Posts in Category: Cerebrovascular Disease/Stroke

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Xiaoming Hu, T. Michael De Silva, Jun Chen, Frank M. Faraci

Structural alterations in endothelial cells are critical for blood–brain barrier (BBB) opening early after ischemic stroke. A, The opening of paracellular pathways: cytoskeletal rearrangements and related signaling in endothelial cells. B, The transcellular pathway of BBB leakage. ADF indicates actin-depolymerizing factor; CaM, calmodulin; LIMK, LIM kinase; MLC, myosin light chain; MLCK, MLC kinase; MLCP, MLC phosphatase; MMP, matrix metallopeptidase; ROCK: Rho kinase; TESK1, testicular protein kinase 1; and ZO, zonula occluden. [Powerpoint File]

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Xiaoming Hu, T. Michael De Silva, Jun Chen, Frank M. Faraci

Pericytes play multifaceted roles in ischemia and reperfusion. Pericytes display both beneficial and detrimental functions during ischemia and reperfusion phases, and contribute significantly to the blood–brain barrier damage and repair. 1. Pericyte contraction and dilation regulate cerebral blood flow in the ischemic and perilesion areas. 2. Pericyte protects other neurovascular unit (NVU) components through releasing protective/trophic factors such as nerve growth factor (NGF), neurotrophin-3 (NT-3), vascular endothelial growth factor (VEGF), angiopoietin (Ang-1), and glial cell line-derived neurotrophic factor (GDNF). 3. Phagocytotic pericytes help to eliminate dead or injured tissue in the ischemic core, which in turn mitigates local inflammation and reduce secondary tissue damage. 4. Pericyte–endothelial cell interaction promotes angiogenesis after stroke. 5) Pericytes have the potential to serve as an origin of NVU components during tissue repair after ischemic stroke. Illustration credit: Ben Smith. [Powerpoint File]

Cardioembolic Stroke

Cardioembolic Stroke

Hooman Kamel, Jeff S. Healey

Overlap among cryptogenic stroke, embolic stroke of undetermined source, and cardioembolic stroke. [Powerpiont File]

Acute Ischemic Stroke Therapy Overview

Acute Ischemic Stroke Therapy Overview

Luciana Catanese, Joseph Tarsia, Marc Fisher

A schematic representation of the cascade of ischemic injury over time. Courtesy of Dr Won-Ki Kim, Seoul Korea (Illustration Credit: Ben Smith). BBB indicates blood–brain barrier. [Powerpoint FIle]

Heart–Brain Axis: Effects of Neurologic Injury on Cardiovascular Function

Heart–Brain Axis: Effects of Neurologic Injury on Cardiovascular Function

Pouya Tahsili-Fahadan, Romergryko G. Geocadin

Neural control of the cardiovascular system. Afferent and efferent pathways are shown in green and red lines, respectively. Some potential sites for therapeutic interventions are illustrated in the blue text boxes. The figure has been simplified to illustrate the major cortical, subcortical, and brain stem areas involved in control of the cardiovascular function. Most of the shown areas are interconnected. For anatomic details and physiological effects of the illustrated pathways, please refer to the text. [Powerpoint File]

Vascular Cognitive Impairment

Vascular Cognitive Impairment

Martin Dichgans, Didier Leys

Major mechanisms underlying vascular cognitive impairment (VCI). A, Vascular causes. B, Brain parenchymal lesions associated with VCI. For explanations, see text. WML indicates white matter lesion (graphical realization: Antonia Weingart, Institute for Stroke and Dementia Research). [Powerpoint File]

Vascular Cognitive Impairment

Vascular Cognitive Impairment

Martin Dichgans, Didier Leys

Pathological findings associated with vascular cognitive impairment (VCI). A, Hemisphere section of a patient with small-vessel disease and extensive white matter rarefication (Luxol fast blue periodic acid Schiff-reaction [LFB-PAS] stain, scale bar 1 cm); the arrowhead marks a lacunar infarct; boxes correspond to higher magnifications in B, C, and D. B, Enlarged perivascular space (LFB-PAS stain, scale bar 200 μm). C, Mild white matter rarefication (pallor; LFB-PAS stain, scale bar 500 μm). D, Marked white matter rarefication (pallor; LFB-PAS stain, scale bar 500 μm). E, Lacunar infarct (hematoxilin and eosin stain, scale bar 500 μm). F, Microhemorrhage with hemosiderin-loaded macrophages (hematoxilin and eosin stain, scale bar 200 μm). G, Microinfarct (hematoxilin and eosin stain, scale bar 200 μm). Images were kindly provided by Thomas Arzberger and Karl Bise, Institute for Neuropathology and Prion Research, LMU, Munich. [Powerpoint File]

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Chirantan Banerjee, Marc I. Chimowitz

Histological cross-section of intracranial atherosclerosis in basilar artery. Image courtesy Dr Tanya Turan. Red arrow—fibrous tissue, blue arrow—vessel wall, and green arrow—lipid [Powerpoint File]

Global Burden of Stroke

Global Burden of Stroke

Valery L. Feigin, Bo Norrving, George A. Mensah

Age-standardized stroke disability-adjusted life-years (DALYs) and mortality rates per 100,000 person-years in various regions of the world in 2013 (both sexes, all ages) [Powerpoint File]