What are white matter hyperintensities made of? Relevance to vascular cognitive impairment.

What are white matter hyperintensities made of? Relevance to vascular cognitive impairment.
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白质超强度是什么?与血管认知障碍有关。

DOI:
10.1161/jaha.114.001140
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发表时间:
2015-06-23
影响因子:
5.4
通讯作者:
Muñoz-Maniega S
Muñoz-Maniega S
中科院分区:
医学2区
文献类型:
--
作者:
Wardlaw JM;Valdés Hernández MC;Muñoz-Maniega S

文献摘要

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白质高信号(WMH)被认为是血管来源,也被称为白质病变,是在老年受试者、中风和痴呆患者的脑磁共振成像(MRI)或计算机断层扫描(CT)上非常常见的发现。它们与认知障碍有关,使中风的风险增加两倍,痴呆的风险增加一倍。他们的病理学知识大多来自于死后的研究,其中许多是几年前的研究。就其性质而言,这些通常很小,从选定的大脑区域取样,可能反映了晚期疾病。他们关注脱髓鞘和轴突变性的特征,这可能比细胞外液的变化更容易在组织病理学上发现。在这里,我们回顾了脑磁共振成像(MRI)的进展,它揭示了早期阶段白质的高强度,以及显示组织病理的正常白质的变化,比WMH发现的更不明显。这些“预先可见”的变化表明,间质液体流动性和含水量的改变可能是可逆的,可能早于脱髓鞘和轴突损伤,而脱髓鞘和轴突损伤不太可能是可逆的,可能是晚期现象。神经影像学也揭示了WMH的动态性质,它们与其他病理特征(如继发性皮质和长束损伤)的相互作用,以及对脑损伤积累的贡献。这些见解为提高对小血管疾病的病因和发病机制的理解提供了机会,并代表了从中年到晚年预防脑损伤积累及其相关认知和身体问题的巨大未完成议程。认识到导致WMH发展的早期阶段将提供重要机会,在早期阶段预防(甚至逆转)小血管疾病造成的脑损伤,并改善其认知、身体、中风和痴呆后果。
White matter hyperintensities (WMH) of presumed vascular origin, also referred to as leukoaraiosis, are a very common finding on brain magnetic resonance imaging (MRI) or computed tomography (CT) in older subjects and in patients with stroke and dementia. They are associated with cognitive impairment, triple the risk of stroke and double the risk of dementia. Knowledge of their pathology derives mostly from post mortem studies, many from some years ago. These, by their nature, were generally small, sampled from selected brain regions and probably reflect late-stage disease. They focus on features of demyelination and axonal degeneration, which may be easier to detect histopathologically than changes in extracellular fluid. Here we review advances in brain magnetic resonance imaging (MRI) that are revealing white matter hyperintensities at earlier stages, and changes in normal-appearing white matter that indicate tissue pathology, less marked than those found in WMH. These “pre-visible” changes show that altered interstitial fluid mobility and water content, which may be reversible, probably predate demyelination and axonal damage, which are less likely to be reversible and are probably a late-stage phenomenon. Neuroimaging is also revealing the dynamic nature of WMH, their interactions with other pathological features such as secondary cortical and long tract damage, and contribution to accumulating brain damage. These insights provide opportunities to improve understanding the etiology and pathogenesis of small vessel disease, and represents an enormous unfinished agenda for preventing accumulation of brain damage, and its associated cognitive and physical problems, from mid to later life. Recognizing the earliest stages leading to WMH development will provide important opportunities to prevent (or even reverse) brain damage due to small vessel disease at the earliest stages, and ameliorate its cognitive, physical, stroke and dementia consequences.