Deptartment of Anatomy & Neurosciences, Clinical Neuroscience, VU University Medical Centre, Amsterdam, The Netherlands.
Prion. 2013 Jan-Feb;7(1):66-75. doi: 10.4161/pri.23499. Epub 2013 Jan 1.
Over the past decade, immunohistochemical studies have provided compelling evidence that gray matter (GM) pathology in multiple sclerosis (MS) is extensive. Until recently, this GM pathology was difficult to visualize using standard magnetic resonance imaging (MRI) techniques. However, with newly developed MRI sequences, it has become clear that GM damage is present from the earliest stages of the disease and accrues with disease progression. GM pathology is clinically relevant, as GM lesions and/or GM atrophy were shown to be associated with MS motor deficits and cognitive impairment. Recent autopsy studies demonstrated significant GM demyelination and microglia activation. However, extensive immune cell influx, complement activation and blood-brain barrier leakage, like in WM pathology, are far less prominent in the GM. Hence, so far, the cause of GM damage in MS remains unknown, although several plausible underlying pathogenic mechanisms have been proposed. This paper provides an overview of GM damage in MS with a focus on its topology and histopathology.
在过去的十年中，免疫组织化学研究提供了令人信服的证据，表明多发性硬化症（MS）中的灰质（GM）病理学广泛存在。直到最近，使用标准磁共振成像（MRI）技术还很难观察到这种 GM 病理学。然而，随着新开发的 MRI 序列的出现，已经清楚地表明 GM 损伤存在于疾病的最早阶段，并随着疾病的进展而累积。GM 病理学具有临床相关性，因为 GM 病变和/或 GM 萎缩与 MS 运动缺陷和认知障碍有关。最近的尸检研究表明 GM 脱髓鞘和小胶质细胞激活显著。然而，像在 WM 病理学中一样，广泛的免疫细胞浸润、补体激活和血脑屏障渗漏在 GM 中并不那么明显。因此，到目前为止，MS 中 GM 损伤的原因仍不清楚，尽管已经提出了几种合理的潜在发病机制。本文重点介绍了 GM 损伤在多发性硬化症中的拓扑结构和组织病理学特征。
