Impact of tobacco smoking on disease-specific outcomes in common neurological disorders: A scoping review.

Although the association of smoking with the risk of incident neurological disorders is well established, less is known about the impact of smoking and smoking cessation on outcomes of these conditions. The objective of this scoping review was to synthesize what is known about the impact of smoking and smoking cessation on disease-specific outcomes for seven common neurological disorders. We included 67 studies on the association of smoking and smoking cessation on disease-specific outcomes. For multiple sclerosis, smoking was associated with greater clinical and radiological disease progression, relapses, risk for disease-related death, cognitive decline, and mood symptoms, in addition to reduced treatment effectiveness. For stroke and transient ischemic attack, smoking was associated with greater rates of stroke recurrence, post-stroke cardiovascular outcomes, post-stroke mortality, post-stroke cognitive impairment, and functional impairment. In patients with cognitive impairment and dementia, smoking was associated with faster cognitive decline, and smoking was also associated with greater cognitive decline in Parkinson's disease, but not motor symptom worsening. Patients with amyotrophic lateral sclerosis who smoked faced increased mortality. Last, in patients with cluster headache, smoking was associated with more frequent and longer cluster attack periods. Conversely, for multiple sclerosis and stroke, smoking cessation was associated with improved disease-specific outcomes. In summary, whereas smoking is detrimentally associated with disease-specific outcomes in common neurological conditions, there is growing evidence that smoking cessation may improve outcomes. Effective smoking cessation interventions should be leveraged in the management of common neurological disorders to improve patient outcomes.

Practice Current: Variability in Smoking Cessation Intervention Practice Patterns After Ischemic Stroke and Transient Ischemic Attack.

People who continue to smoke after ischemic stroke and transient ischemic attack (TIA) are at increased risk for subsequent stroke and cardiovascular events. Although effective smoking cessation strategies exist, smoking rates after stroke remain high. Through case-based discussions with 3 international vascular neurology panelists, this article seeks to explore practice patterns and barriers to smoking cessation for patients with stroke/TIA. We sought to answer these questions: What are the barriers to using smoking cessation interventions for patients with stroke/TIA? Which interventions are most used for hospitalized patients with stroke/TIA? Which interventions are most used for patients who continue smoking during follow-up? Our synthesis of panelists' commentaries is complemented by the preliminary results of an online survey posed to global readership. Together, the interviews and survey results identify practice variability and barriers to smoking cessation after stroke/TIA, suggesting that there is substantial need for research and standardization.

Cost-Effectiveness of Smoking Cessation Interventions in Patients With Ischemic Stroke and Transient Ischemic Attack.

BACKGROUND: Smoking cessation rates after stroke and transient ischemic attack are suboptimal, and smoking cessation interventions are underutilized. We performed a cost-effectiveness analysis of smoking cessation interventions in this population. METHODS: We constructed a decision tree and used Markov models that aimed to assess the cost-effectiveness of varenicline, any pharmacotherapy with intensive counseling, and monetary incentives, compared with brief counseling alone in the secondary stroke prevention setting. Payer and societal costs of interventions and outcomes were modeled. The outcomes were recurrent stroke, myocardial infarction, and death using a lifetime horizon. Estimates and variance for the base case (35% cessation), costs and effectiveness of interventions, and outcome rates were imputed from the stroke literature. We calculated incremental cost-effectiveness ratios and incremental net monetary benefits. An intervention was considered cost-effective if the incremental cost-effectiveness ratio was less than the willingness-to-pay threshold of $100 000 per quality-adjusted life-year (QALY) or when the incremental net monetary benefit was positive. Probabilistic Monte Carlo simulations modeled the impact of parameter uncertainty. RESULTS: From the payer perspective, varenicline and pharmacotherapy with intensive counseling were associated with more QALYs (0.67 and 1.00, respectively) at less total lifetime costs compared with brief counseling alone. Monetary incentives were associated with 0.71 more QALYs at an additional cost of $120 compared with brief counseling alone, yielding an incremental cost-effectiveness ratio of $168/QALY. From the societal perspective, all 3 interventions provided more QALYs at less total costs compared with brief counseling alone. In 10 000 Monte Carlo simulations, all 3 smoking cessation interventions were cost-effective in >89% of runs. CONCLUSIONS: For secondary stroke prevention, it is cost-effective and potentially cost-saving to deliver smoking cessation therapy beyond brief counseling alone.

Impact of Cigarette Smoking and Its Interaction with Hypertension and Diabetes on Cognitive Function in Older Americans.

BACKGROUND: The detrimental impact of tobacco smoking on brain health is well recognized. OBJECTIVE: To evaluate whether smoking acts synergistically with hypertension and diabetes to influence cognitive performance. METHODS: We performed a cross-sectional analysis using the US National Health and Nutrition Examination Survey. Participants were tested for serum cotinine, a validated cigarette smoking/exposure biomarker, and had standardized blood pressure and hemoglobin A1c measurements. Participants were administered four cognitive tests: Digit Symbol Substitution (DSST), Animal Fluency, Immediate Recall, and Delayed Recall. Multivariable linear regression models adjusted for demographics and confounders evaluated the association of cotinine with cognition. Interaction testing evaluated effect modification by hypertension, diabetes, and their continuous measures (systolic blood pressure and hemoglobin A1c). RESULTS: For 3,007 participants, mean age was 69.4 years; 54% were women. Using cotinine levels, 14.9% of participants were categorized as active smokers. Higher cotinine levels were associated with worse DSST performance when modeling cotinine as a continuous variable (ß, -0.70; 95% CI, -1.11, -0.29; p < 0.01) and when categorizing participants as active smokers (ß, -5.63; 95% CI, -9.70, -1.56; p < 0.01). Cotinine was not associated with fluency or memory. Effect modification by hypertension and diabetes were absent, except that cotinine was associated with worse Immediate Recall at lower blood pressures. CONCLUSION: Higher levels of a smoking and secondhand exposure biomarker were associated with worse cognitive performance on a multidomain test. Overall, the relationship of cotinine with cognition was not contingent on or amplified by hypertension or diabetes; smoking is detrimental for brain health irrespective of these comorbidities.

Association between liver fibrosis and incident dementia in the UK Biobank study.

BACKGROUND AND PURPOSE: There is growing recognition that chronic liver conditions influence brain health. The impact of liver fibrosis on dementia risk was unclear. We evaluated the association between liver fibrosis and incident dementia in a cohort study. METHODS: We performed a cohort analysis using data from the UK Biobank study, which prospectively enrolled adults starting in 2007, and continues to follow them. People with a Fibrosis-4 (FIB-4) liver fibrosis score >2.67 were categorized as at high risk of advanced fibrosis. The primary outcome was incident dementia, ascertained using a validated approach. We excluded participants with prevalent dementia at baseline. We used Cox proportional hazards models to evaluate the association between liver fibrosis and dementia while adjusting for potential confounders. RESULTS: Among 455,226 participants included in this analysis, the mean age was 56.5 years and 54% were women. Approximately 2.17% (95% confidence interval [CI] 2.13%-2.22%) had liver fibrosis. The rate of dementia per 1000 person-years was 1.76 (95% CI 1.50-2.07) in participants with liver fibrosis and 0.52 (95% CI 0.50-0.54) in those without. After adjusting for demographics, socioeconomic deprivation, educational attainment, metabolic syndrome, hypertension, diabetes, dyslipidemia, and tobacco and alcohol use, liver fibrosis was associated with an increased risk of dementia (hazard ratio 1.52, 95% CI 1.22-1.90). Results were robust to sensitivity analyses. Effect modification by sex, metabolic syndrome, and apolipoprotein E4 carrier status was not observed. CONCLUSION: Liver fibrosis in middle age was associated with an increased risk of incident dementia, independent of shared risk factors. Liver fibrosis may be an underrecognized risk factor for dementia.

Prescription smoking-cessation medication pharmacy claims after stroke and transient ischemic attack.

Smoking cessation is critical in secondary prevention after stroke and transient ischemic attack. Data regarding use of smoking-cessation interventions after stroke and transient ischemic attack are sparse. We examined the use of prescription smoking-cessation medications in these patients. This is a retrospective cohort study using 2013-2016 data from the INSIGHT Clinical Research Network, comprised of Medicare prescription claims data merged with electronic health record data for patients receiving care across five New York City health care institutions. Active smoking was ascertained based on a validated ICD-9-CM diagnosis code or the presence of an electronic health record active smoking indicator, reflecting clinician-entered data in the health record. The primary outcome was a claim for any prescription smoking-cessation medication (varenicline or bupropion) within 12 months of hospital discharge. We evaluated claims for any statin medication as a comparator because statins are a standard component of stroke secondary prevention. We identified 3,153 patients with stroke or transient ischemic attack who were active smokers at the time of their event. Among these patients, 3.1% (95% CI, 2.5-3.9) had a pharmacy claim for a prescription smoking-cessation medication at 6 months, and 4.7% (95% CI, 3.9-5.6) did at 12 months hospital discharge. In contrast, cumulative statin medication claims rates were 67.5% (95% CI, 65.5-69.5%) at 6 months and 74.6% (95% CI, 72.7-76.6%) at 12 months. Prescription smoking-cessation medications were infrequently used after stroke and transient ischemic attack.

Smoking Cessation in Stroke Survivors in the United States: A Nationwide Analysis.

BACKGROUND: Continued smoking after stroke is associated with a high risk of stroke recurrence and other cardiovascular disease. We sought to comprehensively understand the epidemiology of smoking cessation in stroke survivors in the United States. Furthermore, we compared smoking cessation in stroke and cancer survivors because cancer is another smoking-related condition in which smoking cessation is prioritized. METHODS: We performed a cross-sectional analysis of data from the Centers for Disease Control and Prevention Behavioral Risk Factor Surveillance System, an annual, nationally representative health survey. Using pooled data from 2013 to 2019, we identified stroke and cancer survivors with a history of smoking. We used survey procedures to estimate frequencies and summarize quit ratios with attention to demographic and geographic (state-wise and rural-urban) factors for stroke survivors. The quit ratio is conventionally defined as the proportion of ever smokers who have quit. Then, we used multivariable logistic regression to compare quit ratios in stroke and cancer survivors while adjusting for demographics and smoking-related comorbidities. RESULTS: Among 4 434 604 Americans with a history of stroke and smoking, the median age was 68 years (interquartile range, 59-76), and 45.4% were women. The overall quit ratio was 60.8% (95% CI, 60.1%-61.6%). Quit ratios varied by age group, sex, race and ethnicity, and several geographic factors. There was marked geographic variation in quit ratios, ranging from 48.3% in Kentucky to 71.5% in California. Furthermore, compared with cancer survivors, stroke survivors were less likely to have quit smoking (odds ratio, 0.72 [95% CI, 0.67-0.79]) after accounting for differences in demographics and smoking-related comorbidities. CONCLUSIONS: There were considerable demographic and geographic disparities in smoking quit ratios in stroke survivors, who were less likely to have quit smoking than cancer survivors. A targeted initiative is needed to improve smoking cessation for stroke survivors.

Cognitive Function, Sarcopenia, and Inflammation Are Strongly Associated with Frailty: A Framingham Cohort Study.

BACKGROUND: Frailty is an important contributor to morbidity and mortality in chronic liver disease. Understanding the contributors to frailty has the potential to identify individuals at risk for frailty and may potentially provide targets for frailty-modifying interventions. We evaluated the relationship among cognitive function, inflammation, and sarcopenia and frailty. METHODS: Using cohorts from the Framingham Heart Study (2011-2014), we evaluated for factors associated with frailty. Exposures included cognitive tests (combined Trails A/B test, Animal Naming Test, and combined Digit Span Forward/Backward test), inflammation (interleukin-6 and tumor necrosis factor receptor II), and sarcopenia (creatinine-to-cystatin C ratio). We performed linear and logistic regression to identify the relationship between these exposures and the Liver Frailty Index (LFI). RESULTS: The study population (N = 1208) had a median age of 70 years, was 56% female, and 48.5% had evidence of liver disease. The combined Trails A/B test (ß 0.05, P < .001), creatinine-to-cystatin C (ß -0.17, P = .006), and both inflammatory markers, interleukin-6 levels (ß 0.16, P = .002) and tumor necrosis factor receptor II (ß 0.21, P = .04), were independently associated with the LFI. Using an LFI cutoff of ≥4.5 to define frailty, Trails A/B (odds ratio [OR] 1.21, 95% confidence interval [CI] 1.07-1.37), Animal Naming Test (OR 0.64, 95% CI 0.42-0.97), sarcopenia (OR 0.10, 95% CI 0.01-0.73), and interleukin-6 (OR 4.99, 95% CI 1.03-15.53) were all associated with frailty. Although liver disease did not modify the relationship between the LFI and the Trails A/B test, interleukin-6 was significantly associated with the LFI only in the presence of liver disease. CONCLUSIONS: Cognitive performance, inflammation, and sarcopenia, each highly prevalent in cirrhosis, are associated with the LFI in this population-based study of persons without cirrhosis. Further research is warranted for interventions aiming to prevent frailty by tailoring their approach to the patient's underlying risk factors.

Neurological Outcomes of Patients With Mycotic Aneurysms in Infective Endocarditis.

BACKGROUND AND PURPOSE: Mycotic aneurysms (MA) are rare neurovascular complications of infective endocarditis (IE). The natural history and outcomes of MA under contemporary medical therapy have not been well characterized. The purpose of this study is to describe treatments and outcomes of patients with ruptured and unruptured MA in IE, specifically in relation to medical versus surgical/endovascular treatment. METHODS: Retrospective chart review was performed at 3 US academic medical centers of adult patients with IE and MA. Information was collected regarding risk factors, imaging, treatments, and outcomes, including ischemic stroke, intracerebral hemorrhage, MA size changes, and inhospital mortality. RESULTS: Thirty-five patients with IE had 63 MA. Nineteen patients had at least one ruptured MA; 13 patients underwent invasive treatment and 6 received antibiotics alone. Of 19 patients on antibiotics alone (6 with at least one ruptured MA and 13 with unruptured MA), 14 underwent repeat imaging and 5 had enlarging MA. Of 16 patients treated invasively, 2 had unruptured MA initially treated with antibiotics but ultimately underwent intervention. No MA ruptured after aneurysm discovery. Fifteen patients underwent cardiothoracic surgery (CTS), of which 11 had unsecured MA and 4 had secured MA. No patients suffered perioperiative neurological events attributable to their MA. Three patients treated with antibiotics alone and 3 patients treated invasively died from causes unrelated to their MAs. CONCLUSIONS: For patients with unruptured MA, treatment with antibiotics alone may have similar outcomes to invasive treatment. Further investigation is warranted to determine the risk of undergoing CTS with unsecured MA.

Prior antiplatelet therapy and haematoma expansion after primary intracerebral haemorrhage: an individual patient-level analysis of CLEAR III, MISTIE III and VISTA-ICH.

OBJECTIVE: To evaluate the relationship between prior antiplatelet therapy (APT) and outcomes after primary intracerebral haemorrhage (ICH), and assess if it varies by haematoma location. METHODS: We pooled individual patient data from the Virtual International Stroke Trials Archive-ICH trials dataset, Clot Lysis: Evaluating Accelerated Resolution of Intraventricular Hemorrhage III trial and the Minimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation Phase III trial. The exposure was APT preceding ICH diagnosis. The primary outcome was haematoma expansion at 72 hours. Secondary outcomes were admission haematoma volume, all-cause mortality, death or major disability (modified Rankin Scale (mRS) score ≥4) and shift in mRS distribution. Mixed-effects models were used to assess the relationship between APT and outcomes. Secondary analyses were stratified by ICH location and study cohort. RESULTS: Among 1420 patients with ICH, there were 782 (55.1%) lobar and 596 (42.0%) deep haemorrhages. APT was reported in 284 (20.0%) patients. In adjusted regression models, prior APT was not associated with haematoma expansion (OR, 0.97; 95% CI 0.60 to 1.57), major disability or death (OR, 1.05; 95% CI 0.61 to 1.63), all-cause mortality (OR, 0.89; 95% CI 0.47 to 1.85), admission haematoma volume (beta, -0.17; SE, 0.09; p=0.07) and shift in mRS (p=0.43). In secondary analyses, APT was associated with admission haematoma volume in lobar ICH (beta, 0.25; SE, 0.12; p=0.03), but there was no relationship with other ICH outcomes when stratified by haematoma location or study cohort. CONCLUSIONS: In a large heterogeneous cohort of patients with ICH, prior APT was not associated with haematoma expansion or functional outcomes after ICH, regardless of haematoma location. APT was associated with admission haematoma volumes in lobar ICH.

Association between PNPLA3 rs738409 G variant and MRI cerebrovascular disease biomarkers.

INTRODUCTION: Nonalcoholic fatty liver disease (NAFLD) has been associated with greater cerebral white matter hyperintensity (WMH) volume and microbleeds. The adiponutrin (PNPLA3) rs738409 G variant, a robust NAFLD susceptibility variant, has been variably associated with carotid atherosclerosis. We hypothesized that this variant is associated with WMH volume, microbleeds, covert brain infarction (CBI), and small perivascular spaces. METHODS: We performed a cross-sectional analysis of the Northern Manhattan Study-MRI Substudy. The associations between the rs738409 G variant allele and outcomes were assessed using linear regression for WMH volume, logistic regression for microbleeds and CBI, and Poisson regression for small perivascular spaces. Models were adjusted for age, sex, principal components, diabetes, and body mass index. RESULTS: We included 1063 Northern Manhattan Study participants who had brain MRI and genotype data available (mean age 70 ± 9 years, 61% women). The G allele frequency was 24%. The prevalence of any microbleeds and CBI were 8% and 18%, respectively. The median WMH volume and small perivascular space count score were 7.7 mL and 6, respectively. GG homozygosity, but not heterozygosity, was associated with WMH volume (ß = 0.27; 95% CI, 0.03, 0.51) compared to non-carriers. Having at least one G allele was associated with the presence of microbleeds (Odds ratio, 1.78; 95% CI, 1.02, 3.12); the association was attenuated in other models. No associations were observed for CBI and small perivascular spaces. CONCLUSION: The PNPLA3 rs738409 G allele was associated with greater WMH volume, and inconsistent associations with microbleeds were seen.

Trends in Active Cigarette Smoking Among Stroke Survivors in the United States, 1999 to 2018.

Background and Purpose- Patients who continue to smoke after a stroke face a higher risk of recurrent stroke. While several effective drugs for smoking cessation became available over the past 2 decades, whether active smoking has decreased among stroke survivors is unknown. We, therefore, evaluated trends in active smoking among stroke survivors during this period. Methods- We performed trends analyses using cross-sectional data collected every 1 to 2 years from 2 US health surveys spanning 1999 to 2018. In the National Health and Nutrition Examination Survey (NHANES) and the Behavioral Risk Factor Surveillance System (BRFSS) survey, participants were asked about prior stroke and active tobacco smoking. In NHANES, serum cotinine levels were available as a secondary measure of active smoking. We used multivariable logistic regression models for survey data to assess trends in active smoking among participants with and without prior stroke. Results- Among 49 375 participants in NHANES during 1999 to 2016 and 3 621 741 participants in BRFSS during 2011 to 2018, the prevalence of stroke was ≈3%. The overall prevalence of active smoking among stroke survivors was 24% in NHANES and 23% in BRFSS. Among individuals without prior stroke, the odds of smoking decreased over time in both NHANES (odds ratio, 0.95 per 2 years [95% CI, 0.93-0.96]) and BRFSS (odds ratio, 0.96 per year [95% CI, 0.96-0.96]). In contrast, there was no decrease in smoking among stroke survivors in NHANES (odds ratio, 1.00 [95% CI, 0.93-1.07]) or BRFSS (odds ratio, 0.99 [95% CI, 0.98-1.004]). Results were consistent in secondary analysis using biochemical ascertainment of active smoking in NHANES and in sensitivity analyses accounting for potential demographic changes in stroke epidemiology. Conclusions- In contrast to the general population, the prevalence of active smoking among stroke survivors has not decreased during the past 2 decades.

Symptoms of depression and active smoking among survivors of stroke and myocardial infarction: An NHANES analysis.

Historic concerns about the cardiovascular and neuropsychiatric side effects of smoking-cessation pharmacotherapy have in part limited their use. We sought to evaluate whether depressive symptoms are associated with active smoking among survivors of stroke and myocardial infarction (MI). To do this, we performed a cross-sectional analysis using data from the National Health and Nutrition Examination Survey (2005-2016). We included participants ≥20 years old with prior stroke or MI and any history of smoking. Symptoms of depression, at survey participation, were ascertained using the Patient Health Questionnaire-9. Active smoking was defined using self-report and, secondarily, with cotinine measures. We used logistic regression to evaluate the association between depression and active smoking after adjusting for demographics, smoking-related medical conditions, and health-related behaviors. We found that, among stroke and MI survivors with any history of smoking, 37.9% (95% CI, 34.5-41.3%) reported active smoking and 43.8% (95% CI, 40.3-47.3%) had biochemical evidence of smoking. Rates of active smoking were similar for stroke and MI survivors. Twenty-one percent screened positive for depression. In adjusted models, depression was associated with active smoking in the combined group of stroke and MI survivors (odds ratio, 2.28; 95% CI, 1.24-4.20) and in stroke survivors (odds ratio, 2.97; 95% CI, 1.20-7.38). Tests of heterogeneity by event type did not reveal an interaction. Findings were similar when using cotinine measures. We conclude that symptoms of depression were associated with active smoking among stroke and MI survivors. Stroke and MI survivors with symptoms of depression may require targeted smoking-cessation interventions.

Smoking-cessation pharmacotherapy for patients with stroke and TIA: Systematic review.

Data regarding the efficacy and safety of smoking-cessation pharmacotherapy after stroke are lacking. We systematically reviewed data on this topic by searching Medline, Cochrane, and Clinicaltrials.gov to identify randomized clinical trials (RCT) and observational studies that assessed the efficacy and safety of nicotine replacement therapy (NRT), varenicline, and bupropion in patients with stroke and TIA. We included studies that reported rates of smoking cessation, worsening or recurrent cerebrovascular disease, seizures, or neuropsychiatric events. We identified 2 RCTs and 6 observational studies; 3 included ischemic stroke and TIA, 2 subarachnoid hemorrhage (SAH), and 3 did not specify. Four studies assessed efficacy; cessation rates ranged from 33% to 66% with pharmacological therapy combined with behavioral interventions versus 15% to 46% without, but no individual study demonstrated a statistically significant benefit. Safety data for varenicline and buopropion in ischemic stroke were scarce. Patients with SAH who received NRT had more seizures (9% vs 2%; P = 0.024) and delirium (19% vs 7%; P = 0.006) in one study, but less frequent vasospasm in 3 studies. In conclusion, combined with behavioral interventions, smoking-cessation therapies resulted in numerically higher cessation rates. Limited safety data may prompt caution regarding seizures and delirium in patients with subarachnoid hemorrhage.

Maternal Use of Snus in Pregnancy and Early Childhood Blood Pressure: A Warning for e-Cigarettes?

See Article Nordenstam et al.

The imaging spectrum of posterior reversible encephalopathy syndrome: A pictorial review.

Posterior reversible encephalopathy syndrome (PRES) is characterized by the acute onset of neurologic symptoms (headache, altered mental status, visual changes, seizures) with accompanying vasogenic edema on brain imaging. Risk factors for PRES include infection, uremia, malignancy, autoimmune disorders, the peripartum state and hypertension. PRES is classically described as being posterior (i.e. parieto-occipital) but radiologic variants are increasingly recognized. This pictorial review demonstrates the heterogeneity of the different radiologic presentations of PRES in reference to lesion distribution, hemorrhage, diffusion restriction, contrast enhancement, and other associated findings.

Recurrent Thromboembolic Events after Ischemic Stroke in Patients with Primary Brain Tumors.

BACKGROUND: Stroke mechanisms and the risk of recurrent thromboembolism are incompletely understood in patients with primary brain tumors. We sought to better delineate these important clinical features. METHODS: We performed a retrospective cohort study of adults with primary brain tumors diagnosed with magnetic resonance imaging-confirmed acute ischemic stroke at the Memorial Sloan Kettering Cancer Center from 2005 to 2015. Study neurologists collected data on patients' cancer history, stroke risk factors, treatments, and outcomes. Stroke mechanisms were adjudicated by consensus. The primary outcome was recurrent thromboembolism (arterial or venous) and the secondary outcome was recurrent ischemic stroke. Kaplan-Meier statistics were used to calculate cumulative outcome rates, and Cox hazards analysis was used to evaluate the association between potential risk factors and outcomes. RESULTS: We identified 83 patients with primary brain tumors and symptomatic acute ischemic stroke. Median survival after index stroke was 2.2 years (interquartile range, .5-7.0). Tumors were mostly gliomas (72%) and meningiomas (13%). Most strokes were from unconventional mechanisms, particularly radiation vasculopathy (36%) and surgical manipulation (18%). Small- or large-vessel disease or cardioembolism caused 13% of strokes, whereas 29% were cryptogenic. Cumulative recurrent thromboembolism rates were 11% at 30 days, 17% at 180 days, and 27% at 365 days, whereas cumulative recurrent stroke rates were 5% at 30 days, 11% at 180 days, and 13% at 365 days. We found no significant predictors of outcomes. CONCLUSION: Patients with primary brain tumors generally develop strokes from rare mechanisms, and their risk of recurrent thromboembolism, including stroke, is high.

Imaging characteristics associated with clinical outcomes in posterior reversible encephalopathy syndrome.

PURPOSE: Posterior reversible encephalopathy syndrome (PRES) is a disorder of cerebrovascular autoregulation that can result in brain edema, hemorrhage, and infarction. We sought to investigate whether certain imaging characteristics in PRES are associated with clinically significant patient outcomes. METHODS: We retrospectively reviewed all cases of PRES occurring between 2008 and 2014 at two major academic medical centers. Demographic, clinical, and radiographic data were collected. We analyzed imaging studies for vasogenic edema, hemorrhage, and diffusion restriction. We performed univariate analysis and stepwise logistic regression to assess the association between our radiologic findings of interest and clinical outcomes as defined by hospital discharge disposition and modified Rankin scale (mRS) at time of discharge. RESULTS: We identified 99 cases of PRES in 96 patients. The median age was 55 years (IQR 30-65) and 74% were women. In 99 cases, 60% of patients had active cancer, 19% had history of bone marrow or organ transplantation, 14% had autoimmune disease, and 8% were peripartum. Imaging at clinical presentation showed extensive vasogenic edema in 39%, hemorrhage in 36%, hemorrhage with mass effect in 7%, and restricted diffusion in 16%. In our final logistic regression models, the presence of extensive vasogenic edema, hemorrhage with mass effect, or diffusion restriction was associated with worse clinical outcome as defined by both discharge disposition (OR = 4.3; 95% CI: 1.4-36.3; p = 0.047) and mRS (OR = 3.6; 95% CI: 1.2-10.7; p = 0.019). CONCLUSIONS: Extensive vasogenic edema, hemorrhage, and restricted diffusion on initial imaging in PRES are associated with worse clinical outcomes.