Cognitive Dysfunction After Intracerebral Hemorrhage, Vasculitis, and Other Stroke Syndromes

Smith, Eric E.; Venegas-Torres, José Andrés

doi:10.1007/978-1-4614-7672-6_11

Cited by 1 publication

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References 120 publications

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“…Indeed, 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 ). Additionally, 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 ). Therefore, 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 ).…”

Section: Introductionmentioning

confidence: 99%

White Matter Injury after Intracerebral Hemorrhage: Pathophysiology and Therapeutic Strategies

Tao

et al. 2017

Front. Hum. Neurosci.

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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.

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Section: Introductionmentioning

confidence: 99%

White Matter Injury after Intracerebral Hemorrhage: Pathophysiology and Therapeutic Strategies

Tao

et al. 2017

Front. Hum. Neurosci.

View full text Add to dashboard Cite

show abstract

Cognitive Dysfunction After Intracerebral Hemorrhage, Vasculitis, and Other Stroke Syndromes

Cited by 1 publication

References 120 publications

White Matter Injury after Intracerebral Hemorrhage: Pathophysiology and Therapeutic Strategies

White Matter Injury after Intracerebral Hemorrhage: Pathophysiology and Therapeutic Strategies

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