Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Eur J Neurol. 2020 Oct;27(10):1937-1947. doi: 10.1111/ene.14326. Epub 2020 Jun 26.
Post-hypoxic movement disorders and chronic post-hypoxic myoclonus are rare complications after cardiac arrest in adults. Our study investigates the clinical spectrum, neuroimaging results, therapy and prognosis of these debilitating post-hypoxic sequelae.
This retrospective study included 72 patients from the neurological intensive care unit at a university hospital, who were diagnosed with hypoxic-ischaemic encephalopathy after cardiac arrest between January 2007 and September 2018. Clinical records were screened for occurrence of post-hypoxic movement disorders and chronic post-hypoxic myoclonus. Affected patients were further analysed for applied neuroprognostic tests, administered therapy and treatment response, and the outcome of these movement disorders and neurological function.
Nineteen out of 72 screened patients exhibited post-hypoxic motor symptoms. Basal ganglia injury was the most likely neuroanatomical correlate of movement disorders as indicated by T1 hyperintensities and hypometabolism of this region in magnetic resonance imaging and positron emission tomography computed tomography. Levomepromazine and intrathecal baclofen showed first promising and mostly prompt responses to control these post-hypoxic movement disorders and even hyperkinetic storms. In contrast, chronic post-hypoxic myoclonus best responded to co-application of clonazepam, levetiracetam and primidone. Remission rates of post-hypoxic movement disorders and chronic post-hypoxic myoclonus were 58% and 50%, respectively. Affected patients seemed to present a rather good recovery of cognitive functions in contrast to the often more severe physical deficits.
Post-hypoxic movement disorders associated with pronounced basal ganglia dysfunction might be efficiently controlled by levomepromazine or intrathecal baclofen. Their occurrence might be an indicator for a more unfavourable, but often not devastating, neurological outcome.
成人心脏骤停后出现缺氧后运动障碍和慢性缺氧后肌阵挛是罕见的并发症。本研究旨在调查这些使人衰弱的缺氧后后遗症的临床谱、神经影像学结果、治疗和预后。
本回顾性研究纳入了 2007 年 1 月至 2018 年 9 月期间在一所大学医院神经重症监护病房诊断为心脏骤停后缺氧缺血性脑病的 72 例患者。筛选出缺氧后运动障碍和慢性缺氧后肌阵挛的病例。对受影响的患者进行进一步分析，包括应用神经预后测试、给予的治疗和治疗反应，以及这些运动障碍和神经功能的结果。
在 72 例筛选患者中，有 19 例出现缺氧后运动症状。基底节损伤是运动障碍最可能的神经解剖学相关因素，这一点在磁共振成像和正电子发射断层扫描计算机断层扫描中表现为该区域的 T1 高信号和代谢降低。左美丙嗪和鞘内巴氯芬对控制这些缺氧后运动障碍，甚至对控制过度运动风暴，表现出了最初的有希望的、且主要是迅速的反应。相比之下，慢性缺氧后肌阵挛最好通过联合应用氯硝西泮、左乙拉西坦和扑米酮来治疗。缺氧后运动障碍和慢性缺氧后肌阵挛的缓解率分别为 58%和 50%。与通常更严重的身体缺陷相比，受影响的患者在认知功能方面似乎有较好的恢复。
与明显基底节功能障碍相关的缺氧后运动障碍可以通过左美丙嗪或鞘内巴氯芬有效控制。它们的发生可能是神经预后更差但通常不具破坏性的指标。
