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Cerebrovascular disease is the world's second major cause of mortality and disability, and the fourth major cause of mortality and disability in South Africa. Cerebrovascular disease occurs due to issues of the brain's blood supply, either the blood supply is cut off or a blood artery within the brain bursts. Radiologists have the responsibility to detect cerebrovascular disease. We now have technology which can help them to better detect this disease. Medical imaging plays an important role in detecting diseases. This study presents implementation of a detection system using artificial intelligence model, namely, convolutional neural networks to help in detecting cerebrovascular disease from magnetic resonance imaging (MRI) scans. Brain images using MRI was obtained from kaggle pub-lic dataset. Segmentation process was applied in this study to normalise images since the images came in different sizes. The effectiveness of the concept was demonstrated using a confusion matrix. The accuracy rate was plotted using the Receiver Operating Characteristics (ROC) curve. The evaluation results show that the Convolutional Neural Network (CNN) model detect cerebrovascular disease successfully with validation accu-racy rate of 90% and test accuracy rate of 80%. The training procedure could be improved by using a larger MRI dataset., IBM ETDP SITA

Background Subjective cognitive decline (SCD) has gained recent interest as a potential harbinger of neurodegenerative diseases such as Alzheimer's disease (AD) and cerebrovascular disease (CVD). In addition, SCD can be related to depressive symptomatology. However, the association between AD and CVD biomarkers, depressive symptomatology, and SCD is still unclear. We investigated the association of AD and CVD biomarkers and depressive symptomatology with SCD in individuals with subjective memory complaints (SCD-memory group) and individuals with subjective concentration complaints (SCD-concentration group). Methods We recruited a population-based cohort of 217 individuals (all aged 70 years, 53% female participants, 119 SCD-memory individuals, 23 SCD-concentration individuals, and 89 controls). AD and CVD were assessed through cerebrospinal fluid levels of the A beta 42/40 ratio and phosphorylated tau, and white matter signal abnormalities on magnetic resonance imaging, respectively. Associations between biomarkers, depressive symptomatology, and SCD were tested via logistic regression and correlation analyses. Results We found a significant association between depressive symptomatology with SCD-memory and SCD-concentration. Depressive symptomatology was not associated with AD and CVD biomarkers. Both the phosphorylated tau biomarker and depressive symptomatology predicted SCD-memory, and the A beta 42/40 ratio and depressive symptomatology predicted SCD-concentration. Conclusions The role of depressive symptomatology in SCD may differ depending on the stage within the spectrum of preclinical AD (as determined by amyloid-beta and tau positivity), and does not seem to reflect AD pathology. Our findings contribute to the emerging field of subclinical depressive symptomatology in SCD and clarify the association of different types of subjective complaints with distinct syndromic and biomarker profiles.

In recent years, increasing evidence suggests that commensal microbiota may play an important role not only in health but also in disease including cerebrovascular disease. Gut microbes impact physiology, at least in part, by metabolizing dietary factors and host-derived substrates and then generating active compounds including toxins. The purpose of this current review is to highlight the complex interplay between microbiota, their metabolites. and essential functions for human health, ranging from regulation of the metabolism and the immune system to modulation of brain development and function. We discuss the role of gut dysbiosis in cerebrovascular disease, specifically in acute and chronic stroke phases, and the possible implication of intestinal microbiota in post-stroke cognitive impairment and dementia, and we identify potential therapeutic opportunities of targeting microbiota in this context., Depto. de Farmacología y Toxicología, Depto. de Biología Celular, Fac. de Medicina, Instituto Universitario de Investigación en Neuroquímica (IUIN), TRUE, pub, APC financiada por la UCM

INTRODUCTION: High cardiorespiratory fitness (CRF) has been associated with a lower risk of depression, anxiety, and cerebrovascular disease. The aim was to explore CRF changes over-time associated with these outcomes. METHODS: This large-scale prospective cohort study, using data from Swedish population-wide registries and databases (during 1972-2020), included men (n=131,431), with measures of estimated CRF (estCRF) in late adolescence (maximal cycle test) and adulthood (submaximal cycle test) (mean years between 24.6, SD 8.8). The study explored how change in estCRF was associated with incident depression, anxiety, and cerebrovascular disease using Cox proportional hazards models. Analyses were performed in 2023. RESULTS: Higher estCRF in late adolescence and adulthood were associated with a lower risk of incident depression, anxiety, and cerebrovascular disease later in life. For all three outcomes, an increase in estCRF (mL/min/kg and z-score) between the two-time points was associated with a lower risk. Further, decreasing from moderate or high estCRF in adolescence to low estCRF in adulthood, compared to staying at a moderate or high level, was associated with a higher risk of depression and anxiety (HR: 1.24 95% CI 1.07-1.45 and 1.25 95% CI 1.06-1.49, respectively). Conversely, increasing from moderate to high estCRF was associated with a lower risk of incident anxiety (HR: 0.84 95% CI 0.71-0.99). CONCLUSIONS: The findings indicate that there is a longitudinal association between negative change in estCRF and increased risk of depression, anxiety, and cerebrovascular disease later in life. Decreasing levels of estCRF could be a helpful indicator when identifying these disorders at a population level.

In the brain, the extracellular matrix (ECM) composition shapes the neuronal microenvironment and can undergo substantial changes with cerebral pathology. Brevican is integral to the formation of the ECM's neuroprotective perineuronal nets (PNNs). Decreased brevican levels were reported in vascular dementia (VaD) but not in Alzheimer's disease (AD). However, the status of brevican in clinical cohorts with high concomitance of AD pathological burden and cerebrovascular disease (CeVD) is unclear. In this study, 32 non-cognitively impaired (NCI), 97 cognitively impaired no dementia (CIND), 46 AD, and 23 VaD participants recruited from memory clinics based in Singapore underwent neuropsychological and neuroimaging assessments, together with measurements of serum brevican. Association analyses were performed between serum brevican and neuroimaging measures of CeVDs, including white matter hyperintensities (WMHs), lacunes, cortical infarcts, and cerebral microbleeds. Using an aggregated score for CeVD burden, only CIND participants showed lower brevican levels with higher CeVD compared to those with lower CeVD burden (p = 0.006). Among the CeVD subtypes assessed, only elevated WMH burden was associated with lower brevican levels (OR = 2.7; 95% CI = 1.3-5.5). Our findings suggest that brevican deficits may play a role in early cerebrovascular damage in participants at risk of developing dementia.

BACKGROUND AND PURPOSE Resting brain tissue perfusion in cerebral steno-occlusive vascular disease can be assessed by MR imaging using gadolinium-based susceptibility contrast agents. Recently, transient hypoxia-induced deoxyhemoglobin has been investigated as a noninvasive MR imaging contrast agent. Here we present a comparison of resting perfusion metrics using transient hypoxia-induced deoxyhemoglobin and gadolinium-based contrast agents in patients with known cerebrovascular steno-occlusive disease. MATERIALS AND METHODS Twelve patients with steno-occlusive disease underwent DSC MR imaging using a standard bolus of gadolinium-based contrast agent compared with transient hypoxia-induced deoxyhemoglobin generated in the lungs using an automated gas blender. A conventional multi-slice 2D gradient echo sequence was used to acquire the perfusion data and analyzed using a standard tracer kinetic model. MTT, relative CBF, and relative CBV maps were generated and compared between contrast agents. RESULTS The spatial distributions of the perfusion metrics generated with both contrast agents were consistent. Perfusion metrics in GM and WM were not statistically different except for WM MTT. CONCLUSIONS Cerebral perfusion metrics generated with noninvasive transient hypoxia-induced changes in deoxyhemoglobin are very similar to those generated using a gadolinium-based contrast agent in patients with cerebrovascular steno-occlusive disease.

Brain changes at the end-stage of fragile X-associated tremor/ataxia syndrome (FXTAS) are largely unknown due to mobility impairment. We conducted a postmortem MRI study of FXTAS to quantify cerebrovascular disease, brain atrophy and iron content, and examined their relationships using principal component analysis (PCA). Intracranial hemorrhage (ICH) was observed in 4/17 FXTAS cases, among which one was confirmed by histologic staining. Compared with seven control brains, FXTAS cases showed higher ratings of T2-hyperintensities (indicating cerebral small vessel disease) in the cerebellum, globus pallidus and frontoparietal white matter, and significant atrophy in the cerebellar white matter, red nucleus and dentate nucleus. PCA of FXTAS cases revealed negative associations of T2-hyperintensity ratings with anatomic volumes and iron content in the white matter, hippocampus and amygdala, that were independent from a highly correlated number of regions with ICH and iron content in subcortical nuclei. Post-hoc analysis confirmed PCA findings and further revealed increased iron content in the white matter, hippocampus and amygdala in FXTAS cases compared to controls, after adjusting for T2-hyperintensity ratings. These findings indicate that both ischemic and hemorrhagic brain damage may occur in FXTAS, with the former being marked by demyelination/iron depletion and atrophy, and the latter by ICH and iron accumulation in basal ganglia.

Background: Atrial remodeling is associated with future atrial fibrillation (AF) and stroke. AF has been associated with cognitive impairment and cerebral white matter lesions. We wished to investigate the possible direct association between atrial remodeling and cerebrovascular disease in patients with and without AF documented by implantable loop recorder (ILR). Methods: Cardiac and cerebral magnetic resonance imaging were acquired in a cross-sectional study, including participants ≥70 years of age with stroke risk factors without known AF. Cerebrovascular disease was visually rated using the Fazekas scale and number of lacunar strokes. Left atrial (LA) and ventricular volumes and function were analyzed. Associations between atrial remodeling and cerebrovascular disease were assessed with logistic regression models. The analyses were stratified according to sinus rhythm or any AF during 3 months of continuous ILR monitoring to account for subclinical AF. Results: Of 200 participants investigated, 87% had a Fazekas score ≥1 and 45% had ≥1 lacunar infarct. Within 3 months of ILR monitoring, AF was detected in 28 (14%) participants. For participants with sinus rhythm (n = 172), lower LA passive emptying fraction was associated with Fazekas score after multivariable adjustment (OR [95% CI]: 0.51 [0.27; 0.86] p = 0.02), and increased LA maximum (OR [95% CI]: 1.38 [1.07; 1.82] p = 0.01) and minimum volumes (OR [95% CI]: 1.48 [1.03; 2.17] p = 0.04) were associated with lacunar infarcts. There were no significant associations in patients with AF. Conclusion: In AF-free patients, as documented by ILR monitoring, we found an independent association between LA passive emptying fraction and Fazekas score and between atrial volumes and lacunar infarcts.

The respiratory virus SARS-CoV-2, responsible for the multi-system illness known as COVID-19 and resulting global pandemic of 2020, is increasingly recognized  for its ability to cause cerebrovascular complications. This series of four cases from a single institution during the height of the pandemic is presented to illustrate the virus’s uniquely diverse pathophysiology and corresponding clinical and radiologic manifestations. As no neurologic manifestation specific to SARS-CoV-2 has been identified, it remains of upmost importance that clinicians and radiologists alike maintain a high index of suspicion for these complications, especially when neurological findings present in the young or otherwise atypical demographics.

Pituitary adenomas (PAs) have been shown to cause excess cardiovascular disease comorbidity and mortality. Cerebrovascular disease (CeVD) is a small subset of cardiovascular disease with high morbidity, and its risk in patients with pituitary adenomas has been sparingly explored. In this review, we examine what is known about the prevalence of cerebrovascular disease in patients with PAs, from its initial discovery in 1970 to present. An abundance of literature describes increased cerebrovascular mortality in patients with acromegaly, while research on other PA subtypes is less frequent but shows a similarly elevated CeVD mortality relative to healthy populations. We also review how cerebrovascular risk changes after PAs are treated, with PA treatment appearing to prevent further accumulation of cerebrovascular risk without reversing prior elevations. While acromegaly-associated CeVD appears to be caused by elevated growth hormone (GH) levels and Cushing disease's elevated glucocorticoids similarly cause durable alterations in cerebrovascular structure and function, less is known about the mechanisms behind CeVD in other PA subpopulations. Proposed pathophysiologies include growth hormone deficiency inducing vessel wall damage or other hormone deficits causing increased atherosclerotic disease. Early diagnosis and treatment of PAs may be the key to minimizing lifetime CeVD risk elevations. More research is needed to better understand the mechanisms behind the increased CeVD seen in patients with PAs. Physicians caring for PA patients must remain vigilant for signs and symptoms of cerebrovascular disease in this patient population.

Marta Almeria,1,2 Ignacio Alvarez,2 Jessica Molina-Seguin,1 Sarah Besora,1 Mariateresa Buongiorno,1,2 Silvia Romero,1 Laura Casas,1 Cristina Cano,2 Judith Castejon,2 Sonia Arribas,2 Jerzy Krupinski1,3 1Departament de Neurologia, Fundació Assistencial Hospital Universitari MútuaTerrassa, Terrassa, Barcelona, Spain; 2Fundació per a la Recerca Biomèdica i Social MútuaTerrassa, Terrassa, Barcelona, Spain; 3Healthcare Sciences, Manchester Metropolitan University, Manchester, UKCorrespondence: Marta Almeria, Fundació Assistencial Hospital Universitari MútuaTerrassa, Departament de Neurologia, plaça dels drets humans n 1 (planta -3, despatx. 324), Terrassa, Barcelona, 08222, Spain, Tel +34 937365050, Email malmeria@mutuaterrassa.catIntroduction: Neuroprotective drugs such as citicoline could improve cognitive performance and quality of life. We studied the effect of citicoline treatment and its association with Vascular Risk Factors (VRF) and APOE on cognition in patients with Subjective Cognitive Complaints (SCC) and Mild Cognitive Impairment (MCI).Methods: This is an observational and prospective study with citicoline during 12 months follow-up. Eighty-one subjects who met criteria for SCC/MCI, aged 50– 75 years with VRF were included and prescribed citicoline 1g/day. Subjects with previous cognitive impairment and any other central nervous system affection were excluded. Wilcoxon Signed Ranks test and paired samples t-test were used to analyze the change in neuropsychological performance.Results: Mean age of the sample was 68.2 (SD 6.8) years and 26 (32.09%) were females. Fifteen subjects (24.6%) were APOE-ϵ4 carriers, fifty-six (76.7%) had hypertension, fifty-eight (79.5%) had dyslipidemia, twenty-one (28.8%) had diabetes mellitus and twenty-six (35.6%) had cardiopathy. Thirty-two (43.8%) subjects were diagnosed as SCC and forty-one (56.16%) as MCI. During the follow-up, Tweny-six patients (81.25%) in the group of SCC remained stable, six subjects (

Wenhong Chen,1 Yunping Chen,2 Wenjuan Ye,3 Ting Wang1 1Department of Pediatric Neurology, Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 2Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 3Department of Pediatric, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of ChinaCorrespondence: Ting Wang, Department of Pediatric Neurology, Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, 745 Wuluo Road, Hongshan District, Wuhan, Hubei, People’s Republic of China, Tel +86-27-87169308, Email 67722896@qq.comPurpose: The study aims to identify the characteristics of SSR in patients with AICVD and their correlation with clinical presentations.Methods: SSR of the upper limbs, the National Institute of Health stroke scale (NIHSS), the Barthel index (BI), the Essen stroke risk score (ESRS), and imaging examinations, was evaluated in 30 healthy subjects and 66 patients with AICVD. All results were recorded and analyzed via Statistical Package for the Social Sciences (SPSS 22.0) software. t-test and Spearman rank correlation were used.Results: Compared to the control group, SSR of upper limbs in patients with AICVD showed prolonged latency, reduced amplitude, and disappeared waveform (p=0.000, p=0.015, p=0.004), No statistically significant difference was observed between the affected side and the healthy side (p=0.068, p=0.661). In the case group, the higher the abnormal rate of SSR, the more severe the neurological impairment (NIHSS and ADL scores) and the worse the long-term prognosis. Specific results are as follows: Firstly, the total abnormality rate of SSR, prolonged SSR latency were positively related to the NIHSS, also the ES

Ana Paula Mafla-Mendoza,1,* Esteban David Paredes-Urbano,1,* Enrique Gea-Izquierdo1– 3 1Pontifical Catholic University of Ecuador, Faculty of Medicine, Quito, Ecuador; 2Department of Medical Specialties and Public Health, Rey Juan Carlos University, Madrid, Spain; 3María Zambrano Program, European Union, Rey Juan Carlos University, Madrid, Spain*These authors contributed equally to this workCorrespondence: Enrique Gea-Izquierdo, Pontifical Catholic University of Ecuador, Faculty of Medicine, Quito, Ecuador, Email enriquegea@yahoo.esBackground and Objective: Stroke is one of the most frequent neurological syndromes in the adult population and the cause of 10% of all diagnosed epilepsies. It is attributed to the origin of up to 50% of them in adults > 60 years of age. Although a few risk factors have been described and considered when modeling predictive tools, this aspect is still clinically complex. The objective of this study is to describe and compare predictor scales of post stroke epilepsy (PSE) in adult patients with better performance.Methods: A systematic review and meta-analysis were performed of studies published between 2010 and 2020 and found in PubMed, Scopus, EMBASE, LILACS, BVS, Google Scholar, and CENTRAL databases. Sixteen studies were included with a total of 298,694 patients with a diagnosis of stroke, 5590 presented late seizures (LS).Results: Hemorrhage, cortical involvement, and early seizure were the elements most associated with the risk of presenting late seizures. The SeLECT score demonstrated a low risk of bias with a high predictive ability in patients with ischemic stroke (AUC: 0.77 [95% CI: 0.71– 0.82]). In patients with hemorrhagic stroke, the CAVE score demonstrated adequate predictive ability (AUC: 0.81 [95% CI: 0.76– 0.86]), but an uncertain risk of bias. Research has established risk factors for post ictal epilepsy; however, the numerous ways of assessing data in studies and the difference in their

Background: Low birth weight is associated with an increased risk of adulthood cerebrovascular disease (CVD). Not much is known about effects of early childhood growth. We studied whether the risk of adult CVD is associated with growth or nutritional factors during early childhood. Methods: Within the Northern Finland Birth Cohort 1966, 11 991 persons were followed from birth to 52 years of age. CVD diagnoses were extracted from national hospital and death registers with diagnostic coding based on the World Health Organization recommendations. Cox proportional hazard models were used to estimate associations of childhood growth variables, growth trajectories (by Latent Class Growth Modeling), and nutritional factors with adult CVD, for example, ischemic and hemorrhagic strokes. The analyses were adjusted for childhood socioeconomic status and birth weight. Results: A total of 453 (3.8%) CVDs were recorded during follow-up. Among females, groups with low early childhood weight and height had an increased risk for adulthood ischemic CVDs, with an adjusted hazard ratio of 1.97 (95% CI, 1.21–3.20) and 2.05 (CI, 1.11–3.81), respectively. In addition, females with body mass index over 1 SD at body mass index rebound had an increased risk for ischemic CVDs (adjusted hazard ratio, 1.90 [CI, 1.19–3.04]) compared with females with body mass index −1 to +1 SD. These associations were not found among males. Conclusions: The findings suggest that timing of weight gain during childhood is of significance for development of CVD risk among females.

Cerebrovascular disease is associated with symptoms and pathogenesis of Alzheimers disease (AD) among adults with Down syndrome (DS). The cause of increased dementia-related cerebrovascular disease in DS is unknown. We explored whether protein markers of neuroinflammation are associated with markers of cerebrovascular disease among adults with DS. Participants from the Alzheimers disease in Down syndrome (ADDS) study with magnetic resonance imaging (MRI) scans and blood biomarker data were included. Support vector machine (SVM) analyses examined the relationship of blood-based proteomic biomarkers with MRI-defined cerebrovascular disease among participants characterized as having cognitive decline (n = 36, mean age ± SD = 53 ± 6.2) and as being cognitively stable (n = 78, mean age = 49 ± 6.4). Inflammatory and AD markers were associated with cerebrovascular disease, particularly among symptomatic individuals. The pattern suggested relatively greater inflammatory involvement among cognitively stable individuals and greater AD involvement among those with cognitively decline. The findings help to generate hypotheses that both inflammatory and AD markers are implicated in cerebrovascular disease among those with DS and point to potential mechanistic pathways for further examination.

We determined the extent to which obstructive sleep apnea (OSA) is associated with increased cerebrovascular disease and amyloid burden, and the relation of the two processes across clinical Alzheimers disease (AD) diagnostic groups in adults with Down syndrome (DS). Adults with DS from the Biomarkers of Alzheimers Disease in Down Syndrome (ADDS) study were included given available research MRI (n = 116; 50 ± 8 years; 42% women) and amyloid PET scans (n = 71; 50 ± 7 years; 39% women) at the time of analysis. Participants were characterized as cognitively stable (CS; 64%), with mild cognitive impairment-DS (MCI-DS; 23%), with possible AD dementia (5%), or with definite AD dementia (8%). OSA was determined via medical records and interviews. Models tested the effect of OSA on MRI-derived cerebrovascular biomarkers and PET-derived amyloid burden, and the moderating effect of OSA and AD diagnosis on biomarkers. OSA was reported in 39% of participants, which did not differ by clinical AD diagnostic group. OSA was not associated with cerebrovascular biomarkers but was associated with greater cortical amyloid burden. White matter hyperintensity (WMH) volume (primarily in the parietal lobe), enlarged perivascular spaces, and cortical and striatal amyloid burden were greater across clinical AD diagnostic groups (CS

BACKGROUND AND PURPOSE: Lewy body dementia (LBD), including dementia with Lewy bodies (DLB) and Parkinson's disease dementia, is a common form of neurodegenerative dementia. The frequency and influence of comorbid cerebrovascular disease is not understood but has potentially important clinical management implications. METHODS: A systematic literature search was conducted (MEDLINE and Embase) for studies including participants with DLB and/or Parkinson's disease dementia assessing cerebrovascular lesions (imaging and pathological studies). They included white matter changes, cerebral amyloid angiopathy, cerebral microbleeds (CMB), macroscopic infarcts, microinfarcts and intracerebral haemorrhage. RESULTS: Of 4411 articles, 63 studies were included. Cerebrovascular lesions commonly studied included white matter changes (41 studies) and CMB (18 studies). There was an increased severity of white matter changes on magnetic resonance imaging (visualized as white matter hyperintensities), but not neuropathology, in LBD compared to Parkinson's disease without dementia and age-matched controls. CMB prevalence in DLB was highly variable but broadly similar to Alzheimer's disease (0%-48%), with a lobar predominance. No relationship was found between large cortical or small subcortical infarcts or intracerebral haemorrhage and the presence of LBD. CONCLUSION: The underlying mechanisms of white matter hyperintensities in LBD require further exploration, as their increased severity in LBD was not supported by neuropathological examination of white matter. CMB in LBD had a similar prevalence to Alzheimer's disease. There is a need for larger studies assessing the influence of cerebrovascular lesions on clinical symptoms, disease progression and outcomes.

Purpose: Practical suggestions on clinical decisions about vascular disease management in patients with cognitive impairment are proposed. Methods: The document was produced by the Dementia Committee of the European Stroke Organisation (ESO) based on the evidence from the literature where available and on the clinical experience of the Committee members. This paper was endorsed by the ESO. Findings: Vascular risk factors and cerebrovascular disease are frequent in patients with cognitive impairment. While acute stroke treatment has evolved substantially in last decades, evidence of management of cerebrovascular pathology beyond stroke in patients with cognitive impairment and dementia is quite limited. Additionally, trials to test some daily-life clinical decisions are likely to be complex, difficult to undertake and take many years to provide sufficient evidence to produce recommendations. This document was conceived to provide some suggestions until data from field trials are available. It was conceived for the use of clinicians from memory clinics or involved specifically in cognitive disorders, addressing practical aspects on diagnostic tools, vascular risk management and suggestions on some therapeutic options. Discussion and conclusions: The authors did not aim to do an exhaustive or systematic review or to cover all current evidence. The document approach in a very practical way frequent issues concerning cerebrovascular disease in patients with known cognitive impairment.

Purpose Many daily-life clinical decisions in patients with cerebrovascular disease and cognitive impairment are complex. Evidence-based information sustaining these decisions is frequently lacking. The aim of this paper is to propose a practical clinical approach to cognitive impairments in patients with known cerebrovascular disease. Methods The document was produced by the Dementia Committee of the European Stroke Organisation (ESO), based on evidence from the literature where available and on the clinical experience of the Committee members. This paper was endorsed by the ESO. Findings Many patients with stroke or other cerebrovascular disease have cognitive impairment, but this is often not recognized. With improvement in acute stroke care, and with the ageing of populations, it is expected that more stroke survivors and more patients with cerebrovascular disease will need adequate management of cognitive impairment of vascular etiology. This document was conceived for the use of strokologists and for those clinicians involved in cerebrovascular disease, with specific and practical hints concerning diagnostic tools, cognitive impairment management and decision on some therapeutic options. Discussion and conclusions: It is essential to consider a possible cognitive deterioration in every patient who experiences a stroke. Neuropsychological evaluation should be adapted to the clinical status. Brain imaging is the most informative biomarker concerning prognosis. Treatment should always include adequate secondary prevention.

ObjectivesCerebrovascular disease has increasingly been linked to overall vascular health. Pathologic conditions like diabetes, hypertension, and kidney disease have been shown to affect brain health and cerebrovascular and nervous systems. Acute kidney injury (AKI) and chronic Kidney Disease (CKD) represent a variety of vascular insults that can adversely affect cerebral health. Hypertension, fluctuations in blood pressure, and diabetic vasculopathy are known risk factors for cerebrovascular disease associated with CKD. Other emerging areas of interest include endothelial dysfunction, vascular calcification due to calcium and phosphorus metabolism dysregulation, and uremic neuropathy present the next frontier of investigation in CKD and cerebrovascular health.MethodsIt has become apparent that the interrelation of AKI and CKD with vascular health, chemical homeostasis, and hormonal regulation upset many aspects of cerebral health and functioning. Stroke is an obvious connection, with CKD patients demonstrating a higher proclivity for cerebrovascular accidents. Cerebral bleeding risk, uremic neuropathies, sodium dysregulation with impacts on nervous system, vascular calcification, and endothelial dysfunction are the next salient areas of research that are likely to reveal key breakthroughs in renal-cerebral pathophysiology.ResultsIn this review nephrological definition are discussed in a neuro-centric manner, and the areas of key overlap between CKD and cerebrovascular pathology are discussed. The multifaceted effects of renal function on the health of the brain are also examined.ConclusionThis review article aims to create the background for ongoing and future neurological-nephrological collaboration on understanding the special challenges in caring for patients with cerebrovascular disease who also have CKD.

Background and purpose: For prevention of cerebrovascular diseases at younger age, it is important to understand the risk factors occurring early in life. We investigated the relationship between mothers’ general health during pregnancy and the offspring’s risk of cerebrovascular disease in age of 15 to 52 years. Methods: Within the population-based prospective Northern Finland Birth Cohort 1966, 11,926 persons were followed from antenatal period to 52 years of age. Information on their mother’s ill health conditions, i.e., hospitalizations, chronic diseases, medications, vitamin or iron supplement, fever, anemia, mood, and smoking was collected from 24th gestational week onwards. Ischemic and hemorrhagic cerebrovascular diseases of the offspring were identified from national registers in Finland. Cox proportional hazard models were used to estimate the association of mother’s health conditions with incidence of cerebrovascular disease in the offspring, with adjustments for potential confounders. Results: During 565,585 person-years of follow-up, 449 (2.8%) of the offspring had a cerebrovascular disease. Hospitalization during pregnancy was associated with an increased risk of cerebrovascular disease in the offspring (hazard ratio (HR) = 1.49; 95% confidence interval (CI) 1.06–2.08) after adjustment for confounders, as was having more than three ill health conditions (HR = 1.89; CI 1.14–3.11). Not using vitamin or iron supplement was associated with increased risk for cerebrovascular disease in the offspring (HR = 1.39; CI 1.01–1.89). Conclusions: The results suggest that the risk of cerebrovascular disease may start as early as during the antenatal period, and the health characteristics of mothers during pregnancy may play a role in cerebrovascular disease risk of the offspring.

Background and Purpose: For prevention of cerebrovascular diseases, it is important to understand the risk factors occurring early in life. The aim was to investigate the relationship of maternal and offspring anthropometrics and pregnancy complications with offspring’s risk of ischemic and hemorrhagic stroke and transient ischemic attack in adulthood. Methods: Within the population-based prospective Northern Finland Birth Cohort 1966, 11 991 persons were followed from early pregnancy to 52 years of age. Information on pregnancy and birth complications were collected starting between 24th and 28th gestational week and at birth. Ischemic and hemorrhagic strokes of the offspring were identified from national registers in Finland. Cox proportional hazard models were used to estimate the association of pregnancy and birth complications with incidence of cerebrovascular disease in the offspring, with adjustments for sex, family socioeconomic status, mother’s age, and smoking during pregnancy. Results: During 568 821 person-years of follow-up, 453 (3.8%) of the offspring had a stroke or transient ischemic attack. Small and large gestational weight gain among normal weight mothers were associated with increased ischemic stroke risk in offspring (adjusted hazard ratio [aHR], 1.93 [95% CI, 1.28–2.90] and aHR, 1.54 [95% CI, 1.02–2.31], respectively). Small birth weight for gestational age and small ponderal index were associated with increased risk for ischemic stroke (aHR, 1.95 [CI, 1.21–3.13] and aHR, 1.36 [CI, 1.04–1.77], respectively). Threatening miscarriage was also associated with increased risk of any stroke (aHR, 1.64 [CI 1.14–2.37]). Maternal smoking, hypertension, or birth complications were not associated with increased risk of cerebrovascular disease in the offspring. Conclusions: The results of this study suggest that disturbances in maternal and fetal growth during pregnancy may predispose offspring to developing cerebrovascular diseases in adulthood.

Background:Quantifying the contribution of cerebrovascular disease to the clinical and pathological profile of Alzheimer’s disease is challenging. Objective:We aimed to determine the influence of cerebrovascular disease, amyloid-β (Aβ), and their comorbidity on cognitive decline, hippocampal atrophy, and Aβ deposition, by evaluating data from the Australian Imaging, Biomarker and Lifestyle Study of Ageing. Methods:Two-hundred and eighteen participants underwent Aβ PET, MRI, and cognitive assessment at 18-month intervals for up to 90 months. Aβ status was determined on baseline PET. Participants were also classified as V+ on baseline MRI if they had≥1 large cortical infarcts, subcortical infarcts, or cortical cerebral microinfarcts; or white matter hyperintensity volume greater than the 90th percentile of healthy controls. Linear mixed models were conducted comparing slopes of change in cognition, hippocampal volume, and Aβ load between the four resultant groups. Results:Mean age at baseline was 74 years (range 59–96). One-hundred and fifteen participants were cognitively normal, 54 had mild cognitive impairment, and 49 had Alzheimer’s disease. Compared to the Aβ-/V- group, the Aβ+/V- and Aβ+/V+ groups showed significantly faster cognitive decline and hippocampal atrophy over 90 months. V+ status was associated with greater cognitive decline (Cohen’s d = 0.85, p < 0.001) and hippocampal atrophy (d = 2.05, p < 0.001) in the Aβ+ group but not in the Aβ- group. V+ status was not associated with Aβ accumulation in any group. Conclusion:Comorbidity of cerebrovascular disease and Aβ was associated with cognitive decline and neurodegeneration. Cerebrovascular disease was not associated with the rate of Aβ accumulation.

We examined whether cognitive reserve (CR) impacts level of, or rate of change in, biomarkers of Alzheimer's disease (AD) and small-vessel cerebrovascular disease in >250 individuals who were cognitively normal and middle-aged and older at the baseline. The four primary biomarker categories commonly examined in studies of AD were measured longitudinally: cerebrospinal fluid measures of amyloid (A) and tau (T); cerebrospinal fluid and neuroimaging measures of neuronal injury (N); and neuroimaging measures of white matter hyperintensities (WMHs) to assess cerebrovascular pathology (V). CR was indexed by a composite score including years of education, reading, and vocabulary test performance. Higher CR was associated with lower levels of WMHs, particularly among those who subsequently progressed from normal cognition to MCI. CR was not associated with WMH trajectories. In addition, CR was not associated with either levels of, or rate of change in, A/T/N biomarkers. This may suggest that higher CR is associated with lifestyle factors that reduce levels of cerebrovascular disease, allowing individuals with higher CR to better tolerate other types of pathology.

Elevated low-density lipoprotein-cholesterol (LDL-C) is a causal factor for the development of atherosclerotic cardiovascular disease (ASCVD); accordingly, LDL-C lowering is associated with a decreased risk of progression of atherosclerotic plaques and development of complications. Currently, statins play a central role in any ASCVD management and prevention strategies, in relation to their lipid-lowering action and potentially to pleiotropic effects. After coronary artery disease, stroke is the most frequent cause of ASCVD mortality and the leading cause of acquired disability, a major public health problem. There is often a tendency to aggregate all types of stroke (atherothrombotic, cardioembolic, and haemorrhagic), which have, however, different causes and pathophysiology, what may lead to bias when interpreting the results of the studies. Survivors of a first atherothrombotic ischemic stroke are at high risk for coronary events, recurrent stroke, and vascular death. Although epidemiological studies show a weak relationship between cholesterol levels and cerebrovascular disease as a whole compared with other ASCVD types, statin intervention studies have demonstrated a decrease in the risk of stroke in patients with atherosclerosis of other territories and a decrease in all cardiovascular events in patients who have had a stroke. The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial demonstrated the benefit of high doses of atorvastatin in the secondary prevention of ischemic stroke. In this review, we discuss the evidence, use and recommendations of statins in the primary and secondary prevention of stroke, and their role in other scenarios such as the acute phase of ischemic stroke, cerebral hemorrhage, cardioembolic stroke, small vessel disease, and cognitive impairment.

Mingming Fu,1,&ast; Junfei Guo,2,&ast; Yuqi Zhao,1 Yaqian Zhang,1 Yingze Zhang,2– 4 Zhiqian Wang,1 Zhiyong Hou2,3 1Department of Geriatric Orthopedics, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 2Department of Orthopaedic Surgery, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050051, People’s Republic of China; 3NHC Key Laboratory of Intelligent Orthopeadic Equipment (The Third Hospital of Hebei Medical University), Shijiazhuang, Hebei, 050051, People’s Republic of China; 4Chinese Academy of Engineering, Beijing, 100088, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Zhiqian WangDepartment of Geriatric Orthopedics, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050051, People’s Republic of ChinaEmail w18533112890@163.comZhiyong HouDepartment of Orthopaedic Surgery, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050051, People’s Republic of ChinaEmail drzyhou@gmail.comPurpose: Limited information exists on fall-related fractures in older adults with cerebrovascular disease. This study aimed to determine the characteristics of older adults with cerebrovascular disease who sustained fall-related fractures and identify the associated risk factors for perioperative complications.Patients and Methods: This was a cross-sectional study, which included patients with cerebrovascular disease who sustained fractures between Jan. 2017 and Dec. 2019. The collected data included demographics (age and gender), time and place of fracture occurrence, mechanism of injury, fracture location, type of cerebrovascular disease, complications, and comorbidities.Results: A total of 768 patients with 815 fractures were included; there were 253 males and 515 females, with an average age of 78.3 years. For either males or females, 80– 84 years was the most commonly involved age group. Most (61.0%) patie

Background: Coronary bypass artery grafting (CABG) has a higher procedural risk of stroke than percutaneous coronary intervention (PCI), but may offer better long-term survival. The optimal revascularization strategy for patients with prior cerebrovascular disease (CEVD) remains unclear. Methods and results: The SYNTAXES study assessed the vital status out to 10 year of patients with three-vessel disease and/or left main coronary artery disease enrolled in the SYNTAX trial. The relative efficacy of PCI vs. CABG in terms of 10 year all-cause death was assessed according to prior CEVD. The primary endpoint was 10 year all-cause death. The status of prior CEVD was available in 1791 (99.5%) patients, of whom 253 patients had prior CEVD. Patients with prior CEVD were older and had more comorbidities (medically treated diabetes, insulin-dependent diabetes, metabolic syndrome, peripheral vascular disease, chronic obstructive pulmonary disease, impaired renal function, and congestive heart failure), compared with those without prior CEVD. Prior CEVD was an independent predictor of 10 year all-cause death (adjusted HR: 1.35; 95% CI: 1.04–1.73; p = 0.021). Patients with prior CEVD had a significantly higher risk of 10 year all-cause death (41.1 vs. 24.1%; HR: 1.92; 95% CI: 1.54–2.40; p < 0.001). The risk of 10 year all-cause death was similar between patients receiving PCI or CABG irrespective of the presence of prior CEVD (p-interaction = 0.624). Conclusion: Prior CEVD was associated with a significantly increased risk of 10 year all-cause death which was similar in patients treated with PCI or CABG. These results do not support preferential referral for PCI rather than CABG in patients with prior CEVD. Trial registration: SYNTAX: ClinicalTrials.gov reference: NCT00114972. SYNTAX Extended Survival: ClinicalTrials.gov reference: NCT03417050. Graphic abstract: [Figure not available: see fulltext.].

OBJECTIVE To determine whether a history of cerebrovascular disease (CVD) increases risk of severe coronavirus disease 2019 (COVID-19). METHODS In a retrospective multicenter study, we retrieved individual data from in-patients treated March 1 to April 15, 2020 from COVID-19 registries of three hospitals in Saxony, Germany. We also performed a systematic review and meta-analysis following PRISMA recommendations using PubMed, EMBASE, Cochrane Library databases and bibliographies of identified papers (last search on April 11, 2020) and pooled data with those deriving from our multicenter study. Of 3762 records identified, 11 eligible observational studies of laboratory-confirmed COVID-19 patients were included in quantitative data synthesis. Risk ratios (RR) of severe COVID-19 according to history of CVD were pooled using DerSimonian and Laird random effects model. Between-study heterogeneity was assessed using Cochran's Q and I2-statistics. Severity of COVID-19 according to definitions applied in included studies was the main outcome. Sensitivity analyses were conducted for clusters of studies with equal definitions of severity. RESULTS Pooled analysis included data from 1906 laboratory-confirmed COVID-19 patients (43.9% females, median age ranging from 39 to 76 years). Patients with previous CVD had higher risk of severe COVID-19 than those without [RR 2.07, 95% confidence interval (CI) 1.52-2.81; p < 0.0001]. This association was also observed in clusters of studies that defined severe manifestation of the disease by clinical parameters (RR 1.44, 95% CI 1.22-1.71; p < 0.0001), necessity of intensive care (RR 2.79, 95% CI 1.83-4.24; p < 0.0001) and in-hospital death (RR 2.18, 95% CI 1.75-2.7; p < 0.0001). CONCLUSION A history of CVD might constitute an important risk factor of unfavorable clinical course of COVID-19 suggesting a need of tailored infection prevention and clinical management strategies for this population at risk.

Radboud University, 28 juni 2022, Promotores : Thijssen, D.H.J., Leeuw, H.F. de, Schoon, Y. Co-promotor : Warle, M.C., Item does not contain fulltext

Accurate quantification of cerebral blood flow (CBF) is essential for the diagnosis and assessment of cerebrovascular diseases such as Moyamoya, carotid stenosis, aneurysms, and stroke. Positron emission tomography (PET) is currently regarded as the gold standard for the measurement of CBF in the human brain. PET imaging, however, is not widely available because of its prohibitive costs, use of ionizing radiation, and logistical challenges, which require a co-localized cyclotron to deliver the 2 min half-life Oxygen-15 radioisotope. Magnetic resonance imaging (MRI), in contrast, is more readily available and does not involve ionizing radiation. In this study, we propose a multi-task learning framework for brain MRI-to-PET translation and disease diagnosis. The proposed framework comprises two prime networks: (1) an attention-based 3D encoder-decoder convolutional neural network (CNN) that synthesizes high-quality PET CBF maps from multi-contrast MRI images, and (2) a multi-scale 3D CNN that identifies the brain disease corresponding to the input MRI images. Our multi-task framework yields promising results on the task of MRI-to-PET translation, achieving an average structural similarity index (SSIM) of 0.94 and peak signal-to-noise ratio (PSNR) of 38dB on a cohort of 120 subjects. In addition, we show that integrating multiple MRI modalities can improve the clinical diagnosis of brain diseases., Comment: 7 pages, 6 figures

Contains fulltext : 220510.pdf (Publisher’s version ) (Closed access), Apathy is a reduction in motivated goal-directed behavior (GDB) that is prevalent in cerebrovascular disease, providing an important opportunity to study the mechanistic underpinnings of motivation in humans. Focal lesions, such as those seen in stroke, have been crucial in developing models of brain regions underlying motivated behavior, while studies of cerebral small vessel disease (SVD) have helped define the connections between brain regions supporting such behavior. However, current lesion-based models cannot fully explain the neurobiology of apathy in stroke and SVD. To address this, we propose a network-based model which conceptualizes apathy as the result of damage to GDB-related networks. A review of the current evidence suggests that cerebrovascular disease-related pathology can lead to network changes outside of initially damaged territories, which may propagate to regions that share structural or functional connections. The presentation and longitudinal trajectory of apathy in stroke and SVD may be the result of these network changes. Distinct subnetworks might support cognitive components of GDB, the disruption of which results in specific symptoms of apathy. This network-based model of apathy may open new approaches for investigating its underlying neurobiology, and presents novel opportunities for its diagnosis and treatment.

This dissertation aims to investigate how advanced imaging techniques can improve diagnosis, prognostication and treatment delivery in patients with cerebrovascular disease. Six original publications are presented in which perfusion imaging and new software algorithms are used to address clinical need in two specific cerebrovascular disease entities: acute ischemic stroke (AIS) and dural arteriovenous fistulas (DAVFs). AIS patients with anterior circulation large vessel occlusions (LVO) can be successfully treated with mechanical thrombectomy. Patient triage to thrombectomy requires identification of an LVO, the target of therapy, as well as the likelihood of benefit from reperfusion and the potential risk of complication. This assessment must be accurate, fast and efficient since stroke is a time-critical emergency. This poses a challenge for stroke centres because an increasing number of patients are being screened since extension of the thrombectomy window to 24 hours. Additionally, non-tertiary level hospitals are now required to perform acute stroke imaging despite lacking around-the-clock neuroradiology expertise. The first four publications explore how perfusion imaging and automated software algorithms can be used to expedite triage while maintaining high diagnostic accuracy for identifying patients who are likely to benefit from treatment. The first study introduces and describes a new fully-automated deterministic software algorithm for detecting LVOs on computed tomography (CT) angiography, then validates it in a large cohort of 926 AIS patients that was enriched for LVOs. The algorithm had high sensitivity (97%) and moderate specificity (74%) for detecting LVOs. The second study then applied this algorithm to a consecutive cohort of 477 “code stroke” patients presenting to a large regional hospital, with the aim of field testing it in the real world clinical setting where automated LVO detection tools are most likely to be used. The high sensitivity (94%

Elevated blood pressure (BP) level is one of the most consistently identified risk factors for silent brain disease. BP values obtained at the proximal segment of the aorta (central BP) are more directly involved than brachial BP in the pathogenesis of cardiovascular disease. However, the association between central BP and silent cerebrovascular disease has not been clearly established. Participants in the CABL (Cardiovascular Abnormalities and Brain Lesions) study (n=993; mean age, 71.7±9.3 years; 37.9% men) underwent 2-dimensional echocardiography, arterial wave reflection analysis for determination of central BPs, and brain magnetic resonance imaging. Central BPs were calculated from the radial pulse waveform. Subclinical silent cerebrovascular disease was defined as silent brain infarction and white matter hyperintensity volume. Both brachial (P=0.014) and central pulse pressure (P=0.026) were independently associated with silent brain infarctions after adjustment for clinical variables, but not adjusting for each other. None of the brachial BP values was associated with upper quartile of white matter hyperintensity volume in multivariable analysis. Both central systolic BP (P<0.001) and central pulse pressure (P<0.001) were significantly associated with upper quartile of white matter hyperintensity volume in multivariable analysis, even after adjustment for brachial BP. In a predominantly older population-based cohort, both brachial and central pulse pressure were independently associated with silent brain infarction. However, higher central systolic BP and central pulse pressure, but not brachial BP, were significantly associated with white matter hyperintensity volume.

ObjectiveAdults with Down syndrome (DS) develop Alzheimer disease (AD) pathology by their 5th decade. Compared with the general population, traditional vascular risks in adults with DS are rare, allowing examination of cerebrovascular disease in this population and insight into its role in AD without the confound of vascular risk factors. We examined in vivo magnetic resonance imaging (MRI)-based biomarkers of cerebrovascular pathology in adults with DS, and determined their cross-sectional relationship with age, beta-amyloid pathology, and mild cognitive impairment or clinical AD diagnostic status.MethodsParticipants from the Biomarkers of Alzheimer's Disease in Down Syndrome study (n = 138, 50 ± 7 years, 39% women) with MRI data and a subset (n = 90) with amyloid positron emission tomography (PET) were included. We derived MRI-based biomarkers of cerebrovascular pathology, including white matter hyperintensities (WMH), infarcts, cerebral microbleeds, and enlarged perivascular spaces (PVS), as well as PET-based biomarkers of amyloid burden. Participants were characterized as cognitively stable (CS), mild cognitive impairment-DS (MCI-DS), possible AD dementia, or definite AD dementia based on in-depth assessments of cognition, function, and health status.ResultsThere were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life. There was a monotonic increase in WMH volume, enlarged PVS, and presence of infarcts across diagnostic groups (CS < MCI-DS < possible AD dementia < definite AD dementia). Higher amyloid burden was associated with a higher likelihood of an infarct.InterpretationThe findings highlight the prevalence of cerebrovascular disease in adults with DS and add to a growing body of evidence that implicates cerebrovascular disease as a core feature of AD and not simply a comorbidity. ANN NEUROL 2020;88:1165-1177.

[Abstract] Introduction: There is little control of cardiovascular (CV) risk factors in secondary prevention after an ischaemic stroke, in part due to a lack of adherence to treatment. The CV polypill may contribute to proper treatment adherence, which is necessary for CV disease prevention. This study aimed to establish how and in what cases the CV polypill should be administered. Methods: A group of 8 neurologists drafted consensus recommendations using structured brainstorming and based on their experience and a literature review. Results: These recommendations are based on the opinion of the participating experts. The use of the CV polypill is beneficial for patients, healthcare professionals, and the health system. Its use is most appropriate for atherothrombotic stroke, lacunar stroke, stroke associated with cognitive impairment, cryptogenic stroke with CV risk factors, and silent cerebrovascular disease. It is the preferred treatment in cases of suspected poor adherence, polymedicated patients, elderly people, patients with polyvascular disease or severe atherothrombosis, young patients in active work, and patients who express a preference for the CV polypill. Administration options include switching from individual drugs to the CV polypill, starting treatment with the CV polypill in the acute phase in particular cases, use in patients receiving another statin or an angiotensin ii receptor antagonist, or de novo use if there is suspicion of poor adherence. Nevertheless, use of the CV polypill requires follow-up on the achievement of the therapeutic objectives to make dose adjustments. Conclusions: This document is the first to establish recommendations for the use of the CV polypill in cerebrovascular disease, beyond its advantages in terms of treatment adherence., [Resumen] Introducción. El control de los factores de riesgo cardiovascular (CV) en la prevención secundaria tras un ictus isquémico es bajo, en parte debido a la falta de adherencia terapéutica. La polipíldora CV puede contribuir a la buena cumplimentación del adecuado tratamiento para la prevención cerebrovascular. El objetivo fue establecer cómo y en qué casos se debería administrar. Métodos. Un grupo de 8 neurólogos redactaron recomendaciones consensuadas mediante una técnica de brainstorming estructurado, basándose en su experiencia y en una revisión bibliográfica. Resultados. Los resultados atienden a la opinión de los expertos. El uso de la polipíldora CV tiene ventajas para pacientes, profesionales sanitarios y para el sistema de salud. Las situaciones clínicas más adecuadas para su uso son el ictus aterotrombótico, el lacunar, el asociado a deterioro cognitivo, el criptogénico con factores de riesgo CV y la enfermedad cerebrovascular silente. Su uso preferente incluye la sospecha de mal cumplimiento, a los pacientes polimedicados, ancianos, polivasculares o con alta carga aterotrombótica, jóvenes activos laboralmente y pacientes con preferencias por la polipíldora CV. Las opciones de administración incluyen el paso de fármacos individuales a la polipíldora CV, el inicio directo desde la fase aguda en casos particulares, a los pacientes con otra estatina o con un antagonista del receptor de la angiotensina ii, o de novo si hubiera sospecha de mala adherencia. No obstante, su uso implica realizar seguimiento del cumplimiento de los objetivos terapéuticos para ajustar la dosis. Conclusiones. Este documento es el primero en establecer recomendaciones de uso de la polipíldora CV en enfermedad cerebrovascular, aparte de sus ventajas sobre la adherencia.

Among 1250 robotic radical prostatectomy procedures that were performed at our department, we identified three patients with previous cerebrovascular disease history. Of those, postoperative follow-up was uneventful for two patients. One patient who had a history of cranial meningioma developed urge urinary incontinence and trigerring of epilepsy in the perioperative follow-up, two months after the robot-assisted laparoscopic radical prostatectomy procedure. Medical management resolved the symptoms.