Differential regional infarction, neuronal loss and gliosis in the gerbil cerebral hemisphere following 30 min of unilateral common carotid artery occlusion

2018 ◽  
Vol 34 (1) ◽  
pp. 223-233 ◽  
Author(s):  
Ji Hyeon Ahn ◽  
Minah Song ◽  
Hyunjung Kim ◽  
Tae-Kyeong Lee ◽  
Cheol Woo Park ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
Cerebral Hemisphere ◽  
Neuronal Loss ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Common Carotid Artery Occlusion

scholarly journals Chronic Cerebral Hypoperfusion Induces Vascular Plasticity and Hemodynamics but Also Neuronal Degeneration and Cognitive Impairment

2015 ◽  
Vol 35 (8) ◽  
pp. 1249-1259 ◽  
Author(s):  
Zhen Jing ◽  
Changzheng Shi ◽  
Lihui Zhu ◽  
Yonghui Xiang ◽  
Peihao Chen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Neuronal Degeneration ◽  
Neuronal Loss ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Common Carotid Artery Occlusion

Chronic cerebral hypoperfusion (CCH) induces cognitive impairment, but the compensative mechanism of cerebral blood flow (CBF) is not fully understood. The present study mainly investigated dynamic changes in CBF, angiogenesis, and cellular pathology in the cortex, the striatum, and the cerebellum, and also studied cognitive impairment of rats induced by bilateral common carotid artery occlusion (BCCAO). Magnetic resonance imaging (MRI) techniques, immunochemistry, and Morris water maze were employed to the study. The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO. It returned to the sham level from 3 to 6 weeks companied by the dilation of vertebral arteries after BCCAO. The number of microvessels declined at 2, 3, and 4 weeks but increased at 6 weeks after BCCAO. Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO. Cognitive impairment of ischemic rats was directly related to ischemic duration. Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain. However, this limited compensation cannot prevent neuronal loss and cognitive impairment after permanent ischemia.

scholarly journals Common Carotid Artery Occlusion Treatment: Revealing a Gap in the Current Guidelines

2013 ◽  
Vol 58 (3) ◽  
pp. 846 ◽  
Author(s):  
C. Klonaris ◽  
G.N. Kouvelos ◽  
M. Kafeza ◽  
A. Koutsoumpelis ◽  
A. Katsargyris ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Common Carotid Artery Occlusion ◽  
Current Guidelines

scholarly journals Endovascular Revascularization of a Symptomatic Common Carotid Artery Occlusion

2016 ◽  
Vol 44 (1) ◽  
pp. 120-123 ◽  
Author(s):  
Julie Kromm ◽  
Tim E. Darsaut ◽  
Khurshid Khan ◽  
Robert Ashforth ◽  
Esseddeeg Ghrooda
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
Clinical Presentation ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Common Site ◽  
Extracranial Carotid Artery ◽  
The Common ◽  
Common Carotid Artery Occlusion ◽  
Diagnostic Investigations

AbstractAlthough the common carotid artery is the second most common site for extracranial carotid artery stenosis, complete symptomatic occlusion in the absence of devastating stroke is rare. We present a case of complete common carotid artery occlusion failing medical management and requiring endovascular intervention. The clinical presentation, diagnostic investigations, and management of complete carotid artery occlusions are discussed.

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