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Ketamine for empiric treatment of cortical spreading depolarization after subdural hematoma evacuation
Clinical Neurology and Neurosurgery ( IF 1.9 ) Pub Date : 2021-01-01 , DOI: 10.1016/j.clineuro.2020.106318
Sheshali Wanchoo 1 , Shahab Khazanehdari 1 , Arpan Patel 2 , Amanda Lin 3 , Tania Rebeiz 1 , Celine DeMatteo 1 , Jamie Ullman 1 , David Ledoux 1
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BACKGROUND It is widely known that some patients surgically treated for subdural hematoma (SDH) experience neurologic deficits not clearly explained by the acute brain injury or known sequelae like seizures. There is increasing evidence that cortical spreading depolarization (CSD) may be the cause. A recent article demonstrated that CSD occurred at a rate of 15 % and was associated with neurological deterioration in a subset of patients following chronic subdural hematoma evacuation. Furthermore, CSD can lead to ischemia leading to worsening neurologic deficits. CSD is usually detected on electrocorticography (ECoG) and needs cortical strip electrode placement with equipment and expertise that may not be readily available. CASE DESCRIPTION We report three cases of patients with subdural hematoma (SDH) not undergoing ECoG in whom CSD was suspected to be the cause of their neurologic deficits post evacuation. Extensive workup including neuroimaging and electroencephalography (EEG) were inconclusive. Patients were subsequently treated with ketamine infusion and had resultant neurological recovery. CONCLUSIONS Ketamine infusion can help reverse neurologic deficits in patients with SDH in whom the deficits are not explained by neuroimaging or electrographic seizure. CSD is a known phenomenon that can result in neurological injury and must remain in the differential diagnosis of such patients. Though only limited cases are discussed (n = 3), this small case series provides the basis for conducting clinical trials evaluating the efficacy of ketamine in improving functional outcome in brain-injured patients demonstrating evidence of CSD.

中文翻译:

氯胺酮经验性治疗硬膜下血肿清除后皮层扩散去极化

背景众所周知,一些接受外科手术治疗硬膜下血肿 (SDH) 的患者会出现神经功能缺损,但无法通过急性脑损伤或已知的癫痫等后遗症来明确解释。越来越多的证据表明皮质扩散去极化 (CSD) 可能是原因。最近的一篇文章表明,CSD 的发生率为 15%,并且与慢性硬膜下血肿清除后一部分患者的神经功能恶化有关。此外,CSD 可导致缺血,导致神经功能缺损恶化。CSD 通常在皮层电图 (ECoG) 上检测到,需要使用可能不易获得的设备和专业知识放置皮层条状电极。病例描述 我们报告了三例未接受 ECoG 的硬膜下血肿 (SDH) 患者,其中怀疑 CSD 是导致其疏散后神经功能缺损的原因。包括神经影像学和脑电图 (EEG) 在内的广泛检查尚无定论。患者随后接受氯胺酮输注治疗,神经功能恢复。结论 氯胺酮输注有助于逆转 SDH 患者的神经功能缺损,这些缺损不能通过神经影像学或电图癫痫发作来解释。CSD 是一种已知的可导致神经损伤的现象,必须保留在此类患者的鉴别诊断中。虽然只讨论了有限的情况(n = 3),
更新日期:2021-01-01
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