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Hypertension
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Fibrinoid necrosis of small arteries and arterioles is a consequence of acute elevation of blood pressure, with acute tear of smooth muscle. The artery may but usually does not rupture. This age-independent acute process contrasts with the chronic age-dependent process of elastin fiber fracture in the aorta, consequent on three billion or more cycles acting over decades (see Chapter 15). The lipohyalinosis of intermediate-sized cerebral arteries may represent the effect of a similar phenomenon to that causing fibrinoid necrosis in the smaller vessels (see Chapter 14) (Russell, 1975; Bateman, 2004; Henry-Feugeas et al., 2005). The thesis of Byrom is applicable to the cerebral and renal small arteries in the elderly, hence it is set out in full in Chapter 14.
Stroke
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
FALSE – Atrial fibrillation is a major risk factor; however, the most significant modifiable risk factor is hypertension. This is thought to be a result of the vascular remodelling which occurs with hypertension and the subsequent development of atherosclerosis and lipohyalinosis. Other modifiable risk factors for stroke include diabetes, congestive heart failure, smoking and hypercholesterolaemia.6 Age is the single most important non-modifiable risk factor for stroke.
Structural and Functional Aspects of Brain Damage
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Cristina Sierra, Miguel Camafort, Antonio Coca
Autoregulation of the cerebral circulation enables the maintenance of cerebral blood flow (CBF) at constant levels despite changes in BP. Under normal conditions, autoregulation is effective at between 60 and 150 mmHg. High BP influences the cerebral circulation, causing adaptive vascular changes. Thus, hypertension influences the autoregulation of CBF by shifting both the lower and upper limits of autoregulatory capacity towards higher BP, while hypertensive patients may be especially vulnerable to episodes of hypotension (10), which may play a role in the development of silent cerebrovascular damage. Increased cerebral vascular resistance could be due to narrowing of the small vessels by lipohyalinosis and microatherosclerosis. The effect of high BP on the small vessels is well known, with vascular remodelling occurring in cerebral blood vessels during chronic hypertension. It has been suggested that this structural alteration impairs autoregulation, exposing the white matter to fluctuations in BP. For this reason, it has been hypothesized that changes in cerebral hemodynamic may play a role in the development of WML (10).
Clinical neuroimaging in intracerebral haemorrhage related to cerebral small vessel disease: contemporary practice and emerging concepts
Published in Expert Review of Neurotherapeutics, 2022
Martina Goeldlin, Catriona Stewart, Piotr Radojewski, Roland Wiest, David Seiffge, David J Werring
Postmortem full brain histopathological analysis is the gold standard for diagnosis of CAA [30] but is seldom available in clinical practice. Biopsy is used as a surrogate, with the limitation of possible sampling errors [31]. In clinical practice, only a minority of patients undergo hematoma evacuation offering the possibility of performing brain biopsy. Characteristic changes in CAA histopathology samples include Congo red positive vessel walls and positive immunocytochemistry staining for amyloid [32]. In later stages, fibrinoid vessel wall necrosis and cracking vessels with a ‘vessel-within-a-vessel’ aspect can be observed as well [32]. Typical findings in DPA are lipohyalinosis or fibrinoid necrosis of vessel walls as well as microaneurysms in the basal ganglia and thalamic vessels [32]. Several postmortem neuropathological studies found that DPA and CAA were commonly observed simultaneously in patients with ICH [13,33]. One postmortem study found that in patients with non-lobar intracerebral hemorrhage (generally considered exclusively due to DPA), 6/48 (12.5%) had severe CAA, while among patients with lobar hemorrhage, 48/62 (77%) had evidence of other small vessel disease in addition to CAA [13].
CBF regulation in hypertension and Alzheimer’s disease
Published in Clinical and Experimental Hypertension, 2020
Noushin Yazdani, Mark S. Kindy, Saeid Taheri
The predominant vascular lesions in AD are CAA, as described before, and arteriosclerosis/lipohyalinosis (224). The origin of arteriosclerosis/lipohyalinosis is not clear, though both high MAP and chronic inflammation in endothelial cells have been implicated in the disease (225). Chronic high MAP causes the elevation of the cerebrovascular resistance index, which is associated with cognitive dysfunction in the very-old (226). The activity of Aβ degrading enzymes rises with age and AD (for an in-depth review see (17)). The two most important Aβ degradation enzymes are angiotensin-converting enzyme (ACE) and endothelin converting enzyme (ECE) (227,228). Both are rate-limiting enzymes in the production of endothelin-1 (ET-1) and Angiotensin II (ANG II) (229). The main role of ANG II and ET-1 is to constrict blood vessels, therefore an increased ACE and ET-1 activities to degrade excess Aβ may also contribute to cerebral hypoperfusion in AD (17). These observations highlight the controversial role of ACE in both AD pathology and hypertension. However, more in-depth studies are needed to understand the role of ACE and ECE in connecting hypertension to AD.
Hyperhomocysteinemia can predict the severity of white matter hyperintensities in elderly lacunar infarction patients
Published in International Journal of Neuroscience, 2020
Ling Yu, Lei Yang, Yue Li, Shuna Yang, Hua Gu, Wenli Hu, Shan Gao
Our results also showed older age and stroke history are significantly associated with severe PVWMH. The incidence of WMH and volume may increase exponentially with advanced age [20], and the incidence is greater in individuals with higher levels of and longer exposure to various vascular risk factors, notably hypertension and DM. A research found long-term exposure to high blood pressure could predict WMH, particularly DWMH after followed 28 years follow-up time [21]. Rost et al. [22] found greater WMH burden was associated with small vessel stroke compared with other ischemic stroke subtypes. Lacunar infarction also named hypertensive cSVD. It is strongly associated with ageing, hypertension, DM, and other risk factors. Our subjects were lacunar infarction patients. Lacunar infarction was generally considered to be caused by hypertensive lipohyalinosis. This could explain our findings: age and history of stroke were independent risk factor for WMH.