Risk Stratification Tools to Guide a Personalized Approach for Cardiac Monitoring in Embolic Stroke of Undetermined Source.

Current recommendations support a personalized sequential approach for cardiac rhythm monitoring to detect atrial fibrillation after embolic stroke of undetermined source. Several risk stratification scores have been proposed to predict the likelihood of atrial fibrillation after embolic stroke of undetermined source. This systematic review aimed to provide a comprehensive overview of the field by identifying risk scores proposed for this purpose, assessing their characteristics and the cohorts in which they were developed and validated, and scrutinizing their predictive performance. We identified 11 risk scores, of which 4 were externally validated. The most frequent variables included were echocardiographic markers and demographics. The areas under the curve ranged between 0.70 and 0.94. The 3 scores with the highest area under the curve were the Decryptoring (0.94 [95% CI, 0.88-1.00]), newly diagnosed atrial fibrillation (0.87 [95% CI, 0.79-0.94]), and AF-ESUS (Atrial Fibrillation in Embolic Stroke of Undetermined Source) (0.85 [95% CI, 0.80-0.87]), of which only the latter was externally validated. Risk stratification scores can guide a personalized approach for cardiac rhythm monitoring after embolic stroke of undetermined source.

Decreased monocyte calcium sensing receptor expression in patients with chronic kidney disease is associated with impaired monocyte ability to reduce vascular calcification.

In chronic kidney disease (CKD), calcium-sensing receptor (CaSR) expression and function have been extensively studied in parathyroid tissue and vascular tissues. To examine whether similar changes occurred in other tissues, we measured total and surface CaSR expression in monocytes of patients with various stages of CKD and healthy volunteers respectively in cross-sectional studies. We further explored in vitro the impact of uremic serum on CaSR expression in monocytes (U937 and THP-1 cell lines), and whether human peripheral blood mononuclear cells or U937 and THP-1 monocytes might modify vascular calcium deposition in rat carotid arteries in vitro. CKD was associated with a decrease in peripheral blood mononuclear cell CaSR expression both in total and at the monocyte surface alone (43% and 34%, respectively in CKD stages 4-5). This decrease was associated with a reduction in the ability of monocytes to inhibit vascular calcification in vitro. Pretreatment with the calcimimetic NPSR568 of peripheral blood mononuclear cells isolated from patients with CKD significantly improved monocyte capacity to reduce carotid calcification in vitro. The fewer peripheral blood mononuclear cells expressing cell surface CaSR, the more calcimimetic treatment enhanced the decrease of carotid calcium content. Thus, we demonstrate that monocyte CaSR expression is decreased in patients with CKD and provide in vitro evidence for a potential role of this decrease in the promotion of vascular calcification. Hence, targeting this alteration or following monocyte CaSR expression as an accessible marker might represent a promising therapeutic strategy in CKD-associated arterial calcification.

Cognitive Impairments and Dysexecutive Behavioral Disorders in Chronic Kidney Disease.

The purpose of this study was to characterize cognitive impairments and behavioral disorders in a sample of patients with chronic kidney disease (CKD). A total of 52 patients with CKD were prospectively recruited over a 344-day period. Cognitive functions (memory, action speed, executive function, and language) and behavioral characteristics were assessed with a standardized comprehensive battery. The patients' performances were interpreted with a validated method on the basis of normative data from 1,003 healthy control subjects. Brain MRI and biological data were collected. Multivariable linear regression models and bootstrap analyses were used to identify risk factors for cognitive impairment. Cognitive impairment was observed in 32.5% (95% confidence interval: 17%-48%) of the 40 included patients with full data sets. Action speed and executive functions were the most frequently impaired domains. Dysexecutive behavioral disorders were observed in 27% of patients, and depression was observed in 32.5%. Cognitive impairment was independently associated with stroke volume, high serum parathyroid hormone and uric acid levels, and low serum glucose levels (adjusted R2=0.54, p<0.001 One-third of patients with CKD had cognitive impairments (action speed and executive functions), behavioral dysexecutive disorders (hypoactivity with apathy, irritability, or anosognosia), or depression.

Imaging Characteristics of Venous Parenchymal Abnormalities.

BACKGROUND AND PURPOSE: There are few published data on the patterns of parenchymal imaging abnormalities in a context of cerebral venous thrombosis (CVT). The objectives of the present study were to describe the patterns of parenchymal lesions associated with CVT and to determine the lesion sites. METHODS: We included 44 consecutively hospitalized patients with CVT and parenchymal lesions on magnetic resonance imaging. The diagnosis of CVT had been confirmed by magnetic resonance imaging/magnetic resonance venography. Magnetic resonance imaging patterns for CVT were retrospectively analyzed with regard to the lesion's type, shape, and site. RESULTS: The most frequent stroke subtype was hemorrhagic ischemia (in 56.8% of cases), followed by intracerebral hematoma (in 22.72% of cases) and nonhemorrhagic ischemia (in 20.45% of cases). Although there were no significant differences between these 3 groups with regard to the clinical and radiological characteristics, we observed a nonsignificant trend (P=0.08) toward a shorter time interval between hospital admission and magnetic resonance imaging for nonhemorrhagic stroke. The CVT parenchymal abnormalities were centered on 6 main foci and were related to the site of venous occlusion: (1) the inferior parietal lobule (n=20; 44.5%), associated mainly with occlusion of the transverse sinus (n=10) or pure cortical veins (n=10); (2) the inferior and posterior temporal regions (n=10; 22.75%), associated mainly with occlusion of the transverse sinus (n=9); (3) the parasagittal frontal region (n=6; 13.6%), associated mainly with occlusion of the superior sagittal sinus (n=4) or the transverse sinus (n=4); (4) the thalamus (n=5; 11.3%) associated with occlusion of the straight sinus (n=5); (5) the cerebellar hemisphere (n=2; 4.5%), associated in both cases with occlusion of the transverse sinus; and (6) the deep hemispheric regions (n=3; 6.8%), associated with occlusion of the superior sagittal sinus in all cases. CONCLUSIONS: Parenchymal lesions caused by CVT display specific anatomic patterns, which is mainly determined by the site of venous occlusion.

Prolonged acute migraine with aura and reversible brain MRI abnormalities after liquid sclerotherapy.

Transient visual disturbances constitute the most commonly reported neurological side effect during and immediately after sclerotherapy. A few studies, based on clinical and diffusion-weighted MRI assessments, have suggested that these transient neurological symptoms correspond to migraine with aura. Recently, it has been reported that brain magnetic resonance imaging can reveal transient T2*-weighted abnormalities during the acute phase of migraine with aura. We reported a 36-year-old man who presented with transient neurological symptoms and concomitant T2*-weighted abnormalities on brain magnetic resonance imaging immediately after liquid sclerotherapy. We hypothesize that the reversible nature of the patient's T2*-weighted abnormalities may indicate a relationship with the post-sclerotherapy migraine with aura attack.

Validation of an integrated method for determining cognitive ability: Implications for routine assessments and clinical trials.

INTRODUCTION: Although accurate diagnosis of deficit of mild intensity is critical, various methods are used to assess, dichotomize and integrate performance, with no validated gold standard. This study described and validated a framework for the analysis of cognitive performance. METHODS: This study was performed by using the Groupe de Réflexion sur L'Evaluation des Fonctions EXécutives (GREFEX) database (724 controls and 461 patients) examined by 7 tests assessing executive functions. The first phase determined the criteria for the cutoff scores, the second phase, the effect of test number on diagnostic accuracy and the third phase, the best methods for combining test scores into an overall summary score. Four validation criteria were used: determination of impaired performance as compared to expected one, false-positive rate ≤5%, detection of both single and multiple impairments with optimal sensitivity. RESULTS: The procedure based on 5th percentile cutoffs determined from standardized residuals was the most appropriate procedure. Although area under the curve (AUC) increased with the number of scores (p = .0001), the false-positive rate also increased (p = .0001), resulting in suboptimal sensitivity for detecting selective impairment. Two overall summary scores, the average of the seven process scores and the Item Response Theory (IRT) score, had significantly (p = .0001) higher AUCs, even for patients with a selective impairment, and provided higher resulting prevalence of dysexecutive disorders (p = .0001). CONCLUSIONS: The present study provides and validates a generative framework for the interpretation of cognitive data. Two overall summary score met all 4 validation criteria. A practical consequence is the need to profoundly modify the analysis and interpretation of cognitive assessments for both routine use and clinical research.

Possible involvement of microRNAs in vascular damage in experimental chronic kidney disease.

Chronic kidney disease (CKD) is associated with vascular calcifications and atherosclerosis. There is a need for novel predictors to allow earlier diagnosis of these disorders, predict disease progression, and improve assessment of treatment response. We focused on microRNAs since they are implicated in a variety of cellular functions in cardiovascular pathology. We examined changes of microRNA expression in aortas of CKD and non-CKD wild type mice and apolipoprotein E knock-out mice, respectively. Both vascular smooth muscle-specific miR-143 and miR-145 expressions were decreased in states of atherosclerosis and/or CKD or both, and the expression level of protein target Myocardin was increased. The inflammatory miR-223 was increased in more advanced stages of CKD, and specific protein targets NFI-A and GLUT-4 were dramatically decreased. Expression of miR-126 was markedly increased and expression of protein targets VCAM-1 and SDF-1 was altered during the course of CKD. The drug sevelamer, commonly used in CKD, corrected partially these changes in microRNA expression, suggesting a direct link between the observed microRNA alterations and uremic vascular toxicity. Finally, miR-126, -143 and -223 expression levels were deregulated in murine serum during the course of experimental CKD. In conclusion, these miRNAs could have role(s) in CKD vascular remodeling and may therefore represent useful targets to prevent or treat complications of CKD.

MRI and magnetic resonance angiography findings in patients with multiple sclerosis mimicked by stroke.

We report a 45-year-old woman who presented with a first demyelinating event with abnormalities seen on both MRI and magnetic resonance angiography that were highly suggestive of acute ischemic stroke. This report highlights the problem of differential diagnosis of acute neurological symptoms in adult subjects.

Cognitive disorders and dementia in CKD: the neglected kidney-brain axis.

Epidemiologic data suggest that individuals at all stages of CKD have a higher risk of developing cognitive disorders and dementia. This risk is generally explained by the high prevalence of both symptomatic and subclinical ischemic cerebrovascular lesions. However, other potential mechanisms, including direct neuronal injury by uremic toxins, could also be involved, especially in the absence of obvious cerebrovascular disease. We discuss the prevalence and characteristics of cognitive disorders and dementia in patients with CKD, brain imaging findings, and traditional and nontraditional risk factors. Understanding the pathophysiologic interactions between renal impairment and brain function is important in order to minimize the risk for future cognitive impairment.

Cognitive impairment after cerebral venous thrombosis: a two-center study.

The objective of this observational study of consecutive patients hospitalized for cerebral venous thrombosis (CVT) was to determine the prevalence of post-CVT cognitive impairment and identify factors associated with this condition. Out of a total of 73 patients hospitalized for CVT, 52 were included in the study and 44 were assessed with a comprehensive neuropsychological battery. At the last outpatient visit (mean ± SD time since CVT: 22 ± 13 months), a standardized, neuropsychological assessment was administered. Cognitive impairment was defined as significant impairment (with a cut-off at the 5th percentile) in at least two of the cognitive domains tested in the neuropsychological battery or severe aphasia or cognitive disorders with MMSE score ≤ 17 out of 30. Cognitive impairment was observed in 16 patients (31 %; 95 % CI 18-43 %): 4 with major disability precluding comprehensive assessment (3 with severe aphasia, 1 with MMSE ≤ 17) and 12 with significant impairments in at least two cognitive domains. Determinants of long-term cognitive impairment were straight sinus involvement (OR 22.4; 95 % CI 1.79-278.95; p = 0.016) and the presence of parenchymal lesions on follow-up magnetic resonance imaging (OR 7.8; 95 % CI 1.40-43.04; p = 0.019). The sole predictor of failure to return to full-time employment was cognitive impairment (OR 21.0; 95 % CI 3.35-131.44; p = 0.001). Cognitive impairment persists in up to one-third of cases of CVT. It is more frequent in patients with deep CVT and persistent parenchymal lesions and is associated with failure to return to full-time employment.

Cognitive impairment and dementia after intracerebral hemorrhage: a cross-sectional study of a hospital-based series.

BACKGROUND: Frequencies of cognitive impairment and dementia have not been assessed in spontaneous intracerebral hemorrhage (ICH). The objective of this study was to determine the frequencies and patterns of cognitive impairment and dementia in a cross-sectional study of consecutive patients hospitalized in a single university medical center. METHODS: Of 183 consecutive patients hospitalized between 2002 and 2006, 80 survivors were contacted and 78 were included (mean time since stroke 40 months). Thirty patients were scored with the Informant Questionnaire on Cognitive Decline in the Elderly and Instrumental Activities of Daily Living in a telephone interview, and 48 underwent a comprehensive clinical and neuropsychological assessment. RESULTS: Dementia was observed in 18 of 78 patients (23%; 95% confidence interval [CI] 13-32%) and cognitive impairment without dementia was seen in 37 of 48 patients (77%; 95% CI 65-89%). The cognitive disorders mainly concerned episodic memory (52%), psychomotor speed (44%), and executive function (37%), followed by language and visuoconstructive abilities. In a logistic regression analysis, Rankin score >1 at discharge and hemorrhage volume were the initial factors to be selected as a predictor of long-term dementia. CONCLUSIONS: This single-center, cross-sectional study revealed that the prevalence of dementia and cognitive impairment without dementia after ICH are high and are similar to those observed in cerebral infarct. Further longitudinal, prospective studies are required to assess accurately the prevalence, mechanisms and predictors of post-ICH dementia.

Posterior Cerebral Infarction following Loss of Guide Wire.

Stroke after internal jugular venous cannulation typically leads to acute carotid or vertebral arteries injury and cerebral ischemia. We report the first case of delayed posterior cerebral infarction following loss of guide wire after left internal jugular venous cannulation in a 46-year-old woman with a history of inflammatory bowel disease. Our observation highlights that loss of an intravascular guide wire can be a cause of ischemic stroke in patients undergoing central venous catheterization.

NIHSS and acute complications after anterior and posterior circulation strokes.

BACKGROUND: The purpose of this study was to determine whether the National Institutes of Health Stroke Scale (NIHSS) score was associated with inhospital neurological and medical complications (NMC) in patients with posterior circulation infarction. METHODS: This retrospective study included all patients admitted to our stroke unit during a one-year period (n = 289). NMC included neurological deterioration (ie, worsening by 4 points or more of the NIHSS score during the hospital stay) and all other medical complications based on what was recorded in the patients' charts. RESULTS: Seventy-nine patients (27%) experienced NMC. In posterior circulation infarction patients (n = 90), patients with NMC had a higher baseline NIHSS score (10.9 versus 2.2, P = 0.004) and a baseline NIHSS score >2 (78% versus 36%, P = 0.003). In stepwise logistic regression, an NIHSS score >2 (odds ratio: 8.2; 95% confidence interval: 1.64-41.0; P = 0.01) was associated with NMC. Similar results were observed for anterior circulation infarction patients but with a higher cutoff value for NIHSS score. CONCLUSION: In ischemic stroke patients, an increased baseline NIHSS score was associated with an increased risk of NMC. This association applied to anterior-circulation as well as posterior circulation stroke, although zero on the NIHSS for posterior circulation stroke does not mean the absence of NMC during hospitalization. The clinical significance of these findings requires further evaluation in larger prospective studies.

Attenuation of brain white matter lesions after lacunar stroke.

White matter lesions (WMLs) are commonly observed in stroke patients with small vessel disease (SVD) and are thought to result from a progressive, irreversible disease process following arteriolosclerosis. In this study, we report a case of partial disappearance of WMLs 1 year after a lacunar stroke in a 69-year-old man with evidence of SVD. We also discuss possible mechanisms associated with this observation.