neurology, Hyogo Rehabilitation Center Hospital.
Rinsho Shinkeigaku. 2012;52(9):672-6. doi: 10.5692/clinicalneurol.52.672.
Delayed posthypoxic leukoencephalopathy (DPL) is a rare and less well known complication of hypoxic brain injury. Although it is well known that anoxic or hypoxic injury produces acute neurologic deficits, DPL typically manifests days to weeks after apparent recovery from an obtunded state, and patients with DPL demonstrate cognitive impairment, high brain dysfunction, parkinsonism, or psychosis. MRI findings of the brain demonstrate deep white matter abnormalities. We report 2 cases of DPL after hypoxia due to benzodiazepine overdose. Both of our patients had normal arylsulfatase A activity. Although DPL is seen in carbon monoxide poisoning, pseudodeficiency of arylsulfatase A activity, or drug overdose with heroin or morphine, there are only some previous studies of DPL caused by an overdose with benzodiazepine. It is unclear whether neurotoxicity from the drug in addition to hypoxia alone is involved, however, it is important to note that overdose of common drugs as sleeping medicine can cause DPL. Since DPL may often be misdiagnosed and be subjected to unnecessary treatments, it is also important to understand its unique clinical course and MRI findings. With prompt recognition of DPL, we expect that more cases of DPL caused by overdose with benzodiazepine will be diagnosed, because benzodiazepine overdoses are common.
迟发性缺氧后白质脑病（DPL）是缺氧性脑损伤一种罕见且鲜为人知的并发症。虽然众所周知缺氧或低氧损伤会导致急性神经功能缺损，但DPL通常在从昏迷状态明显恢复数天至数周后出现，且DPL患者表现出认知障碍、高级脑功能障碍、帕金森综合征或精神病症状。脑部MRI检查结果显示深部白质异常。我们报告2例因苯二氮䓬类药物过量导致缺氧后的DPL病例。我们的两名患者芳基硫酸酯酶A活性均正常。虽然DPL可见于一氧化碳中毒、芳基硫酸酯酶A活性假性缺乏或海洛因或吗啡药物过量，但之前仅有一些关于苯二氮䓬类药物过量导致DPL的研究。尚不清楚除了单纯缺氧外药物的神经毒性是否也起作用，然而，需要注意的是作为安眠药的常用药物过量可导致DPL。由于DPL常可能被误诊并接受不必要的治疗，了解其独特的临床病程和MRI表现也很重要。随着对DPL的及时识别，我们预计将会诊断出更多由苯二氮䓬类药物过量导致的DPL病例，因为苯二氮䓬类药物过量很常见。
