Pathology Of Cerebral Vessels Research Articles

Associations of renin-angiotensin system inhibitor use with brain insulin signaling and neuropathology.

To examine the associations of renin-angiotensin system (RAS) inhibitor use with postmortem brain insulin signaling and neuropathology. Among Religious Orders Study participants, 150 deceased and autopsied older individuals (75 with diabetes matched to 75 without by age at death, sex, and education) had measurements of insulin receptor substrate-1 (IRS-1) and RAC-alpha serine/threonine protein kinase (AKT1) collected in the prefrontal cortex using ELISA and immunohistochemistry. Alzheimer's disease (AD), brain infarcts, and cerebral vessel pathology data were assessed by systematic neuropathologic evaluations. RAS inhibitor use was determined based on visual inspection of medication containers during study visits. The associations of RAS inhibitor use with brain insulin signaling measures and neuropathology were examined using adjusted regression analyses. Of the 90 RAS inhibitor users (54 with diabetes), 65 had used only angiotensin-converting enzyme inhibitors, 11 only angiotensin II receptor blockers, and 14 used both. RAS inhibitor use was associated with lower pT308AKT1/total AKT1, but not with pS307IRS-1/total IRS-1 or the density of cells stained positive for pS616 IRS-1. RAS inhibitor use was not associated with the level of global AD pathology or amyloid beta burden, but it was associated with a lower tau-neurofibrillary tangle density. Additionally, we found a significant interaction between diabetes and RAS inhibitors on tangle density. Furthermore, AKT1 phosphorylation partially mediated the association of RAS inhibitor use with tau tangle density. Lastly, RAS inhibitor use was associated with more atherosclerosis, but not with other cerebral blood vessel pathologies or cerebral infarcts. Late-life RAS inhibitor use may be associated with lower brain AKT1 phosphorylation and fewer neurofibrillary tangles.

Correlation of Black Blood MRI with Image- Based Blood Flow Simulations in Intracranial Aneurysms

Abstract Intracranial aneurysms (IA) is not-uncommon pathology of cerebral vessels. Vessel wall magnetic resonance imaging can visualize the vascular walls of IAs. In some aneurysms, the wall-adjacent and a luminal hyperintense signal was detected. The signal was attributed to the inflammation and specific hemodynamic features of aneurysms. But, up to now, the studies investigating luminal enhancement combined with flow analysis are limited. Therefore, in this study, investigation of the luminal enhancement is further carried out by comparison to computational fluid dynamics. The latter provides the possibility of calculating hemodynamic parameters, which can give information such as velocity, pressure, and shear stress fields throughout a heart cycle. The data of the IAs is specific to each patient and builds the basis for the enhancement analysis and simulations. Specific hemodynamic parameters like kinetic energy and vortex formation evaluated in the simulations show a dependency to signal suppression recorded with vessel wall magnetic resonance imaging

Клінічний випадок артеріовенозної мальформації у вагітної жінки

Extragenital pathology during pregnancy and childbirth occupies a leading place in maternal mortality and perinatal pathology. One of the main ways to maintain the health of mother and child is to identify somatic diseases in pregnant women and timely treat them. Nervous system diseases that occur in pregnant women are mainly epilepsy, multiple sclerosis, brain tumors, cerebrovascular disorders, although remain poorly understood, but require immediate decisions to prolong pregnancy, obstetric tactics during childbirth, conservative or conservative surgery. The pathology of cerebral vessels (arterial aneurysms and arteriovenous malformations) also remains an urgent problem, despite many years of experience in their diagnosis and treatment. The sudden development of symptoms, severity of clinical manifestations and high mortality in rupture of an aneurysm or arteriovenous malformation of cerebral vessels determine the urgency of this problem and increased interest in its study, especially in pregnant women. Material and methods. The paper presents a clinical case of arteriovenous malformation in a 25-year-old pregnant woman, her treatment and delivery. Results and discussion. Arteriovenous malformation is considered a congenital cerebrovascular pathology, which is accompanied by a sudden rupture of abnormal vessels with the development of hemorrhagic stroke, without specific clinical symptoms and precursors, which complicates lifelong diagnosis. Endovascular embolization during pregnancy saved the lives of women and children. An effective result was obtained after neurosurgical treatment of arteriovenous malformation in a pregnant woman in the second trimester of pregnancy (17 weeks), which allowed to bring the pregnancy to the physiological time of delivery. Taking into account the complex neurological pathology, neurosurgery, which requires the exclusion of a powerful period of childbirth, a pregnant woman gave birth by cesarean section at 38 weeks of pregnancy. Conclusion. An effective result was obtained after neurosurgical treatment of arteriovenous malformation in a pregnant woman in the second trimester of pregnancy, which allowed to bring the pregnancy to the physiological time of delivery. The obtained results indicated the possibility of full-term pregnancy, reduction of maternal and perinatal morbidity and mortality in pregnant women with arteriovenous malformation with timely preventive and curative measures with timely referral of pregnant women to the perinatal center on the basis of a multidisciplinary clinical institution to prevent complications

Сase of Progressive Fibrodysplasia Ossificans in Combination with a Rupture of Cerebral Arterial Aneurysm and Hyperparathyroidism

A rare clinical observation of a 24-year-old patient with clinical and radiological manifestations of Fibrodysplasia Ossificans Progressiva, combined with rupture of saccular cerebral aneurysm and hyperparathyroidism, is presented. A characteristic feature of this case was a combined pathology of cerebral vessels with Fibrodysplasia Ossificans Progressiva, the first manifestations of which appeared after intracranial haemorrhage with the development of severe motor neurological deficiency. It was accompanied by articulate and severe spastic syndromes, tough muscle and joint contractures, and the signs of Vitamin D deficiency and hyperparathyroidism were found later.

Modeling of the optimal scenario of arteriovenous malformation embolization

Cerebral arteriovenous malformation is a congenital developmental pathology of cerebral vessels, in which the arterial and venous blood vessels are connected directly by randomly interlaced degenerate vessels. This is a dangerous disease affecting the functioning of the brain, at which the risk of intracerebral hemorrhage is high. One of the methods of treatment of arteriovenous malformation is embolization – endovascular filling of arteriovenous malformation vessels with a special medical embolizing composition for blocking blood flow through them. This method is widely used, but still in some cases accompanied by intraoperative rupture of arteriovenous malformation. In this paper, on the basis of a one-dimensional model of joint two-phase filtration of blood and an embolizing composition, the optimal scenario of embolization is studied from the point of view of safety and efficiency. The methods of admissible and optimal embolization, which reduce the risk of rupture of arteriovenous malformation vessels, are considered.

Cerebral vascular syndrome of connective tissue dysplasia as a cause of subarachnoid hemorrhage in young patients

To clarify the role of connective tissue dysplasia (CTD) in the development and course of intracranial arterial aneurysm (IAA) and arteriovenous malformation (AVM) in young patients. The first stage of the study was a prospective 7-year follow-up of 549 patients with CDT signs, aged from 18 to 45 years, mean 23.51±8.67 years. The first stage included a comparative analysis of clinical characteristics of patients with DST with asymptomatic pathology of cerebral vessels and patients with DST without this pathology. At the second stage, there was a comparative study in 2 groups of patients with symptomatic pathology of cerebral vessels (AAA and/or AVM): with CTD (n=58) and without CTD (n=135). Symptomatic AAA and/or AVM were identified in 10.56% of young people with CTD including 37 patients with subarachnoid hemorrhages (SAH). The age of clinical manifestations was 25.55±8.13 years. Expressed manifestations of CTD were more frequent in the group of patients with cerebral vascular pathology compared to patients without CTD (p=0.008). The majority of patients had CTD manifestations of 3 or more systems, less than 2 systems were not involved, 12 patients had small abnormalities and/or malformations of the heart and other vessels. Hypertension, pathology of the vertebral arteries, skin, spine, veins, fully open Willis circle were independent risk factors for symptomatic pathology of cerebral vessels in patients with CTD. AVM and AAA in young patients with CTD compared with patients without CTD were characterized by the manifestation at an earlier age (25.55±8.13 years and 36.10±10.58 years, respectively; p=0.000), a more frequent combination with a fully open Willis circle (56.90 and 25.19%, respectively; df=1; p=0.000), more frequent multiple pathologies (15.52 and 4.44%, respectively, p=0.008), EAA in the posterior vascular bed (15.52 and 3.70%, respectively, p=0.004), SAH (63.79 and 35.56%, respectively, p=0.000) with lesser effects of general population risk factors. EAA and AVM in patients with CTD are likely to be considered in the context of vascular syndrome of connective tissue dysmorphogenesis, and CTD as a factor of adverse prognosis of IAA and AVM.

Relation of cerebral vessel disease to Alzheimer's disease dementia and cognitive function in elderly people: a cross-sectional study

BackgroundFew pathologic data are available on cerebral vessel disease, dementia, and cognition. This cross-sectional study examined associations of cerebral atherosclerosis and arteriolosclerosis neuropathology with probable and possible Alzheimer’s disease (AD) dementia and level of cognitive function, in a large group of older persons who came to autopsy.Methods1,143 older women or men (median age-at-death = 88.8 years; 42% with AD dementia) underwent annual clinical evaluations and agreed to brain autopsy at time-of-death, as part of one of two cohort studies of aging. Neuropsychological data proximate-to-death were used to create summary measures of global cognition and cognitive domains. Data across all years were used to determine presence of the clinical syndrome of AD dementia. Systematic neuropathologic evaluations documented severity of cerebral large (atherosclerosis) and small vessel disease (arteriolosclerosis). Using regression analyses adjusted for demographics, gross and micro-infarcts and AD pathology, we examined associations of vessel disease severity with odds of probable and possible AD dementia and level of cognition.FindingsModerate-to-severe atherosclerosis was present in 445 (39%) subjects, and arteriolosclerosis in 401 (35%). The odds of AD dementia was higher with moderate-to-severe atherosclerosis (OR=1.33; 95%CI:1.11–1.58) and arteriolosclerosis (OR=1.20; 95%CI:1.04–1.40). Atherosclerosis was associated with lower scores for global cognition (estimate= −0.10, SE=0.04; p=0.00096) and four cognitive domains (episodic memory, semantic memory, perceptual speed and visuospatial abilities; all p<0.019) but not working memory (p=0.21). Arteriolosclerosis was associated with lower scores for global cognition (estimate= −0.10, SE=0.03; p=0.0015) and four domains (all p<0.046), and a borderline/non-significant association was noted for visuospatial abilities (p=0.052). Findings were unchanged in analyses controlling for APOEε4 and vascular risk factors.InterpretationCerebral atherosclerosis and arteriolosclerosis each contribute to the odds of AD dementia by 20–30% per level increase in severity, and are associated with lower scores in most cognitive domains. Associations remain after taking into account AD and infarct pathologies, and vascular factors. Cerebral vessel pathology may be an under-recognized risk factor for AD dementia.FundingUnited States National Institutes of Health.

The Relationship of Cerebral Vessel Pathology to Brain Microinfarcts.

The relationship of cerebral vessel pathology to brain microinfarcts is not fully understood. We examined associations of cerebral vessel pathology with microinfarcts among community-dwelling persons who came to autopsy. Brain specimens were derived from 1,066 deceased subjects (mean age-at-death = 88 years, 65% women) participating in a cohort study of aging. Microinfarcts were classified by number, age and location. Severity of vessel pathologies was graded semi-quantitatively. Almost a third of subjects (n = 300; 28%) had at least one chronic microinfarct, including 128 cortical only, 120 subcortical only, and 47 with both. Moderate-to-severe atherosclerosis was present in 430 (41%) subjects, arteriolosclerosis in 382 (36%), and amyloid angiopathy in 374 (35%). The odds of one or multiple microinfarct(s) was increased for more severe atherosclerosis (OR =1.22; 95%CI: 1.03-1.45), arteriolosclerosis (OR =1.18; 95%CI: 1.02-1.37) and amyloid angiopathy (OR =1.13; 95%CI: 1.00-1.28). Separately, the odds of subcortical microinfarct(s) was increased for atherosclerosis (OR =1.49; 95%CI: 1.20-1.84) and arteriolosclerosis (OR =1.39; 95%CI: 1.16-1.67) but not amyloid angiopathy; whereas the odds of cortical microinfarct(s) was increased for amyloid angiopathy (OR =1.26; 95%CI: 1.09-1.46) only. While cerebral vessel pathologies are associated with microinfarct burden, atherosclerosis and arteriolosclerosis are associated with subcortical microinfarcts, and amyloid angiopathy with cortical microinfarcts.

The relationship of cerebral vessel pathology to brain microinfarcts

The relationship of cerebral vessel pathology to brain microinfarcts

Персонифицированная оценка риска развития неблагоприятных сердечно-сосудистых проявлений у пациентов молодого возраста с дисплазией соединительной ткани

Adverse cardiovascular manifestations (ACVM) were registered during 7-year follow-up of young patients with undifferentiated connective tissue dysplasia (CTD). ACVM developed in 28.42% of patients. Most frequent ACVMs were extension/aneurysm of the thoracic aorta (10.75%), cerebral vascular syndrome (10.56%), and arrhythmias (9.11%). Most significant risk factors for extension/aneurysm of the aorta were pathology of vertebral arteries, common risk factors (arterial hypertension, alcohol/drugs, smoking, heavy physical work, sports activities), bicuspid aortic valve); for pathology of cerebral vessels--completely open Willis' Circle, pathology of vertebral arteries, CTD related changes of skin and spine, diagnostic CTD coefficient > 23, chronic diseases of veins; clinically significant cardiac rhythm disturbances--combined valve manifestations of CTD, myxomatous degeneration of heart valves, pathology of the aorta, male sex, metabolic changes of the myocardium, deviations of circadian index, predominance of sympathetic tone, and diastolic dysfunction. Analysis of clinical characteristics (age, symptoms and severity of CTD, QTc dispersion ≥ 50 ms) and presence of unfavorable genetic polymorphisms in β1-adrenergic receptor gene (Ser49Gly, rs1801252), transcription factor Sp4 gene (A80807T, rs1011168), genes of matrix metalloproteinases type 3 (5A/6A) and type 9 (8202 A/G) allowed to evaluate overall risk of ACVM.

Abstract TP171: Purpose in Life and Risk of Cerebral Infarction

Background: Purpose in life (PIL), the sense that life has meaning and direction, is associated with a reduced risk of Alzheimer’s disease, incident disability, and mortality among community-dwelling older persons. Objective: To test the hypothesis that PIL is associated with reduced risk of cerebral infarction. Methods: Longitudinal clinical-pathologic cohort study. Subjects were from the Rush Memory and Aging Project (MAP). Older persons without dementia completed a standard measure of PIL using a structured interview and 10-item scale derived from Ryff’s Scales of Psychological Well-Being. The number of chronic gross &amp; microscopic cerebral infarctions (each expressed as 0,1, or &gt;1) were identified on a uniform neuropathologic examination blinded to clinical information. Semiquantitative assessments (0 to 3) of atherosclerosis and lipohyalinosis were also performed. The associations of PIL with cerebral infarction, cerebral vessel pathology were examined using linear regression and mixed models adjusted for age, sex, &amp; education. Results: 347 subjects had both PIL and brain pathology assessed. Scores on the measure of PIL ranged from 2.1 to 5.0 (mean 3.5, SD 0.48). On postmortem examination, gross/macroscopic cerebral infarcts were found in 112 (32.28%) persons (51 with 1, 61 with &gt;1) and microinfarcts were found in 84 (24.21%) (54 with 1, 30 with &gt; 1). PIL was associated with a reduced odds of gross cerebral infarcts (estimate = 0.57, SE = 0.24, p = 0.02) and there was a trend (p = 0.096) toward an association with microinfarcts. PIL was not related to the type or severity of cerebral vessel pathology. In subsequent logistic regression models, the association of PIL with gross cerebral infarcts persisted after adjustment for depressive symptoms, BMI, smoking, diabetes, and measures of socioeconomic status. However, the association of PIL with gross infarcts was reduced to a trend (estimate = 0.46, SE = 0.26, p = 0.08) after adjustment for systolic blood pressure, suggesting partial mediation. Conclusions: Lower PIL may be a risk factor for macroscopic cerebral infarction in old age without a direct effect on atherosclerotic cerebral vessel pathology.

Vascular parkinsonism — an update

Vascular parkinsonism (VP) is a heterogeneous clinical entity. The idea of a relationship between cerebral vascular disease and parkinsonism may be traced back to the 1920s, when the diagnostic unit called “arteriosclerotic parkinsonism”, a predecessor of VP, was established. This review is concerned with historical and contemporary views regarding the possible vascular genesis of parkinsonism. Confusion persists as a result of vaguely defined diagnostic criteria. The following types of simultaneous occurrence of parkinsonism and cerebral vascular disease (CVD) may be recognised: 1. gait disorders of the lower body parkinsonism type are caused mostly by white matter lesions in the frontal lobes; such disorders may require a diagnosis of vascular origin. We suggest replacing the term “lower body parkinsonism” with a more appropriate term not including the word “parkinsonism”: an alternative term could be “cerebrovascular gait disorder”; 2. if the signs and symptoms are typical for idiopathic Parkinson's disease (IPD), the coincidence of IPD and CVD should be considered; 3. if the symptoms of parkinsonism are neither typical for IPD nor for VP, and there are clinical or MR signs of CVD, VP should be regarded as possible when alternative causes are excluded; 4. if the symptoms of parkinsonism and clinical and MR signs are typical for VP, VP should be regarded as probable; 5. if a stroke affecting the contralateral basal ganglia is followed by the occurrence of hemiparkinsonism, the diagnosis of VP is unambiguous. Vascular parkinsonism (VP) is probably one of the most frequently erroneous neurological diagnoses. The reason for this misdiagnosis is that both cerebral vascular disease (CVD) and parkinsonism usually occur at the same age. Due to the high incidence of CVD, it is possible for CVD and idiopathic Parkinson's disease (IPD) to coincide in some cases. Another reason for the misdiagnosis is that the concept of VP lacks clarity. This review aims to contribute to an improved understanding of VP in clinical practice. In this context, the term “CVD” is understood in the broad sense of a brain impairment caused by cerebral vessel pathology. It covers various concepts, as some authors use the term CVD to mean a manifestation of vascular lesions in pathologico-anatomical material or in the imaging techniques; others mean the history and clinical manifestation of cerebral ischaemia, or, more rarely, haemorrhage. The term CVD may cover large vessel disease as well as small vessel disease. This means that territorial and lacunar infarcts and white matter lesions (WML) are all considered as CVD.