在初级渐进性多发性硬化症中,神经障碍和大脑灰质缩是由微观结构的损伤变化决定的,而不是由损伤负荷决定的
Theodoros Ladopoulos1,2, Zainab Abbas3, Britta Krieger4
1Department of Neurology, St Josef Hospital, Ruhr University, Gudrunstr. 56, 44791, Bochum, Germany. Theodoros.Ladopoulos@rub.de.
Journal of neurology
|April 1, 2025
概括
多发性硬化 (MS) 病变的定量MRI测量,而不仅仅是病变负载,与渐进性MS的灰质缩和残疾相关. 这些发现突显了MS亚型之间的病变病理学的差异.
科学领域:
- 神经成像是一种神经成像.
- 神经学 神经学
- 放射学 放射学是一门学科.
背景情况:
- 传统的MRI指标,如多发性硬化症 (MS) 中的病变数和体积,缺乏特异性,无法完全解释临床残疾或大脑缩.
- 脱线性斑块在复发性和渐进性多发性硬化症亚型中显示出明显的组织病理特征.
- 定量MRI提供了对MS病变及其影响的更详细评估.
研究的目的:
- 用定量MRI评估MS病变的微观结构特征.
- 调查这些定量MRI参数,灰质 (GM) 缩和不同MS亚型的临床残疾之间的关联.
主要方法:
- 56名对照组,121名复发性复发性多发性硬化症 (RRMS) 患者和38名初级进展性多发性硬化症 (PPMS) 患者接受了1.5TMRI扫描和临床评估.
- 使用SAMSEG进行了损伤和大脑细分;使用MDME序列和SyMRI软件估计了放松率和髓体积分数.
- 分析了定量MRI参数 (损伤和正常出现的白质) 与转基因缩和临床残疾之间的关联.
主要成果:
- 与RRMS患者相比,PPMS患者的脑区域体积和定量损伤/NAWMMMRI参数显著降低.
- 定量损伤MRI参数与皮质/深层GM体积和RRMS和PPMS的残疾分数显著相关,特别是在PPMS中.
- 与RRMS不同的是,单独的病变体积与PPMS组的GM缩或临床残疾没有相关性.
结论:
- 对MS病变的定量MRI测量,与简单的病变负载不同,与PPMS的临床残疾和GM缩有很强的相关性.
- 这些发现表明,不同的病变病理有助于不同类型的多发性硬化症的疾病进展.
- 定量核磁共振 (MRI) 提供了有价值的见解,了解病变特征与MS的临床结果之间的关系.
相关概念视频
Multiple Sclerosis l: Introduction
19
Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
19
Alzheimer Disease ll: Pathophysiology
32
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
32


