White Matter Injury After Intracerebral Hemorrhage.

Xiongjie Fu,Jianfeng Zhuang,Yucong Peng,Hang Zhou,Feng Yan,Jianru Li,Yang Cao,Lin Wang,Guoyang Zhou,Chaoran Xu,Hanhai Zeng,Gao Chen

doi:10.3389/fneur.2021.562090

Xiongjie Fu, Jianfeng Zhuang + Show 10 more

Open Access

https://doi.org/10.3389/fneur.2021.562090

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Abstract

Spontaneous intracerebral hemorrhage (ICH) accounts for 15% of all stroke cases. ICH is a devastating form of stroke associated with high morbidity, mortality, and disability. Preclinical studies have explored the mechanisms of neuronal death and gray matter damage after ICH. However, few studies have examined the development of white matter injury (WMI) following ICH. Research on WMI indicates that its pathophysiological presentation involves axonal damage, demyelination, and mature oligodendrocyte loss. However, the detailed relationship and mechanism between WMI and ICH remain unclear. Studies of other acute brain insults have indicated that WMI is strongly correlated with cognitive deficits, neurological deficits, and depression. The degree of WMI determines the short- and long-term prognosis of patients with ICH. This review demonstrates the structure and functions of the white matter in the healthy brain and discusses the pathophysiological mechanism of WMI following ICH. Our review reveals that the development of WMI after ICH is complex; therefore, comprehensive treatment is essential. Understanding the relationship between WMI and other brain cells may reveal therapeutic targets for the treatment of ICH.

Highlights

Spontaneous intracerebral hemorrhage (ICH) is a serious disease and a global public healthcare challenge
We conducted a systematic online search in PubMed, without time limits, for papers published in English, appearing with the following keywords: white matter injury (WMI), white matter lesion, white matter hyperintensities, white matter change, leukoaraiosis or leukoencephalopathy, ICH, intracerebral hemorrhage, spontaneous intracerebral hemorrhage, or cerebral hemorrhage
Iron deposition after ICH causes inflammatory cell activation and the release of inflammatory cytokines, which induce WMI and neurological dysfunction. Iron chelators such as 2,2′-dipyridyl and deferoxamine can suppress the inflammatory response through the tumor necrosis factor (TNF)-α/receptorinteracting protein kinase 1 (RIPK1) and Jun N-terminal kinase (JNK) pathways [39, 103, 106]

Summary

INTRODUCTION

Spontaneous intracerebral hemorrhage (ICH) is a serious disease and a global public healthcare challenge. Multiple studies are focused on white matter injury (WMI). They discuss its mechanism of injury and the relationship between WMI and ICH outcomes [14,15,16,17,18]. The proportion of white matter in the rodent brain is 10–20%; it is 50% in humans [11, 20] This indicates that WMI plays a vital role after ICH; it is important to understand it in detail. This review summarizes the latest findings on the development of WMI after ICH in terms of anatomical structure, function, mechanism of injury, potential treatment, and repair of WMI after ICH to improve the outcome of ICH patients

METHOD

Findings

LIMITATIONS