Department of Neurology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Department of Public Health, Center for Medical Decision Sciences, Erasmus Medical Center, Rotterdam, The Netherlands.
Acta Neurol Scand. 2022 Jun;145(6):649-657. doi: 10.1111/ane.13617. Epub 2022 Mar 31.
Patients with chronic subdural hematoma (CSDH) can have transient neurological deficits deficit (TND) mimicking transient ischemic attacks. The prevalence of TNDs in CSDH varies between 1%-24%, depending on TND definition. Despite this high prevalence the pathophysiology of TND in CSDH is not clear in many cases. In this systematic review, we aim to unravel the responsible mechanism. Pubmed and Embase were searched for all articles concerning the pathophysiology of TND as a presenting symptom in patients with CSDH. There were no publication date restrictions for the articles in the search. Two reviewers independently selected studies for inclusion and subsequently extracted the necessary data. Out of 316 identified references, 15 met the inclusion criteria. Several articles mentioned multiple pathophysiological mechanisms. One of the proposed etiologies of TND was epileptic activity, stated by three articles. In contrast, three different studies stated that seizures are unlikely to cause TND. Five papers suggested that obstruction of blood flow, caused by the hematoma or subsequent swelling, might be the cause. Six articles made no definite statement on the responsible pathophysiological mechanism of TND. Different mechanisms have been proposed to be the cause of TNDs in patients with CSDH. Based on this review, the exact pathophysiology of TND remains unclear. We suggest that future studies on this topic should incorporate MRI of the brain (with diffusion-weighted imaging) and EEG, to provide better insight into TND pathophysiology. The knowledge resulting from future studies might contribute to better understanding of TND and optimal treatment in CSDH.
慢性硬脑膜下血肿（CSDH）患者可能会出现短暂性神经功能缺损（TND），类似于短暂性脑缺血发作。TND 在 CSDH 中的发生率在 1%-24%之间，具体取决于 TND 的定义。尽管如此，TND 在 CSDH 中的病理生理学在许多情况下仍不清楚。在这项系统评价中，我们旨在阐明其负责的机制。在 PubMed 和 Embase 上搜索了所有关于 TND 作为 CSDH 患者首发症状的病理生理学的文章。搜索时对文章没有出版日期限制。两位审稿人独立选择纳入的研究，并随后提取必要的数据。在 316 篇确定的参考文献中，有 15 篇符合纳入标准。有几篇文章提到了多种病理生理机制。有三篇文章提出 TND 的一个发病机制是癫痫活动。相比之下，有三篇不同的研究表明癫痫不太可能导致 TND。五篇论文认为血肿或随后的肿胀引起的血流阻塞可能是原因。六篇文章没有明确说明 TND 的负责病理生理机制。已经提出了不同的机制来解释 CSDH 患者 TND 的发生。基于本综述，TND 的确切病理生理学仍不清楚。我们建议，未来关于这一主题的研究应包括大脑 MRI（包括弥散加权成像）和 EEG，以更好地了解 TND 病理生理学。未来研究的结果可能有助于更好地理解 TND 和 CSDH 的最佳治疗。
