Gupta Harsh V, Caviness John N
Department of Neurology, Mayo Clinic, Scottsdale, AZ, USA.
Tremor Other Hyperkinet Mov (N Y). 2016 Sep 17;6:409. doi: 10.7916/D89C6XM4. eCollection 2016.
Myoclonus may occur after hypoxia. In 1963, Lance and Adams described persistent myoclonus with other features after hypoxia. However, myoclonus occurring immediately after hypoxia may demonstrate different syndromic features from classic Lance-Adams syndrome (LAS). The aim of this review is to provide up-to-date information about the spectrum of myoclonus occurring after hypoxia with emphasis on neurophysiological features.
A literature search was performed on PubMed database from 1960 to 2015. The following search terms were used: "myoclonus," "post anoxic myoclonus," "post hypoxic myoclonus," and "Lance Adams syndrome." The articles describing clinical features, neurophysiology, management, and prognosis of post-hypoxic myoclonus cases were included for review.
Several reports in the literature were separated clinically into "acute post-hypoxic myoclonus," which occurred within hours of severe hypoxia, and "chronic post-hypoxic myoclonus," which occurred with some recovery of mental status as the LAS. Acute post-hypoxic myoclonus was generalized in the setting of coma. Chronic post-hypoxic myoclonus presented as multifocal cortical action myoclonus that was significantly disabling. There was overlap of neurophysiological findings for these two syndromes but also different features. Treatment options for these two distinct clinical-neurophysiologic post-hypoxic myoclonus syndromes were approached differently.
The review of clinical and neurophysiological findings suggests that myoclonus after hypoxia manifests in one or a combination of distinct syndromes: acute and/or chronic myoclonus. The mechanism of post-hypoxic myoclonus may arise either from cortical and/or subcortical structures. More research is needed to clarify mechanisms and treatment of post-hypoxic myoclonus.
缺氧后可能发生肌阵挛。1963年，兰斯（Lance）和亚当斯（Adams）描述了缺氧后出现的持续性肌阵挛及其他特征。然而，缺氧后立即出现的肌阵挛可能表现出与经典兰斯-亚当斯综合征（LAS）不同的综合征特征。本综述的目的是提供有关缺氧后肌阵挛谱系的最新信息，重点是神经生理学特征。
在PubMed数据库中对1960年至2015年的文献进行检索。使用了以下检索词：“肌阵挛”、“缺氧后肌阵挛”、“低氧后肌阵挛”和“兰斯·亚当斯综合征”。纳入描述缺氧后肌阵挛病例的临床特征、神经生理学、管理和预后的文章进行综述。
文献中的几份报告在临床上分为“急性缺氧后肌阵挛”，其发生在严重缺氧数小时内，以及“慢性缺氧后肌阵挛”，其发生在精神状态有所恢复时，如同LAS。急性缺氧后肌阵挛在昏迷状态下为全身性。慢性缺氧后肌阵挛表现为多灶性皮质动作性肌阵挛，具有明显的致残性。这两种综合征的神经生理学发现存在重叠，但也有不同特征。针对这两种不同的临床-神经生理学缺氧后肌阵挛综合征的治疗选择有所不同。
对临床和神经生理学发现的综述表明，缺氧后肌阵挛表现为一种或多种不同综合征的组合：急性和/或慢性肌阵挛。缺氧后肌阵挛的机制可能源于皮质和/或皮质下结构。需要更多研究来阐明缺氧后肌阵挛的机制和治疗方法。
