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Ageing
Published in Henry J. Woodford, Essential Geriatrics, 2022
Atherosclerosis accumulates as we age. This may be promoted by lipid peroxidation. Its formation is accelerated by associated co-morbidities (i.e. hypertension, diabetes and renal disease). Additional factors may include reduced physical activity and obesity. Large blood vessels become dilated and their walls become thickened. Amyloid deposition occurs in the walls of cerebral vessels (termed ‘cerebral amyloid angiopathy', see page 218) and is associated with an increased risk of intracerebral haemorrhage. Bleeding risk tends to increase due to lower platelet counts and changes in clotting factors.
Neurosurgery: Cerebrovascular diseases
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Geriatric Neuroanesthesia, 2019
Paolo Gritti, Luigi Andrea Lanterna, Francesco Ferri, Carlo Brembilla, Ferdinando Luca Lorini
Hemorrhagic stroke is the third most frequent cause of stroke after AIS and TIA (2). Hypertensive hemorrhages (11%–15.5%) compared with hemorrhage due to ruptured aneurysms and vascular malformations (4.5%–7%) have a higher overall incidence in the context of the major CVD (2). Primary hypertensive ICH is the mundane “spontaneous” brain hemorrhage (9). It is predominantly due to chronic hypertension and degenerative changes in cerebral arteries. In recent decades, with increased awareness of the need to control BP, the percentage of hemorrhages caused by factors other than hypertension has greatly increased. In order of frequency, ICH is classified according to its anatomical site or presumed etiology. The most common sites of ICH are supratentorial (85%–95%), including deep (50%–75%) and lobar (25%–40%). The most common causes are hypertension (30%–60%), cerebral amyloid angiopathy (10%–30%), anticoagulation (1%–20%), and vascular structural lesions (3%–8%), while undetermined causes account for about 5%–20% of cases (27).
Case 34: An Elderly Man with Confusion
Published in Layne Kerry, Janice Rymer, 100 Diagnostic Dilemmas in Clinical Medicine, 2017
Amyloidosis is a term encompassing a number of conditions where insoluble amyloid proteins form deposits within tissues, resulting in disease. In cerebral amyloid angiopathy, fibrils of β-amyloid protein are deposited within the tunica media and adventitia of cerebral and leptomeningeal blood vessels. β-Amyloid may accumulate either due to processes causing increased production or because of impaired clearance by endocytosis. Cerebral amyloid angiopathy is not related to systemic amyloidosis. β-Amyloid deposition causes increased fragility of the vessels making them prone to haemorrhage.
The aquaporin-4 water channel and updates on its potential as a drug target for Alzheimer’s disease
Published in Expert Opinion on Therapeutic Targets, 2023
Bret Silverglate, Xiaoyi Gao, Hannah P. Lee, Peter Maliha, George T. Grossberg
Modulating AQP4 activity in AD requires the drug to cross the blood-brain barrier, a perennial challenge when trying to create drugs that are active in the CNS. Previous postmortem and recent neuroimaging studies showed that the BBB is disrupted in patients with AD, including capillary leakages, aberrant angiogenesis, and degeneration of BBB-associated cells (pericytes and endothelial cells) [70]. Cerebral amyloid angiopathy, a pathological hallmark of AD, also causes BBB disruption by damaging blood vessels. In many neurodegenerative diseases, including AD, PD, and HIV-associated dementia, disruption of P-glycoprotein-mediated active efflux transport at BBB leads to the accumulation of toxic agents. The changes in BBB in AD pose another challenge to the discovery of AQP4-targeting drugs, and research on these changes in BBB is required to determine the correct dosage.
Considerations when restarting anticoagulants in patients with atrial fibrillation after bleeding
Published in Expert Review of Hematology, 2019
Monika Kozieł, Wern Yew Ding, Zbigniew Kalarus, Gregory Y. H. Lip
Administration of NOACs or VKAs may be restarted 4–8 weeks after intracerebral hemorrhage when the risk of ischaemic stroke is estimated to be high and the risk of a further intracerebral hemorrhage is predicted to be lower [36]. However, factors such as hypertension, old age, and previous stroke are predictive for both ischaemic stroke and intracerebral hemorrhage [40]. Individual assessment of not restarting anticoagulation in intracerebral hemorrhage AF patients with optional advice of multidisciplinary team is highlighted. The balance between risk of ischemic stroke and rebleeding should be analyzed for the individual patient. A multidisciplinary team should be composed of cardiologists, neurologists, neuroradiologists and neurosurgeons. Suggested factors that should contribute to the risk/benefit evaluation of restarting anticoagulation include: patient’s age, renal function, the location of bleeding and greater number of cerebral microbleeds on magnetic resonance imaging [56]. Patients with cerebral amyloid angiopathy are at very high risk of recurrent intracerebral hemorrhage and should not be treated with OACs [57]. Long-term coagulation after a lobar hemorrhage remains still a matter of debate [58]. In case of absolute contraindication for OAC, left atrial appendage occlusion should be considered [14,36].
The extracellular matrix of the blood–brain barrier: structural and functional roles in health, aging, and Alzheimer’s disease
Published in Tissue Barriers, 2019
May J. Reed, Mamatha Damodarasamy, William A. Banks
It is accepted that BM thickening occurs in response to stress such as sheer forces. The impact of longstanding vascular flow on the BM has led to consensus that normal aging results in eventual BM thickening.20,88 Whether these changes confer functional alteration is less clear. It is also noted that specific brain regions demonstrate differential changes in BM ECM with aging in both mouse and humans.89–91 Changes with AD are likely similar to that of aging, with a general increase in BM thickening, but accurate assessment is again complicated by the regional changes that are a foundation of AD progression and classification.92 AD patients with cerebral amyloid angiopathy (CAA) provide additional difficulty in the study.46 Although CAA primarily affects arterioles, this pathology induces alterations in BM that exceed, or at the minimum differ from, that found in microvasculature without significant Abeta deposition.90,93 It should also be noted that in most human samples, autofluorescence and the presence of residual blood contents in brain specimens can make the differentiation of changes in ECM content difficult to discern, and can reflect regional bias that affects analysis within and among brain specimens.94 Measures of BM ECM are further complicated by whether the quality is considered in the evaluation of immunostaining (for example, linear integrity of the BM) or discrete bands on electrophoresis.