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基底动脉尖分布区创伤性缺血性损伤:病例报告。

Traumatic ischemic injury in a top of the basilar distribution: a case report.

机构信息

Department of Neurosurgery, University of California San Diego, La Jolla, 1335 Sunset Cliffs Boulevard, San Diego, CA, 92107, USA.

Department of Neurosurgery, Massachusetts General Hospital, Boston, MA, USA.

出版信息

BMC Neurol. 2021 Apr 27;21(1):178. doi: 10.1186/s12883-021-02207-7.

DOI:10.1186/s12883-021-02207-7
PMID:33902491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8077958/
Abstract

BACKGROUND

Top of the basilar syndrome is a rare, heterogeneous disorder that has previously only been described in the setting of acute ischemic stroke in predominantly elderly patients. We present the first reported case of traumatic brain injury (TBI) causing ischemia in a top of the basilar distribution.

CASE PRESENTATION

A 19-year-old woman suffered an acute subdural hematoma and sustained hypoxemia after being struck by a motor vehicle. Neurosurgical evacuation of the hematoma was undertaken. Magnetic resonance imaging revealed ischemic injury in the midbrain and diencephalic structures fitting a top of the basilar distribution. No associated vascular injury was identified. The patient was eventually discharged in a state of persistent unresponsive wakefulness.

CONCLUSIONS

Ischemia in a top of the basilar distribution may occur in the setting of TBI. A high degree of clinical suspicion is required to identify this disorder. Further study of the complex inflammatory microenvironment and associated tissue perfusion dynamics in TBI are needed in order to elucidate the mechanisms underlying ischemic injury patterns, develop management paradigms and predict prognosis.

摘要

背景

基底动脉尖综合征是一种罕见的、异质性的疾病,以前仅在主要为老年患者的急性缺血性卒中中描述过。我们报告了首例外伤性脑损伤(TBI)导致基底动脉尖分布区域缺血的病例。

病例介绍

一名 19 岁女性被机动车撞击后发生急性硬膜下血肿并伴有低氧血症。进行了血肿的神经外科清除术。磁共振成像显示中脑和间脑结构存在符合基底动脉尖分布的缺血性损伤。未发现相关血管损伤。患者最终处于持续无反应性觉醒的状态出院。

结论

TBI 可发生基底动脉尖分布区域的缺血。需要高度的临床怀疑来识别这种疾病。需要进一步研究 TBI 中的复杂炎症微环境和相关组织灌注动力学,以阐明缺血性损伤模式的机制,制定管理范式并预测预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f15/8077958/f5f2cedd1206/12883_2021_2207_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f15/8077958/326e68387d3e/12883_2021_2207_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f15/8077958/f5f2cedd1206/12883_2021_2207_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f15/8077958/326e68387d3e/12883_2021_2207_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f15/8077958/f5f2cedd1206/12883_2021_2207_Fig2_HTML.jpg

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Neuropharmacology. 2019 Feb;145(Pt B):230-246. doi: 10.1016/j.neuropharm.2018.08.004. Epub 2018 Aug 4.
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Response of the cerebral vasculature following traumatic brain injury.创伤性脑损伤后脑血管系统的反应。
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Pathophysiologic Mechanisms of Cerebral Ischemia and Diffusion Hypoxia in Traumatic Brain Injury.
颅脑创伤中脑缺血和弥散性缺氧的病理生理机制。
JAMA Neurol. 2016 May 1;73(5):542-50. doi: 10.1001/jamaneurol.2016.0091.
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