Development and initial validation of a patient-centered stroke outcome measure in young stroke survivors.

BACKGROUND AND PURPOSE: This study was undertaken to develop a patient-centered stroke outcome measure and initial validation of the proposed Young Stroke Questionnaire (YSQ). METHODS: This study assessed the reliability and discriminant validity of the YSQ. The initial questionnaire evolved from a focus group comprised of six young stroke survivors and six stroke neurologists centralized around four patient-centered domains. To determine the reliability and discriminant validity of the YSQ, 100 young stroke survivors were recruited and provided consent. Standardized clinical assessments completed included the modified Rankin Scale (mRS), National Institutes of Health Stroke Scale, and Stroke Impact Scale. Additionally, all patients were asked to complete the patient-centered YSQ. RESULTS: Of the 100 enrolled patients in the study (mean age ± standard deviation = 49 ± 11.3, 58% females, 53% African American, 44% White), Cronbach alpha for all domains was >0.7. Moreover, Cronbach alpha for entire questionnaire was >0.9, indicating that the scale, with four subdomains, is internally consistent and reproducible. Discriminant validity of the scale was assessed by comparing the means of each subdomain of the YSQ among healthy subjects to the groups of stroke patients as defined by the mRS. The YSQ was able to differentiate subjects with good outcome (mRS = 0-1) from subjects with varying degree of disability as defined by the mRS (p = 0.026). CONCLUSIONS: Standardized clinical assessments are not sensitive to disabilities in young stroke survivors. When compared to standardized clinical assessments, the YSQ is significantly capable of differentiating the young survivor perspective of the impact of stroke in all four subdomains.

Chronic Periodontitis is Associated With Cerebral Atherosclerosis -A Nationwide Study.

Introduction Chronic periodontitis and atherosclerosis share common risk factors and produce the same inflammatory markers. Many studies found a high prevalence of chronic periodontitis in patients with atherosclerosis but there is no strong evidence to support a specific association of chronic periodontitis with cerebral atherosclerosis. We aimed to study the concurrent prevalence and association of chronic periodontitis with cerebral atherosclerosis and cerebrovascular diseases among the US population. Methods We performed a cross-sectional analysis of a Nationwide Inpatient Sample with adult hospitalizations to identify the primary diagnosis of cerebrovascular diseases [acute ischemic stroke (AIS), hemorrhagic stroke (HS), and transient ischemic attack (TIA)] with concurrent cerebral atherosclerosis and chronic periodontitis. Multivariate survey logistic regression models were fitted to evaluate the linkage of chronic periodontitis with cerebral atherosclerosis and cerebrovascular diseases. Results Of total 56,499,788 hospitalizations, 0.01% had chronic periodontitis. Prevalence of chronic periodontitis was higher in 50-64 years (36.18% vs. 23.91%), males (59.19% vs. 41.06% in females), Afro-Americans (25.93% vs. 15.21%), and 0-25th percentile median-household-income-category (38.31% vs. 30.15%) compared to non-chronic periodontitis. There was significantly higher prevalence of cerebral atherosclerosis (0.71% vs. 0.41%; p<0.0001) with weak evidence of high prevalence of cerebrovascular diseases (AIS:2.21% vs. 1.97%; p=0.1563; HS:0.57% vs. 0.46%; p=0.1560) among chronic periodontitis compared to non-chronic periodontitis. In regression analysis, odds of having cerebral atherosclerosis were 2.48-folds higher in patients with chronic periodontitis compared to that without-chronic periodontitis, and cerebral atherosclerosis patients were associated with higher odds of TIA (aOR:2.40; p<0.0001), AIS (aOR:3.35; p<0.0001), and HS (aOR:1.51; p<0.0001) compared to without-cerebral atherosclerosis. No significant relationship between chronic periodontitis and cerebrovascular diseases was observed. Conclusion Although chronic periodontitis may not directly increase the risk of cerebrovascular diseases, it increases the burden of cerebrovascular diseases by evidently increasing the risk of cerebral atherosclerosis. Early identification of chronic periodontitis and atherosclerotic risk factors may help to mitigate the risk of cerebrovascular diseases.

Early Anticoagulation or Antiplatelet Therapy Is Critical in Craniocervical Artery Dissection: Results from the COMPASS Registry.

INTRODUCTION: Craniocervical artery dissection (CeAD) is a leading cause of stroke in the young patient population. Recent studies reported a low rate of major adverse cardiac events (MACEs) in patients with CeAD, with no significant difference between patients randomized to anticoagulation or antiplatelet therapy. OBJECTIVE: To compare the effectiveness of anticoagulation and antiplatelet therapy in patients with CeAD. METHODS: All CeAD patients from 2015 to 2017 were consecutively identified by an electronic medical record-based application and enrolled in this prospective longitudinal registry. CeAD was confirmed by imaging and graded using the Denver scale for blunt cerebrovascular injury. Patients were followed for 12 months for MACE defined as stroke, transient ischemic attack (TIA), or death. RESULTS: The cohort included 111 CeAD patients (age 53 ± 15.9 years, 56% Caucasian, 50% female). CeAD was detected by magnetic resonance (5%), computed tomography (88%), or catheter angiography (7%). CeAD was noted in the carotid (59%), vertebral (39%), and basilar (2%) arteries, 82% of which were extracranial dissections. CeAD was classified as grade I, II, III, and IV in 16, 33, 19, and 32%, respectively. A total of 40% of dissections were due to known trauma. A predisposing factor was noted in the majority (78%) of patients, including violent sneezing (21%), carrying a heavy load (19%), sports/recreational activity (11%), chiropractic manipulation (9%), abrupt/prolonged rotation of head (9%), and prolonged phone use (9%). At presentation, 41% had a stroke, 5% had TIA, 39% had headache, and 36% were asymptomatic. Favorable outcome defined as a modified Rankin Scale score of 0-2 was noted in 68% at 3 months and 71% at 12 months. The rate of MACEs at 3 and 12 months was 11 and 14%, respectively, with more events observed in patients who were not receiving anticoagulation/antiplatelet therapy due to contraindications (p = 0.008). CONCLUSIONS: We report diagnostic characteristics, as well as short- and long-term outcomes of CeAD. A high MACE rate was observed within the first 2 weeks of CeAD diagnosis, notably in patients not initiated on anticoagulation or antiplatelet therapy.

Stroke-Associated Pneumonia: A Retrospective Study of Risk Factors and Outcomes.

INTRODUCTION: Pneumonia is the most common complication after stroke, but our knowledge on risk factors and predictors of stroke-associated pneumonia (SAP) is limited. We sought to evaluate the predictors and outcomes of SAP among acute ischemic stroke (AIS) hospitalizations. METHODS: This is a cross-sectional study of the Nationwide Inpatient Sample database from the year 2003 to 2014. We identified adult hospitalizations with AIS using International Classification of Diseases, ninth revision, clinical modification (ICD-9-CM) codes. The SAP was identified by the presence of a secondary diagnosis of hospital-acquired pneumonia and ventilator-associated pneumonia. Multivariable survey logistic regression models were utilized to evaluate the predictors of SAP. RESULTS: Overall, 4,224,924 AIS hospitalizations were identified, of which 149,169 (3.53%) had SAP. The prevalence of SAP decreased from 3.72% in 2003 to 3.17% in 2014 (P<0.0001). Mortality [17.12% vs. 4.77%; adjusted odds ratio (aOR): 1.71; P<0.0001] and morbidity (22.53% vs. 3.28%; aOR: 1.86; P<0.0001) were markedly elevated in SAP group compare to non-SAP group. The significant risk factors of pneumonia among AIS hospitalization were nasogastric tube (aOR: 1.21; P=0.0179), noninvasive mechanical ventilation (aOR: 1.65; P<0.0001), invasive mechanical ventilation (aOR: 4.09; P<0.0001), length of stay between 1 to 2 weeks (aOR: 1.99; P<0.0001), >2 weeks (aOR: 3.90; P<0.0001), hemorrhagic conversion (aOR: 1.17; P=0.0002), and epilepsy (aOR: 1.09; P=0.0009). Other concurrent comorbidities which increased the risk of SAP among AIS patients were acquired immune deficiency syndrome (aOR: 1.88; P<0.0001), alcohol abuse (aOR: 1.60; P=0.0006), deficiency anemia (aOR: 1.26; P<0.0001), heart failure (aOR: 1.62; P<0.0001), pulmonary disease (aOR: 1.73; P<0.0001), diabetes (aOR: 1.29; P=0.0288), electrolyte disorders (aOR: 1.50; P<0.0001), paralysis (aOR: 1.22; P<0.0001), pulmonary circulation disorders (aOR: 1.22; P<0.0001), renal failure (aOR: 1.12; P<0.0001), coagulopathy (aOR: 1.13; P=0.0006), and weight loss (aOR: 1.39; P<0.0001). CONCLUSION: Our data underline the considerable epidemiological and prognostic impact of SAP in patients with AIS leading to higher mortality, morbidity, length of stay, and hospital cost despite advancements in care.

Hypocalcemia and Vitamin D Deficiency amongst Migraine Patients: A Nationwide Retrospective Study.

Background and Objectives: Inadequate vitamin D and calcium intake have been linked to many health issues including chronic headaches. Some studies suggested an association between low vitamin D levels and increase the risk of frequent headaches in middle-aged and older men; however, no single study reported the role of these deficiencies in migraine patients. We aimed to investigate the association of hypocalcemia and vitamin D deficiency with migraine hospitalizations. Materials and Methods: A population-based retrospective cross-sectional analysis of the Nationwide Inpatient Sample (NIS) (years 2003-2014) in migraine hospitalizations was performed. The prevalence, demographic characteristics and All Patient Refined Diagnosis Related Groups severity/disability association were compared in patients with hypocalcemia and vitamin D deficiency to those without deficiencies, using ICD-9-CM codes. Weighted analyses using Chi-Square, paired Student's t-test, and Cochran-Armitage trend test were performed. Survey logistic regression was performed to find an association between deficiencies and migraine hospitalizations and deficiency induced disability amongst migraineurs. Results: Between years 2003 and 2014, of the total 446,446 migraine hospitalizations, 1226 (0.27%) and 2582 (0.58%) presented with hypocalcemia and vitamin D deficiency, respectively. In multivariable analysis, hypocalcemia [Odds Ratio (OR): 6.19; Confidence Interval (CI): 4.40-8.70; p < 0.0001] and vitamin D deficiency (OR: 3.12; CI: 2.38-4.08; p < 0.0001) were associated with markedly elevated odds of major/extreme loss of function. There was higher prevalence (3.0% vs. 1.5% vs. 1.6%; p < 0.0001) and higher odds of migraine among vitamin D deficiency (OR: 1.97; CI: 1.89-2.05; p < 0.0001) patients in comparison to patients with hypocalcemia (OR: 1.11; CI: 1.03-1.20; p = 0.0061) and no-deficiency, respectively. Conclusions: In this study, we demonstrated a significant association between hypocalcemia and vitamin D deficiency with migraine attacks and deficiency induced loss of function among migraineurs. Early preventive measures may reduce the disability in migraineurs.

Migraine Age of Onset and Association With Ischemic Stroke in Late Life: 20 Years Follow-Up in ARIC.

BACKGROUND AND PURPOSE: To evaluate the association between cumulative exposure to migraine and incidence of ischemic stroke in the Atherosclerosis Risk in Communities (ARIC) study. METHODS: In this ongoing, prospective longitudinal community-based cohort, participants were interviewed to ascertain migraine history at the third visit (1993-1995), followed for ischemic stroke incidence over 20 years. We performed a post hoc analysis to evaluate the association between the age of migraine onset and ischemic stroke. RESULTS: We identified 447 migraineurs with aura (MA) and 1128 migraineurs without aura (MO) among 11,592 black and white participants. There was an association between the age of MA onset ≥50 years old (average duration = 4.75 years) and ischemic stroke when compared to no headache group (multivariable adjusted HR = 2.17, 95% CI [1.39-3.39], P < .001). MA onset <50 years old (average duration = 28.17 years) was not associated with stroke (multivariable adjusted HR = 1.31, 95% CI [0.86-2.02], P = .212). These results were consistent with our logistic regression model. MO was not associated with increased stroke regardless of the age of onset. The absolute risk for stroke in migraine with aura is 37/447 (8.27%) and migraine without aura is 48/1128 (4.25%). CONCLUSION: As compared to the no headache participants, increased stroke risk in late life was observed in participants with late onset of MA. In this cohort, longer cumulative exposure to migraine with visual aura, as would be expected with early onset of migraine, was not associated with increased risk of ischemic stroke in late life. This study underscores the importance of the age of onset of MA in assessing stroke risk in older migraineurs.

Ischemic stroke subtypes and migraine with visual aura in the ARIC study.

OBJECTIVE: To investigate the association among migraine, ischemic stroke, and stroke subtypes in the Atherosclerosis Risk in Communities (ARIC) study. METHODS: In this ongoing, prospective, longitudinal community-based cohort study, participants were given an interview ascertaining migraine history in 1993-1995, and were followed for all vascular events, including stroke. All stroke events over the subsequent 20 years were adjudicated and classified into stroke subtypes by standard definitions. Cox proportional hazards models adjusted for stroke risk factors were used to study the relationship between migraine and ischemic stroke, overall, as well as stroke subtypes (cardioembolic, lacunar, or thrombotic). RESULTS: We identified 1,622 migraineurs among 12,758 participants. Mean age of the study population at the 3rd clinical visit was 59 years. When compared to nonheadache participants, there was a significant association between migraine with visual aura and ischemic stroke (hazard ratio [HR] 1.7, 95% confidence interval [CI] 1.2-2.6, p = 0.008). Migraine without visual aura was not significantly associated with ischemic stroke (HR 1.2, CI 1.0-1.8, p = 0.28) when compared to nonheadache participants. Among the 3 subtypes of ischemic stroke evaluated, migraine with visual aura was significantly associated only with cardioembolic stroke (HR 3.7, 95% CI 1.6-8.7, p = 0.003). CONCLUSION: In participants with migraine with visual aura in late middle age, increased risk of cardioembolic stroke was observed. Migraine with visual aura was linked to increased stroke risk, while migraine without visual aura was not, over the period of 20 years. These results are specific to older migraineurs.

The association of insular stroke with lesion volume.

The insula has been implicated in many sequelae of stroke. It is the area most commonly infarcted in people with post-stroke arrhythmias, loss of thermal sensation, hospital acquired pneumonia, and apraxia of speech. We hypothesized that some of these results reflect the fact that: (1) ischemic strokes that involve the insula are larger than strokes that exclude the insula (and therefore are associated with more common and persistent deficits); and (2) insular involvement is a marker of middle cerebral artery (MCA) occlusion. We analyzed MRI scans of 861 patients with acute ischemic hemispheric strokes unselected for functional deficits, and compared infarcts involving the insula to infarcts not involving the insula using t-tests for continuous variables and chi square tests for dichotomous variables. Mean infarct volume was larger for infarcts including the insula (n = 232) versus excluding the insula (n = 629): 65.8 ± 78.8 versus 10.2 ± 15.9 cm(3) (p < 0.00001). Even when we removed lacunar infarcts, mean volume of non-lacunar infarcts that included insula (n = 775) were larger than non-lacunar infarcts (n = 227) that excluded insula: 67.0 cm(3) ± 79.2 versus 11.5 cm(3) ± 16.7 (p < 0.00001). Of infarcts in the 90th percentile for volume, 87% included the insula (χ(2) = 181.8; p < 0.00001). Furthermore, 79.0% infarcts due to MCA occlusion included the insula; 78.5% of infarcts without MCA occlusion excluded the insula (χ(2) = 93.1; p < 0.0001). The association between insular damage and acute or chronic sequelae likely often reflects the fact that insular infarct is a marker of large infarcts caused by occlusion of the MCA more than a specific role of the insula in a range of functions. Particularly in acute stroke, some deficits may also be due to ischemia of the MCA or ICA territory caused by large vessel occlusion.

Association of Dietary Factors with Progression of AA in Stroke/TIA Patients.

OBJECTIVE: To investigate the effect of dietary factors such as calorie intake and dietary fats on the progression of aortic arch atheroma (AA). BACKGROUND: In stroke/TIA patients, progression of AA is associated with recurrent vascular events. DESIGN/METHODS: Consecutive patients with measurable (>1 mm) AA atheroma on baseline transesophageal echocardiogram (TEE) evaluation consented to a protocol mandated follow-up TEE at 12 months. Patients that had adequate paired AA images were assessed for progression, defined as Δ ≥ 1 grade worsening (based on plaque thickness over 12 months). Stroke risk factors and fasting lipid profile were assessed at baseline. The patient's nutritional intake was measured at baseline using the Gladys Block Food Frequency Questionnaire. RESULTS: One-hundred-nine patients (70 strokes, 33 TIAs) had sequential TEEs, of whom 27% (N=30) progressed and 73% (N=79) did not. Patients with progression had higher daily calorie (1778 ± 623 vs. 1378 ± 406 Calories, p=0.008), fat (76 ± 33 vs. 52 ± 23 grams, p=0.0002), carbohydrate (208 ± 78 vs. 169 ± 57 grams, p=0.01) and protein (73 ± 26 vs. 57 ± 21 grams, p=0.005) intake. On Further analysis among different fats showed a higher consumption of saturated fats (25 ± 12 vs. 17 ±8 grams, p=0.00051) as well as unsaturated fats (44 ± 20 vs. 30 ± 13 grams, p=0.002). These differences remained significant after we adjusted for the medication use. However the significance of these differences was attenuated after adjusting for the calorie intake. Cholesterol consumption did not differ between the progression and no-progression group (262 ± 125 vs. 213 ± 149 mg, p=0.2). CONCLUSIONS/RELEVANCE: Calorie intake plays a significant role in the progression of AA. Further studies are needed to confirm these findings and determine the specific dietary modifications that may prevent AA progression and associated recurrent vascular events.