Abstract
Intracerebral hemorrhage (ICH) accounts for 10%–30% of all types of stroke. Bleeding within the brain parenchyma causes gray matter (GM) destruction as well as proximal or distal white matter (WM) injury (WMI) due to complex pathophysiological mechanisms. Because WM has a distinct cellular architecture, blood supply pattern and corresponding function, and its response to stroke may vary from that of GM, a better understanding of the characteristics of WMI following ICH is essential and may shed new light on treatment options. Current evidence using histological, radiological and chemical biomarkers clearly confirms the spatio-temporal distribution of WMI post- ICH. Although certain types of pathological damage such as inflammatory, oxidative and neuro-excitotoxic injury to WM have been identified, the exact molecular mechanisms remain unclear. In this review article, we briefly describe the constitution and physiological function of brain WM, summarize evidence regarding WMI, and focus on the underlying pathophysiological mechanisms and therapeutic strategies.
Highlights
Intracerebral hemorrhage (ICH) accounts for approximately 10%–15% of all strokes in Western countries and 20%–30% of strokes in Asia and has a high mortality and poor functional outcome
We further found that the significant demyelination and axonal damage 3 days post-ICH were highly associated with brain edema and neurologic dysfunction using an ICH rat model in which autologous blood was infused into the pons, indicating that WMI plays a vital role in neurologic impairment (Tao et al, 2016)
WMI that is characterized by demyelination, axonal damage and loss of oligodendrocytes frequently occurs within 3 days of the onset of ICH, implying that a relatively wide therapeutic time window may exist in ICH which is advantageous for the design of potential treatments
Summary
Intracerebral hemorrhage (ICH) accounts for approximately 10%–15% of all strokes in Western countries and 20%–30% of strokes in Asia and has a high mortality and poor functional outcome. ICH leads to both gray matter (GM) and white matter (WM) injury (WMI). The typical clinical syndromes, such as contralateral hemiplegia due to injury to the corticospinal tracts (CSTs) and corticonuclear tracts, hemidysesthesia due to injury to the central thalamic radiations and hemianopia due to damage to the optic radiation after deep basal ganglia ICH are the main sequelae resulting from WMI (Chung et al, 2000; Qureshi et al, 2001). The cognitive dysfunction following striatal ICH may predominantly reflect injury to adjacent WM pathways rather than damage to the putamen or caudate (Smith and Venegas-Torres, 2014). WMI is a great contributor to the neurological deficits after ICH, but experimental and clinical studies focus more on GM damage than WMI, which may be partially responsible for the failure of treatments with massive neuroprotectants targeting degenerating neuronal cells (Wasserman and Schlichter, 2008). A comprehensive review of the pertinent literature that discusses the pathophysiological mechanisms underlying WMI, potential therapeutic targets and novel treatment modalities is essential
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