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American Indians experience substantial health disparities relative to the US population, including vascular brain aging. Poorer cognitive test performance has been associated with cranial magnetic resonance imaging findings in aging community populations, but no study has investigated these associations in elderly American Indians.
We examined 786 American Indians aged 64 years and older from the Cerebrovascular Disease and its Consequences in American Indians study (2010–2013). Cranial magnetic resonance images were scored for cortical and subcortical infarcts, hemorrhages, severity of white matter disease, sulcal widening, ventricle enlargement, and volumetric estimates for white matter hyperintensities (WMHs), hippocampus, and brain. Participants completed demographic, medical history, and neuropsychological assessments including testing for general cognitive functioning, verbal learning and memory, processing speed, phonemic fluency, and executive function.
Processing speed was independently associated with the presence of any infarcts, white matter disease, and hippocampal and brain volumes, independent of socioeconomic, language, education, and clinical factors. Other significant associations included general cognitive functioning with hippocampal volume. Nonsignificant, marginal associations included general cognition with WMH and brain volume; verbal memory with hippocampal volume; verbal fluency and executive function with brain volume; and processing speed with ventricle enlargement.
Brain-cognition associations found in this study of elderly American Indians are similar to those found in other racial/ethnic populations, with processing speed comprising an especially strong correlate of cerebrovascular disease. These findings may assist future efforts to define opportunities for disease prevention, to conduct research on diagnostic and normative standards, and to guide clinical evaluation of this underserved and overburdened population.
Anecdotal evidence suggests the use of bolus tube feeding is increasing in the long-term home enteral tube feed (HETF) patients. A cross-sectional survey to assess the prevalence of bolus tube feeding and to characterise these patients was undertaken. Dietitians from ten centres across the UK collected data on all adult HETF patients on the dietetic caseload receiving bolus tube feeding (n 604, 60 % male, age 58 years). Demographic data, reasons for tube and bolus feeding, tube and equipment types, feeding method and patients’ complete tube feeding regimens were recorded. Over a third of patients receiving HETF used bolus feeding (37 %). Patients were long-term tube fed (4·1 years tube feeding, 3·5 years bolus tube feeding), living at home (71 %) and sedentary (70 %). The majority were head and neck cancer patients (22 %) who were significantly more active (79 %) and lived at home (97 %), while those with cerebral palsy (12 %) were typically younger (age 31 years) but sedentary (94 %). Most patients used bolus feeding as their sole feeding method (46 %), because it was quick and easy to use, as a top-up to oral diet or to mimic mealtimes. Importantly, oral nutritional supplements (ONS) were used for bolus feeding in 85 % of patients, with 51 % of these being compact-style ONS (2·4 kcal (10·0 kJ)/ml, 125 ml). This survey shows that bolus tube feeding is common among UK HETF patients, is used by a wide variety of patient groups and can be adapted to meet the needs of a variety of patients, clinical conditions, nutritional requirements and lifestyles.
No data exist on the associations of dietary tomato and lycopene consumption with total and cause-specific mortality. Using the National Health and Nutrition Examination Surveys (NHANES) 1999-2010, we evaluted the long-term impact of tomato and lycopene intake on total and cause-specific (coronary heart disease [CHD] and cerebrovascular disease) mortality. We also assessed the changes in cardio-metabolic risk factors according to tomato and lycopene intake. Vital status through December 31, 2011 was ascertained. Cox proportional hazard regression models (followed by propensity score-matching) were used to investigate the link between tomato and lycopene consumption total, CHD and cerebrovascular mortality. Among the 23,935 participants included (mean age = 47.6 years, 48.8% men), 3403 deaths occurred during 76.4 months of follow-up. Tomato intake was inversely associated with total (risk ratio (RR):0.86, 95% confidence interval (CI):0.81-0.92), CHD (0.76, 95%CI: 0.70-0.85) and cerebrovascular (0.70, 95%CI: 0.62-0.81) mortality. Similar inverse associations were found between lycopene consumption, total (0.76, 95%CI: 0.72-0.81), CHD (0.73, 95%CI: 0.65-0.83) and cerebrovascular (0.71, 95%CI: 0.65-0.78) mortality; these associations were independent of anthropometric, clinical and nutritional parameters. Age and obesity did not affect the associations of tomato and lycopene consumption with total, CHD and cerebrovascular mortality. C-reactive protein significantly moderated the link between lycopene and tomato intake with total, CHD and cerebrovascular mortality. Analysis of co-variance showed that participants with a higher tomato and lycopene consumption had a more cardio-protective profile compared with those with a lower intake. Our results highlighted the favorable effect of tomato and lycopene intake on total and cause-specific mortality as well as to cardio-metabolic risk factors. These findings should be taken into consideration for public health strategies.
Introduction: Dizziness is among the most common presenting complaints in the emergency department (ED). Although the vast majority of these cases are the result of a benign, self-limiting process, many patients undergo computed tomography (CT) of the head. The objective of this study was to define the yield of and diagnostic accuracy of CT in dizziness in addition to defining high-risk clinical features predictive of an abnormal CT. Methods: At a tertiary care ED we performed a medical records review from Jan 2015-2018 including adult patients with a triage complaint of dizziness (vertigo, unsteady, lightheaded), excluding those with symptoms >14days, recent trauma, GCS < 15, hypotensive, or syncope/loss of consciousness. Five trained reviewers used a standardized data collection sheet to extract data. Our outcome was a central cause defined as: cerebrovascular accident (CVA), brain tumor (BT) or intracranial haemorrhage (ICH) diagnosed on CT or magnetic resonance imaging. Univariate analysis/logistic regression were performed and odds ratios reported. A sample size of 796 was calculated based on an expected prevalence of 5% with an 80% power and 95% confidence interval to detect an odds ratio greater than 2. Results: 2310 patients were recruited, 800 (35%) underwent CT head, 471(59%) female and a mean age of 62.8 years (+/−17.5 years). The top three diagnoses for patients undergoing CT were peripheral vertigo/benign positional vertigo (153 – 19%), vertigo not-otherwise-specified (137 – 17%) and dizziness not-otherwise-specified (137 – 17%). The number of CT scans considered abnormal was 30 (3.7%). The top three diagnoses for patients with an abnormal CT were CVA (22 – 75%), BT (9 – 26%) and ICH (6-17%). High risk clinical findings associated (p < 0.001) with an abnormal head CT were dysmetria, objective motor neurological signs, positive Rhomberg, ataxia and inability to walk 3 steps. Objective motor neurological signs (OR 8.4 [95% CI 3.27-21.72]) and ataxia (OR 3.4 [95% CI 1.62-7.41]) were both independently associated with an abnormal CT. Patients without any high risk findings on exam had a 0.7%(3/381 – 2 CVA,1 Tumour) probability of an abnormal CT. Sensitivity of CT for a central cause of dizziness was 71.43%(95%CI 55.4-84.3%), specificity 100%(95%CI 99.5-100%). Conclusion: Current rate of imaging in dizziness is high and inefficient. CT should be the first imaging test in those with high-risk clinical features, but a normal result does not rule out a central cause.
Objective: Post-stroke cognitive impairment is common, but mechanisms and risk factors are poorly understood. Frailty may be an important risk factor for cognitive impairment after stroke. We investigated the association between pre-stroke frailty and acute post-stoke cognition. Methods: We studied consecutively admitted acute stroke patients in a single urban teaching hospital during three recruitment waves between May 2016 and December 2017. Cognition was assessed using the Mini-Montreal Cognitive Assessment (min=0; max=12). A Frailty Index was used to generate frailty scores for each patient (min=0; max=100). Clinical and demographic information were collected, including pre-stroke cognition, delirium, and stroke-severity. We conducted univariate and multiple-linear regression analyses with covariates forced in (covariates included were: age, sex, stroke severity, stroke-type, pre-stroke cognitive impairment, delirium, previous stroke/transient ischemic attack) to investigate the association between pre-stroke frailty and post-stroke cognition. Results: Complete data were available for 154 stroke patients. Mean age was 68 years (SD=11; range=32–97); 93 (60%) were male. Median mini-Montreal Cognitive Assessment score was 8 (IQR=4–12). Mean Frailty Index score was 18 (SD=11). Pre-stroke cognitive impairment was apparent in 13/154 (8%) patients. Pre-stroke frailty was significantly associated with lower post-stroke cognition (Standardized-Beta=−0.40; p<0.001) and this association was independent of covariates (Unstandardized-Beta=−0.05; p=0.005). Additional significant variables in the multiple regression model were age (Unstandardized-Beta=−0.05; p=0.002), delirium (Unstandardized-Beta=−2.81; p<0.001), pre-stroke cognitive impairment (Unstandardized-Beta=−2.28; p=0.001), and stroke-severity (Unstandardized-Beta=−0.20; p<0.001). Conclusions: Pre-stroke frailty may be a moderator of post-stroke cognition, independent of other well-established post-stroke cognitive impairment risk factors. (JINS, 2019, 25, 501–506)
We conducted a study to describe food profile, health status and stroke risk factors in the population of the Aeolian Islands.
Self-administrated questionnaires regarding eating habits, health status and stroke risk factors were obtained from a sample of the general Aeolian population. We analysed the difference from common healthy eating habits indicated by the Italian Institute of Nutrition.
Current evidence finds the Mediterranean diet is a protective factor for cardio- and cerebrovascular diseases. The Aeolian Islands are an interesting study setting because of their peculiarity in the epidemiology of cerebrovascular and neurodegenerative diseases.
Individuals (n 586; age range 15–93 years; mean 52 (sd 18) years) living in the Aeolian Islands.
We found low fish consumption in 13·3% and vitamin intake deficiency in 5·8% of participants. A marked excess of saturated fats was observed in 71·0% of participants. Sodium excess was reported almost in half of participants (49·0%). Eating habits were characterized by high consumption of fruits and vegetables, consistent use of olive oil and scanty use of cured meat. Health status as evaluated by the General Health Questionnaire was characterized by ‘normal distress’ level in the majority of participants.
Study findings show the eating habits and health status of the Aeolian people in an interesting setting of low incidence of cerebrovascular disease. This nutrition regimen has been proved to be protective against cerebrovascular disease. Nutrition is likely to contribute to the low incidence of stroke in this population.
Background: Anatomic variants of the circle of Willis (CW) are commonly observed in healthy subjects. Genetic and environmental factors influencing these variants remain unclear. Our aim was to assess the genetic and environmental background affecting variant CW phenotypes. Methods: A total of 122 adult healthy twins from the Hungarian Twin Registry (39 monozygotic (MZ) and 22 dizygotic (DZ) pairs, average age 49.7 ± 13.4 years) underwent Time-of-Flight magnetic resonance angiography and transcranial Doppler sonography. We investigated the anterior and posterior CW according to morphological categories. Prevalence and concordance rates of CW variants were calculated. MZ twins discordant for CW variants were analyzed for cardiovascular risk factors and altered blood flow. Results: Complete CW (45.0%) and bilaterally absent posterior communicating artery (PCoA) (22.5%) were the most prevalent variants in the anterior and posterior CW, respectively. There was no significant difference regarding the prevalence of variants across zygosity except for bilaterally hypoplastic PCoA (p = .02). DZ concordance was higher compared to MZ twins regarding morphological categories of the CW. Cardiovascular risk factors were not significantly associated with variant CW in MZ twins discordant to CW morphology. Flow parameters did not differ significantly among MZ twins discordant to CW variants. Conclusion: CW variants may not be determined by substantial genetic effects and are not influenced by altered blood flow in healthy individuals. Further investigations are needed to identify potential environmental factors affecting these variants.
Background The long-term cognitive and quality-of-life (QoL) outcomes after treatment of ruptured anterior communicating artery (ACoA) aneurysms are unknown. Methods Potential participants were all consecutive patients with ruptured ACoA aneurysms who were treated at one institution from July 1992 to December 2008. All potential participants were asked to complete the Cognitive Failures Questionnaire (CFQ), Center for Epidemiology Studies-Depression (CES-D) questionnaire, Short Form 36 (SF-36) questionnaire, and Telephone Interview for Cognitive Status-Modified (TICS-M). Patient charts were retrospectively reviewed for baseline demographics and clinical status, intra-operative details, and post-operative course. Reporting of cognitive and QoL assessment results was stratified by treatment method (endovascular coil embolization and surgical clipping by pterional craniotomy or orbitocranial craniotomy). Results In total, 82 patients (18 treated with coiling, 27 by orbitocranial craniotomy, and 37 by pterional craniotomy) were included in this study. In total, 32 patients (9 treated by coiling, 11 by orbitocranial craniotomy, and 16 by pterional craniotomy) completed follow-up cognitive and QoL questionnaires. The mean follow-up for patients who completed the questionnaires was 8.64±3.81 years. The three groups did not differ in questionnaires assessing cognitive status (TICS-M p=0.114, CFQ p=0.111). Moreover, there were no observed differences in QoL or depression scores between the three groups. Conclusions At long-term follow-up, QoL, cognitive, and depression test scores of patients with ruptured ACoA aneurysms are similar across open surgery and coiling modalities. Our results emphasize the importance of considering long-term outcomes with validated daily measures of functioning when reporting on outcomes after treatment for ruptured intracranial aneurysms. Larger prospective studies are required to further explore the results.
To investigate the predictive ability of the previously established global cerebrovascular disease (CeVD) burden scale on long-term clinical outcomes in a longitudinal study of Asian elderly participants across the spectrum of cognitive impairment.
A case-control study was conducted over a 2-year period involving participants with no cognitive impairment, cognitive impairment-no dementia (CIND), and Alzheimer's disease (AD). Annually, cognitive function was assessed with a comprehensive neuropsychological battery and the clinical dementia rating (CDR) scale was used to stage disease severity.
Of 314 participants, 102 had none/very mild CeVD, 31 mild CeVD, 94 moderate CeVD, and 87 severe CeVD at baseline. There was a 1.14 and 1.42 units decline per year on global cognitive z-scores in moderate and severe CeVD groups, respectively, compared to none/very mild CeVD. Moderate-severe CeVD predicted significant functional deterioration at year 2 (HR = 2.0, 95% CI = 1.2–3.4), and conversion to AD (HR = 6.3, 95% CI = 1.7–22.5), independent of medial temporal atrophy.
The global CeVD burden scale predicts poor long-term clinical outcome independent of neurodegenerative markers. Furthermore, CeVD severity affects the rate of cognitive and functional deterioration. Hence, cerebrovascular burden, which is potentially preventable, is a strong prognostic indicator, both at preclinical and clinical stages of AD, independent of neurodegenerative processes.
Canadian contributions to cerebrovascular neurosurgery have been disproportionately large and, with some exceptions, relatively unrecognized. In this review, some of the efforts in the advancement of cerebrovascular neurosurgery by Canadian neurologists and neurosurgeons are described.
Cerebrovascular reactivity monitoring has been used to identify the lower limit of pressure autoregulation in adult patients with brain injury. We hypothesise that impaired cerebrovascular reactivity and time spent below the lower limit of autoregulation during cardiopulmonary bypass will result in hypoperfusion injuries to the brain detectable by elevation in serum glial fibrillary acidic protein level.
We designed a multicentre observational pilot study combining concurrent cerebrovascular reactivity and biomarker monitoring during cardiopulmonary bypass. All children undergoing bypass for CHD were eligible. Autoregulation was monitored with the haemoglobin volume index, a moving correlation coefficient between the mean arterial blood pressure and the near-infrared spectroscopy-based trend of cerebral blood volume. Both haemoglobin volume index and glial fibrillary acidic protein data were analysed by phases of bypass. Each patient’s autoregulation curve was analysed to identify the lower limit of autoregulation and optimal arterial blood pressure.
A total of 57 children had autoregulation and biomarker data for all phases of bypass. The mean baseline haemoglobin volume index was 0.084. Haemoglobin volume index increased with lowering of pressure with 82% demonstrating a lower limit of autoregulation (41±9 mmHg), whereas 100% demonstrated optimal blood pressure (48±11 mmHg). There was a significant association between an individual’s peak autoregulation and biomarker values (p=0.01).
Individual, dynamic non-invasive cerebrovascular reactivity monitoring demonstrated transient periods of impairment related to possible silent brain injury. The association between an impaired autoregulation burden and elevation in the serum brain biomarker may identify brain perfusion risk that could result in injury.
Prenatal exposure to famine is associated with an increased risk of metabolic and cardiovascular diseases in the offspring at adult age. The aim of this study was to assess whether prenatal exposure to undernutrition increases the risk of stroke. This study was performed in the Dutch famine birth cohort, which consist of 2414 members who were born between 1943 and 1947 in the Netherlands. In a subsample of 1177 individuals, interviews were conducted using standardized questionnaires to obtain information about medical history (which included specific questions regarding stroke) and lifestyle. Information on stroke-related mortality was collected by linking the cohort with Statistics Netherlands. A Cox’s proportional hazard analysis was performed to calculate hazard ratios (HRs) comparing the incidence of non-fatal stroke between participants who were exposed, subdivided into early, mid and late gestation, and unexposed to famine prenatally. Three cohort members died of stroke. Of the 1177 subjects who responded to the questionnaires 49 (4.2%) survived a stroke. Unadjusted and adjusted HRs for the risk of non-fatal stroke did not show a significant difference between the unexposed and exposed subjects: HR 1.23 (95% CI 0.53–2.83), HR 1.23 (95% CI 0.53–2.82), HR 1.12 (95% CI 0.46–2.71) for those exposed in late, mid and early gestation, respectively. We were unable to find evidence for a major effect of prenatal exposure to famine on the risk of stroke in later life, although one should be aware that this study was underpowered and the study population too selected and young to identify smaller risks.
Objectives: The present study examined differences in neurocognitive outcomes among non-Hispanic Black and White stroke survivors using the NIH Toolbox-Cognition Battery (NIHTB-CB), and investigated the roles of healthcare variables in explaining racial differences in neurocognitive outcomes post-stroke. Methods: One-hundred seventy adults (91 Black; 79 White), who participated in a multisite study were included (age: M=56.4; SD=12.6; education: M=13.7; SD=2.5; 50% male; years post-stroke: 1–18; stroke type: 72% ischemic, 28% hemorrhagic). Neurocognitive function was assessed with the NIHTB-CB, using demographically corrected norms. Participants completed measures of socio-demographic characteristics, health literacy, and healthcare use and access. Stroke severity was assessed with the Modified Rankin Scale. Results: An independent samples t test indicated Blacks showed more neurocognitive impairment (NIHTB-CB Fluid Composite T-score: M=37.63; SD=11.67) than Whites (Fluid T-score: M=42.59, SD=11.54; p=.006). This difference remained significant after adjusting for reading level (NIHTB-CB Oral Reading), and when stratified by stroke severity. Blacks also scored lower on health literacy, reported differences in insurance type, and reported decreased confidence in the doctors treating them. Multivariable models adjusting for reading level and injury severity showed that health literacy and insurance type were statistically significant predictors of the Fluid cognitive composite (p<.001 and p=.02, respectively) and significantly mediated racial differences on neurocognitive impairment. Conclusions: We replicated prior work showing that Blacks are at increased risk for poorer neurocognitive outcomes post-stroke than Whites. Health literacy and insurance type might be important modifiable factors influencing these differences. (JINS, 2017, 23, 640–652)
Arterial wall thickening, stimulated by low-grade systemic inflammation, underlies many cardiovascular events. As diet is a significant moderator of systemic inflammation, the dietary inflammatory index (DIITM) has recently been devised to assess the overall inflammatory potential of an individual’s diet. The primary objective of this study was to assess the association of the DII with common carotid artery–intima-media thickness (CCA–IMT) and carotid plaques. To substantiate the clinical importance of these findings we assessed the relationship of DII score with atherosclerotic vascular disease (ASVD)-related mortality, ischaemic cerebrovascular disease (CVA)-related mortality and ischaemic heart disease (IHD)-related mortality more. The study was conducted in Western Australian women aged over 70 years (n 1304). Dietary data derived from a validated FFQ (completed at baseline) were used to calculate a DII score for each individual. In multivariable-adjusted models, DII scores were associated with sub-clinical atherosclerosis: a 1 sd (2·13 units) higher DII score was associated with a 0·013-mm higher mean CCA–IMT (P=0·016) and a 0·016-mm higher maximum CCA–IMT (P=0·008), measured at 36 months. No relationship was seen between DII score and carotid plaque severity. There were 269 deaths during follow-up. High DII scores were positively associated with ASVD-related death (per sd, hazard ratio (HR): 1·36; 95 % CI 1·15, 1·60), CVA-related death (per sd, HR: 1·30; 95 % CI 1·00, 1·69) and IHD-related death (per sd, HR: 1·40; 95 % CI 1·13, 1·75). These results support the hypothesis that a pro-inflammatory diet increases systemic inflammation leading to development and progression of atherosclerosis and eventual ASVD-related death.
Introduction: Age and systolic blood pressure (SBP) are important predictors of Acute Cerebrovascular Syndrome (ACVS). Yet, the effect of SBP is confounded by age, making its independent contribution to ACVS risk difficult to quantify. Here we use logistic regression to explore the role of SBP in younger and older ED patients. Methods: Data comprised 1019 ED patients (ACVS 70%, 30% non-ACVS) enrolled during a 28-month period of an ongoing prospective, observational, multi-site stroke biomarker study (SpecTRA). We used logistic regression to examine the effects of age, sex, and the age:SBP interaction as predictive markers of the diagnosis of ACVS. Results: Participants (53% male) ranged in age from 18 to 97 years (Q1=58, median=70, Q3=80). SBP ranged from 84 to 248 mmHg (Q1=137, median=154, Q3=174). In our initial regression model, age, sex, SBP and the age:SBP interaction were all significant (p<0.01). Using cubic regression splines for age, sbp and their interaction yields the same conclusion (p<0.01). To better understand the role of SBP in younger vs. older patients, we stratified the sample at the median age (70 years of age). In the younger group (n=510), participants were 55% male, 60% ACVS, and had SBP ranging from 91 to 236 mmHg (Q1=133, median=148, Q3=165). In the older group (n=509), participants were 51% male, 82% ACVS and had SBP ranging from 84 to 248 mmHg (Q1=143, median=159, Q3=179), a shift of approximately 10 mmHg between the groups. The logistic regression model was then fit separately to each group without the age:SBP interaction term. In the younger group, we found SBP to be highly significant (p<0.001), with an odds-ratio (OR) of 1.18 per 10 mmHg (95% CI: 1.10-1.29). In the older group, we found that SBP was not significant (p=0.91), with an OR of 1.00 per 10 mmHg (95% CI: 0.91-1.08). Age and sex were also significant risk factors in the younger group (each p<0.01), though not in the older group (both p>0.07). Conclusion: Our findings suggest that for ED patients suspected of ACVS, SBP is a clinically relevant predictor for younger patients, with higher SBP associated with an increased risk of ACVS, regardless of patient age and sex. SBP does not appear to be a strong predictor for patients over 70. ED physicians can leverage this finding by attributing greater importance to elevated SBP in younger patients than older patients when working toward a clinical suspicion of ACVS.