Disorders of the Cerebrovascular System

2015 ◽  
pp. 103-120 ◽  
Author(s):  
Larry E. Davis ◽  
Sarah Pirio Richardson
2021 ◽  
pp. 107385842110122
Author(s):  
Tamara L. Baker ◽  
Denes V. Agoston ◽  
Rhys D. Brady ◽  
Brendan Major ◽  
Stuart J. McDonald ◽  
...  

The diagnosis, prognosis, and treatment of mild traumatic brain injuries (mTBIs), such as concussions, are significant unmet medical issues. The kinetic forces that occur in mTBI adversely affect the cerebral vasculature, making cerebrovascular injury (CVI) a pathophysiological hallmark of mTBI. Given the importance of a healthy cerebrovascular system in overall brain function, CVI is likely to contribute to neurological dysfunction after mTBI. As such, CVI and related pathomechanisms may provide objective biomarkers and therapeutic targets to improve the clinical management and outcomes of mTBI. Despite this potential, until recently, few studies have focused on the cerebral vasculature in this context. This article will begin by providing a brief overview of the cerebrovascular system followed by a review of the literature regarding how mTBI can affect the integrity and function of the cerebrovascular system, and how this may ultimately contribute to neurological dysfunction and neurodegenerative conditions. We then discuss promising avenues of research related to mTBI biomarkers and interventions that target CVI, and conclude that a clinical approach that takes CVI into account could result in substantial improvements in the care and outcomes of patients with mTBI.


Stroke ◽  
2003 ◽  
Vol 34 (5) ◽  
pp. 1197-1202 ◽  
Author(s):  
M. Müller ◽  
O. Bianchi ◽  
S. Erülkü ◽  
C. Stock ◽  
K. Schwerdtfeger

2001 ◽  
Vol 42 (6) ◽  
pp. 560-562 ◽  
Author(s):  
R. Klingebiel ◽  
C. Zimmer ◽  
P. Rogalla ◽  
D. Kivelitz ◽  
G. Bohner ◽  
...  

2001 ◽  
Vol 42 (6) ◽  
pp. 560-562
Author(s):  
R. Klingebiel ◽  
C. Zimmer ◽  
P. Rogalla ◽  
D. Kivelitz ◽  
G. Bohner ◽  
...  

2021 ◽  
Vol 20 ◽  
Author(s):  
Mustafa Etli ◽  
Oguz Karahan

Abstract Moyamoya disease is a rare disorder that involves the cerebrovascular system. Usually, it leads to occlusion of the arteries of the cerebral system and causes cerebral circulatory complaints. A 48-year-old female patient was admitted to our clinic with intermittent claudication in both legs. Biphasic and monophasic waveform patterns were detected bilaterally in distal (trifurcation arteries) lower extremities with Doppler sonography. The patient therefore underwent systemic vascular examination. Computed tomography angiography revealed bilateral carotid occlusion at the level of supraclinoid segments, and opacifications were detected at the distal segments of the bilateral anterior cerebellar and middle cerebellar arteries. The patient was diagnosed with moyamoya disease, and anticoagulant treatment was started. In conclusion, most previous reports have presented the cerebrovascular involvement of moyamoya disease. However, this disease can involve different peripheral vascular systems and careful and systemic vascular examination is necessary for an exact diagnosis.


Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
David H Cribbs ◽  
Giselle Passos ◽  
Vitaly Vasilevko

Hypertension is a major risk factor for intracerebral hemorrhage (ICH), and the accumulation of amyloid-beta (Aβ) in the cerebrovascular system, cerebral amyloid angiopathy (CAA), is also a significant risk factor for intracerebral hemorrhage ICH. Currently, there are no animal studies demonstrating a direct involvement of hypertension in the accumulation of Alzheimer’s disease-like pathology. To address this issue we have developed several mouse models that combine hypertension protocols with amyloid precursor protein (APP) transgenic mice (Tg2576), which accumulate significant CAA in the large cerebral vessels and the meninges by 18 months of age. The goal of this study was to determine the effect of acute and chronic hypertension on ICH in wildtype and a transgenic mouse model overexpressing a mutant human amyloid precursor protein (Tg2576 mice) associated with early onset AD and CAA. Fifteen-month-old Tg2576 mice and non-transgenic (nTg) littermates were treated with an angiotensin II (AngII) infusion (1000 ng/kg/min) and L-NAME (100 mg/kg/day) in drinking water to produce chronic hypertension. One week later, transient acute hypertension was induced by daily AngII injections (0.5 μg/g, s.c., twice daily) to produce ICH. A similar increase in mean blood pressure was observed in Tg2576 and nTg mice when evaluated 2 weeks after initiation of treatment. However Tg2576 mice had a higher incidence of signs of stroke compared with nTg littermates (P > 0.05). These data suggest that the accumulation of Aβ in the brain has an important role in development of ICH. Moreover, there was robust glial activation and increase in CAA in the gray matter of Tg2576 mice showing that hypertension may affect gray as well as white matter in the brain. Further studies may provide insights into the hypertension-induced changes in the cerebral vascular system that initiated the increase in CAA. The accumulation of Aβ in the cerebrovascular system is a significant risk factor for intracerebral hemorrhage (ICH), and has been linked to endothelial transport failure and blockage of perivascular drainage. While management of hypertension and atherosclerosis can reduce the incidence of ICH, there are currently no approved therapies for attenuating CAA.


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