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慢性硬脑膜下血肿清除术后迟发性波动神经功能缺损可能与播散性去极化有关。

Spreading depolarization may represent a novel mechanism for delayed fluctuating neurological deficit after chronic subdural hematoma evacuation.

机构信息

Departments of1Neurosurgery.

2Neurology.

出版信息

J Neurosurg. 2020 Mar 27;134(3):1294-1302. doi: 10.3171/2020.1.JNS192914. Print 2021 Mar 1.

DOI:10.3171/2020.1.JNS192914
PMID:32217801
Abstract

OBJECTIVE

Most patients with chronic subdural hematoma (cSDH) recover after surgical evacuation with a straightforward course. There is a subset of patients who develop transient and fluctuating deficits not explained by seizures, stroke, or mass effect after evacuation. The objective of this study was to investigate whether these postoperative neurological deficits may be related to temporary brain dysfunction caused by cortical spreading depolarizations (SDs).

METHODS

The authors conducted a prospective observational study of 40 patients who underwent cSDH evacuation. At the time of surgery, a 1 × 6 subdural electrode strip was placed on the cortex parallel to the subdural drain. Clinical outcomes were assessed utilizing the Markwalder Grading Scale, need for clinical EEG for new deficit, and presence of new deficits.

RESULTS

Definitive SD was detected in 6 (15%) of 40 patients. Baseline and cSDH characteristics did not differ between patients with and without SD. More patients experienced postoperative neurological deterioration if they had SD (50%) compared to those without SD (8.8%; p = 0.03). Only 2 patients in the entire cohort demonstrated early neurological deterioration, both of whom had SD. One of these cases demonstrated a time-locked new focal neurological deficit (aphasia) at the start of a series of multiple clusters of SD.

CONCLUSIONS

This is the first observation of SD occurring after cSDH evacuation. SD occurred at a rate of 15% and was associated with neurological deterioration. This may represent a novel mechanism for otherwise unexplained fluctuating neurological deficit after cSDH evacuation. This could provide a new therapeutic target, and SD-targeted therapies should be evaluated in prospective clinical trials.

摘要

目的

大多数慢性硬脑膜下血肿(cSDH)患者在手术清除后会恢复,且过程顺利。但有一部分患者在清除血肿后会出现短暂且波动的神经功能缺损,这些缺损不能用癫痫发作、中风或肿块效应来解释。本研究旨在探讨这些术后神经功能缺损是否与皮质扩散性抑制(SD)引起的暂时性脑功能障碍有关。

方法

作者对 40 例行 cSDH 清除术的患者进行了前瞻性观察研究。在手术时,将一个 1×6 的硬脑膜下电极条平行于硬脑膜引流管放置在皮质上。利用 Markwalder 分级量表、新缺陷的临床脑电图需要以及新缺陷的存在来评估临床结果。

结果

在 40 例患者中,有 6 例(15%)明确检测到 SD。有 SD 的患者与无 SD 的患者的基线和 cSDH 特征没有差异。如果患者有 SD(50%),则比无 SD 的患者(8.8%)更有可能出现术后神经功能恶化(p=0.03)。在整个队列中,只有 2 例患者出现早期神经功能恶化,且均有 SD。其中一例患者在一系列多发性 SD 簇开始时表现出时间锁定的新局灶性神经功能缺损(失语症)。

结论

这是首次观察到 cSDH 清除术后发生 SD。SD 的发生率为 15%,且与神经功能恶化有关。这可能代表了 cSDH 清除术后出现的其他不明原因波动的神经功能缺损的新机制。这可能为新的治疗靶点提供了依据,应该在前瞻性临床试验中评估针对 SD 的治疗方法。

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