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低温脑损伤后常温下年轻女性 N20 电位的双侧重现。

Bilateral Reappearance of the N20 Potential in a Normothermic Young Woman Post-Anoxic Brain Injury.

机构信息

American University of Beirut Medical Center, Beirut, Lebanon.

出版信息

J Clin Neurophysiol. 2022 Jul 1;39(5):e21-e25. doi: 10.1097/WNP.0000000000000928. Epub 2022 Feb 2.

DOI:10.1097/WNP.0000000000000928
PMID:35239554
Abstract

Hypoxic-ischemic brain injury is a well-known consequence of cardiac arrest and providing an accurate prognostication remains a challenge, especially in decisions related to withdrawal of care. Bilateral absence of the cortical response (N20 potential) on median somatosensory evoked potentials, on days 1 to 3 after the return of spontaneous circulation, is widely considered as the most reliable predictor of poor outcome with a high specificity and a low false-positive rate. The authors describe the case of a young comatose woman after hypoxic injury because of cardiac arrest whose initial median somatosensory evoked potentials revealed bilateral absence of the N20 response associated with evidence of selective injury to both perirolandic cortices and basal ganglia on brain MRI. This patient made a substantial recovery associated with bilateral reappearance of the N20 potential and resolution of the neuroimaging abnormalities.This case revealed that an acute selective and reversible hypoxic injury to both perirolandic cortices may lead to a temporary loss of the N20 responses and an inaccurate prediction of poor outcome after cardiac arrest. It emphasizes on the importance of adopting a multimodal approach in the prognostic assessment of survivors of cardiac arrest.

摘要

缺氧缺血性脑损伤是心脏骤停的已知后果,提供准确的预后仍然是一个挑战,特别是在与停止治疗相关的决策中。在自主循环恢复后的 1 至 3 天内,正中感觉诱发电位双侧皮质反应(N20 电位)缺失被广泛认为是预后不良的最可靠预测指标,具有高特异性和低假阳性率。作者描述了一名年轻的昏迷女性心脏骤停后缺氧损伤的病例,其初始正中感觉诱发电位显示双侧 N20 反应缺失,同时脑 MRI 显示双侧岛盖皮质和基底节选择性损伤的证据。该患者出现了显著的恢复,双侧 N20 电位再次出现,神经影像学异常也得到了缓解。该病例表明,双侧岛盖皮质的急性选择性和可逆性缺氧损伤可能导致 N20 反应的暂时丧失,并对心脏骤停后预后不良的不准确预测。这强调了在心脏骤停幸存者的预后评估中采用多模态方法的重要性。

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J Neurol. 2023 Dec;270(12):5999-6009. doi: 10.1007/s00415-023-11951-4. Epub 2023 Aug 28.