C-reactive protein and D-dimer in cerebral vein thrombosis: Relation to clinical and imaging characteristics as well as outcomes in a French cohort study.

Introduction: Cerebral venous sinus thrombosis (CVST) is a rare disease with highly variable clinical presentation and outcomes. Clinical studies suggest a role of inflammation and coagulation in CVST outcomes. The aim of this study was to investigate the association of inflammation and hypercoagulability biomarkers with CVST clinical manifestations and prognosis. Methods: This prospective multicenter study was conducted from July 2011 to September 2016. Consecutive patients referred to 21 French stroke units and who had a diagnosis of symptomatic CVST were included. High-sensitivity C-reactive protein (hs-CRP), neutrophil-to-lymphocyte ratio (NLR), D-dimer, and thrombin generation using calibrated automated thrombogram system were measured at different time points until 1 month after anticoagulant therapy discontinuation. Results: Two hundred thirty-one patients were included. Eight patients died, of whom 5 during hospitalization. The day 0 hs-CRP levels, NLR, and D-dimer were higher in patients with initial consciousness disturbance than in those without (hs-CRP: 10.2 mg/L [3.6-25.5] vs 23.7 mg/L [4.8-60.0], respectively; NLR: 3.51 [2.15-5.88] vs 4.78 [3.10-9.59], respectively; D-dimer: 950 µg/L [520-2075] vs 1220 µg/L [950-2445], respectively). Patients with ischemic parenchymal lesions (n = 31) had a higher endogenous thrombin potential5pM than those with hemorrhagic parenchymal lesions (n = 31): 2025 nM min (1646-2441) vs 1629 nM min (1371-2090), respectively (P = .0082). Using unadjusted logistic regression with values >75th percentile, day 0 hs-CRP levels of >29.7 mg/L (odds ratio, 10.76 [1.55-140.4]; P = .037) and day 5 D-dimer levels of >1060 mg/L (odds ratio, 14.63 [2.28-179.9]; P = .010) were associated with death occurrence. Conclusion: Two widely available biomarkers measured upon admission, especially hs-CRP, could help predict bad prognosis in CVST in addition to patient characteristics. These results need to be validated in other cohorts.

Determinants of disability at 6 months after stroke: The GRECogVASC Study.

BACKGROUND AND PURPOSE: The aim of this study was to determine the contributions of background disorders responsible for participation restriction as indexed by a structured interview for the modified Rankin Scale (mRS-SI). METHODS: A subset of 256 patients was assessed at 6 months after stroke using the National Institutes of Health Stroke Scale (NIHSS), gait score, comprehensive cognitive battery (yielding a global cognitive Z-score), behavioral dysexecutive disorders (DDs), anxiety and depressive symptoms, epilepsy, and headache. Following bivariate analyses, determinants of participation restriction were selected using ordinal regression analysis with partial odds. RESULTS: Poststroke participation restriction (mRS-SI score > 1) was observed in 59% of the patients. In bivariate analyses, mRS-SI score was associated with prestroke mRS-SI score, 6-month NIHSS score, gait score, global cognitive Z-score, behavioral DDs, and presence of anxiety and depression (all: p = 0.0001; epilepsy: p =0.3; headache: p = 0.7). After logistic regression analysis, NIHSS score was associated with increasing mRS-SI score (p = 0.00001). Prestroke mRS-SI score (p = 0.00001), behavioral DDs (p = 0.0008) and global cognitive Z-score (p = 0.01) were associated with both mRS-SI score > 1 and mRS-SI score > 2. In addition, gait score was associated with mRS-SI score > 2 (p = 0.00001). This model classified 85% of mRS-SI scores correctly (p = 0.001). Structural equation modeling showed the contributions of gait limitation (standardized coefficient [SC]: 0.68; p = 0.01), prestroke mRS-SI (SC: 0.41; p = 0.01), severity of neurological impairment (SC: 0.16; p = 0.01), global cognitive Z-score (SC: -0.14; p = 0.05), and behavioral DDs (SC: 0.13; p = 0.01). CONCLUSION: These results provide a statistical model of weights of determinants responsible for poststroke participation restriction and highlight a new independent determinant: behavioral DDs.

Cerebral Venous Thrombosis: Clinical, Radiological, Biological, and Etiological Characteristics of a French Prospective Cohort (FPCCVT)-Comparison With ISCVT Cohort.

Introduction: Cerebral venous thrombosis (CVT) is a rare disease with highly variable clinical presentation and outcome. Etiological assessment may be negative. The clinical and radiological presentation and evolution can be highly variable. The mechanisms involved in this variability remain unknown. Objective: The aim of this multicenter French study registered on ClinicalTrials.gov (NCT02013635) was therefore to prospectively recruit a cohort of patients with cerebral venous thrombosis (FPCCVT) in order to study thrombin generation and clot degradation, and to evaluate their influence on clinical radiological characteristics. The first part of the study was to compare our cohort with a reference cohort. Methods: This prospective, multicenter, French study was conducted from July 2011 to September 2016. Consecutive patients (aged >15 years) referred to the stroke units of 21 French centers and who had a diagnosis of symptomatic CVT were included. All patients gave their written informed consent. The diagnosis of CVT had to be confirmed by imaging. Clinical, radiological, biological, and etiological characteristics were recorded at baseline, at acute phase, at 3 months and at last follow-up visit. Thrombophilia screening and the choice of treatment were performed by the attending physician. All data were compared with data from the International Study on CVT published by Ferro et al. Results: Two hundred thirty-one patients were included: 117 (50.6%) had isolated intracranial hypertension, 96 (41.5%) had focal syndrome. During hospitalization, 229 (99.1%) patients received anticoagulant treatment. Median length of hospital stay was 10 days. Five patients died during hospitalization (2.2%). At 3 months, 216 patients (97.0%) had follow-up with neurological data based on an outpatient visit. The mean duration of antithrombotic treatment was 9 months, and the mean time to last follow-up was 10.5 months. At the end of follow-up, eight patients had died, and 26 patients were lost to follow-up. At least one risk factor was identified in 200 patients. Conclusions: We demonstrated that the FPCCVT cohort had radiological, biological, and etiological characteristics similar to the historical ISCVT cohort. Nevertheless, the initial clinical presentation was less severe in our study probably due to an improvement in diagnostic methods between the two studies.

Patent foramen ovale closure in stroke patients with migraine in the CLOSE trial. The CLOSE-MIG study.

BACKGROUND AND PURPOSE: The efficacy of patent foramen ovale (PFO) closure to reduce the frequency of migraine attacks remains controversial. METHODS: This was a planned sub-study in migraine patients enrolled in a randomized, clinical trial designed to assess the superiority of PFO closure plus antiplatelet therapy over antiplatelet therapy alone to prevent stroke recurrence in patients younger than 60 years with a PFO-associated cryptogenic ischaemic stroke. The main outcome was the mean annual number of migraine attacks in migraine patients with aura and in those without aura, as recorded at each follow-up visit by study neurologists. RESULTS: Of 473 patients randomized to PFO closure or antiplatelet therapy, 145 (mean age 41.9 years; women 58.6%) had migraine (75 with aura and 70 without aura). Sixty-seven patients were randomized to PFO closure and 78 to antiplatelet therapy. During a mean follow-up of about 5 years, there were no differences between antiplatelet-only and PFO closure groups in the mean annual number of migraine attacks, both in migraine patients with aura (9.2 [11.9] vs. 12.0 [19.1], p = 0.81) and in those without aura (12.1 [16.1] vs. 11.8 [18.4], p > 0.999). There were no differences between treatment groups regarding cessation of migraine attacks, migraine-related disability at 2 years and use of migraine-preventive drugs during follow-up. CONCLUSIONS: In young and middle-aged adults with PFO-associated cryptogenic stroke and migraine, PFO closure plus antiplatelet therapy did not reduce the mean annual number of migraine attacks compared to antiplatelet therapy alone, in migraine patients both with and without aura.

Aortic root dilatation in PFO-related cryptogenic stroke: A propensity score-matched analysis.

BACKGROUND: Dilatation of the ascending aorta has an important role in the anatomical conformation of interatrial septum (IAS) especially when a patent foramen ovale (PFO) is present. The aim of the study was to investigate the relationship between ascending aortic dilation and PFO-related cryptogenic stroke in a cohort of cryptogenic strokes. METHODS: It is a retrospective, single-center echocardiographic study assessing aortic root dilatation in 315 consecutive patients with cryptogenic stroke between January 2011 and January 2019. Aortic root dilatation was defined by a diameter of the Valsalva sinuses of the proximal aorta >40 mm. Predictive factors of PFO were assessed by a multivariate analysis. Propensity score matching was applied to account for clinical differences. RESULTS: Of the 315 patients, 68 (22%) had an aortic root dilatation and 167 (53%) had a PFO. In the aortic root dilation group, PFO was more often diagnosed (n = 47/68 [69%], vs n = 120/247 [49%], P = .004). In the PFO group with aortic dilatation, IAS was more mobile (n = 37/47[79%] vs n = 69/120[57%], P < .012) and smaller (2.3 ± 0.5 vs 2.5 ± 0.5 mm, P < .009). On multivariate analysis, aortic root dilatation (OR: 2.6; 95% CI [1.2-5.6]; P = .001) and IAS hypermobility (OR: 5.2 95% CI [2.7-10]; P = .001) were associated with PFO. After propensity matching, aortic root dilatation remained strongly associated with PFO (n = 34/107 [32%] vs 15/107[14%], P = .002). CONCLUSION: Aortic root dilation and IAS hypermobility were strongly associated with PFO-related cryptogenic stroke.

Who should undergo a comprehensive cognitive assessment after a stroke? A cognitive risk score.

OBJECTIVE: To validate the ability of a specifically developed cognitive risk score to identify patients at risk of poststroke neurocognitive disorders (NCDs) who are eligible for a comprehensive cognitive assessment. METHODS: After assessing 404 patients (infarct 91.3%) in the Groupe de Réflexion pour l'Evaluation Cognitive VASCulaire (GRECogVASC) cross-sectional study with the National Institute of Neurological Disorders and Stroke-Canadian Stroke Network battery 6 months after stroke, we used multivariable logistic regression and bootstrap analyses to determine factors associated with NCDs. Independent, internally validated factors were included in a cognitive risk score. RESULTS: Cognitive impairment was present in 170 of the 320 patients with a Rankin Scale score ≥1. The backward logistic regression selected 4 factors (≥73% of the permutations): NIH Stroke Scale score on admission ≥7 (odds ratio [OR] 2.73, 95% confidence interval [CI] 1.29-4.3, p = 0.005), multiple strokes (OR 3.78, 95% CI 1.6-8, p = 0.002), adjusted Mini-Mental State Examination (MMSEadj) score ≤27 (OR 6.69, 95% CI 3.9-11.6, p = 0.0001), and Fazekas score ≥2 (OR 2.34, 95% CI 1.3-4.2, p = 0.004). The cognitive risk score computed with these 4 factors provided good calibration, discrimination (overoptimism-corrected C = 0.793), and goodness of fit (Hosmer-Lemeshow test p = 0.99). A combination of Rankin Scale score ≥1, cognitive risk score ≥1, and MMSEadj score ≥21 selected 230 (56.9%) of the 404 patients for a comprehensive assessment. This procedure yielded good sensitivity (96.5%) and moderate specificity (43%; positive predictive value 0.66, negative predictive value 0.91) and was more accurate (p ≤ 0.03 for all) than the sole use of screening tests (MMSE or Montréal Cognitive Assessment). CONCLUSION: The GRECogVASC cognitive risk score comprises 4 easily documented factors; this procedure helps to identify patients at risk of poststroke NCDs who must therefore undergo a comprehensive assessment. CLINICALTRIALSGOV IDENTIFIER: NCT01339195.

Neuroimaging Determinants of Poststroke Cognitive Performance.

Background and Purpose- We aimed to define the neuroimaging determinants of poststroke cognitive performance and their relative contributions among a spectrum of magnetic resonance imaging markers, including lesion burden and strategic locations. Methods- We prospectively included patients with stroke from the GRECogVASC study (Groupe de Réflexion pour l'Évaluation Cognitive Vasculaire) who underwent 3-T magnetic resonance imaging and a comprehensive standardized battery of neuropsychological tests 6 months after the index event. An optimized global cognitive score and neuroimaging markers, including stroke characteristics, cerebral atrophy markers, and small vessel diseases markers, were assessed. Location of strategic strokes was determined using a specifically designed method taking into account stroke size and cerebral atrophy. A stepwise multivariable linear regression model was used to identify magnetic resonance imaging determinants of cognitive performance. Results- Data were available for 356 patients (mean age: 63.67±10.6 years; 326 [91.6%] of the patients had experienced an ischemic stroke). Six months poststroke, 50.8% of patients presented with a neurocognitive disorder. Strategic strokes (right corticospinal tract, left antero-middle thalamus, left arcuate fasciculus, left middle frontal gyrus, and left postero-inferior cerebellum; R2=0.225; P=0.0001), medial temporal lobe atrophy ( R2=0.077; P=0.0001), total brain tissue volume ( R2=0.028; P=0.004), and stroke volume ( R2=0.013; P=0.005) were independent determinants of cognitive performance. Strategic strokes accounted for the largest proportion of the variance in the cognitive score (22.5%). The white matter hyperintensity burden, brain microbleeds, and dilated perivascular spaces were not independent determinants. Conclusions- Optimized global cognitive score and combined approach of both quantitative measures related to structure loss and qualitative measures related to the presence of strategic lesion are required to improve the determination of structure-function relationship of cognitive performance after stroke.

Patent Foramen Ovale Closure or Anticoagulation vs. Antiplatelets after Stroke.

BACKGROUND: Trials of patent foramen ovale (PFO) closure to prevent recurrent stroke have been inconclusive. We investigated whether patients with cryptogenic stroke and echocardiographic features representing risk of stroke would benefit from PFO closure or anticoagulation, as compared with antiplatelet therapy. METHODS: In a multicenter, randomized, open-label trial, we assigned, in a 1:1:1 ratio, patients 16 to 60 years of age who had had a recent stroke attributed to PFO, with an associated atrial septal aneurysm or large interatrial shunt, to transcatheter PFO closure plus long-term antiplatelet therapy (PFO closure group), antiplatelet therapy alone (antiplatelet-only group), or oral anticoagulation (anticoagulation group) (randomization group 1). Patients with contraindications to anticoagulants or to PFO closure were randomly assigned to the alternative noncontraindicated treatment or to antiplatelet therapy (randomization groups 2 and 3). The primary outcome was occurrence of stroke. The comparison of PFO closure plus antiplatelet therapy with antiplatelet therapy alone was performed with combined data from randomization groups 1 and 2, and the comparison of oral anticoagulation with antiplatelet therapy alone was performed with combined data from randomization groups 1 and 3. RESULTS: A total of 663 patients underwent randomization and were followed for a mean (±SD) of 5.3±2.0 years. In the analysis of randomization groups 1 and 2, no stroke occurred among the 238 patients in the PFO closure group, whereas stroke occurred in 14 of the 235 patients in the antiplatelet-only group (hazard ratio, 0.03; 95% confidence interval, 0 to 0.26; P<0.001). Procedural complications from PFO closure occurred in 14 patients (5.9%). The rate of atrial fibrillation was higher in the PFO closure group than in the antiplatelet-only group (4.6% vs. 0.9%, P=0.02). The number of serious adverse events did not differ significantly between the treatment groups (P=0.56). In the analysis of randomization groups 1 and 3, stroke occurred in 3 of 187 patients assigned to oral anticoagulants and in 7 of 174 patients assigned to antiplatelet therapy alone. CONCLUSIONS: Among patients who had had a recent cryptogenic stroke attributed to PFO with an associated atrial septal aneurysm or large interatrial shunt, the rate of stroke recurrence was lower among those assigned to PFO closure combined with antiplatelet therapy than among those assigned to antiplatelet therapy alone. PFO closure was associated with an increased risk of atrial fibrillation. (Funded by the French Ministry of Health; CLOSE ClinicalTrials.gov number, NCT00562289 .).

Creation of an intensive care unit and organizational changes in an adult emergency department: Impact on acute stroke management.

BACKGROUND AND PURPOSE: Following the reorganization of a University Medical Center onto a single campus, an Intensive Care Unit was created within the adult Emergency Department (ED ICU). We assessed the effects of these organizational changes on acute stroke management and the intravenous administration of recombinant tissue plasminogen activator (IV rtPA), as characterized by the thrombolysis rate, door-to-needle time (DNT) and outcome at 3months. METHODS: Between October 2013 and September 2015, we performed a retrospective, observational, single-center, comparative study of patients admitted for ischemic stroke and treated with IV rtPA during two 321-day periods (before and after the creation of the ED ICU). All patients with ischemic stroke were included. Multivariable logistic regression models were performed. The DNT was stratified according to a threshold of 60min. A favorable long-term outcome was defined as a modified Rankin score≤2 at 3months. RESULTS: A total of 1334 ischemic stroke patients were included. Among them, 101 patients received IV rtPA. The frequency of IV rtPA administration was 5.8% (39 out of 676) before the creation of the ED ICU, and 9.3% (62 out of 668) afterwards (odds ratio (OR) [95% confidence interval (CI)]: 1.67 [1.08-2.60]; p=0.02). Additionally, the DNT was shorter (OR [95%CI]: 4.30 [1.17-20.90]; p=0.04) and there was an improvement in the outcome (OR [95%CI]=1.30 [1.01-2.10]; p=0.045). CONCLUSION: Our results highlight the benefits of a separate ED ICU within conventional ED for acute stroke management, with a higher thrombolysis rate, reduced intrahospital delays and better safety.

Phenotypic variability in ARCA2 and identification of a core ataxic phenotype with slow progression.

Autosomal recessive cerebellar ataxia 2 (ARCA2) is a recently identified recessive ataxia due to ubiquinone deficiency and biallelic mutations in the ADCK3 gene. The phenotype of the twenty-one patients reported worldwide varies greatly. Thus, it is difficult to decide which ataxic patients are good candidates for ADCK3 screening without evidence of ubiquinone deficiency. We report here the clinical and molecular data of 10 newly diagnosed patients from seven families and update the disease history of four additional patients reported in previous articles to delineate the clinical spectrum of ARCA2 phenotype and to provide a guide to the molecular diagnosis. First signs occurred before adulthood in all 14 patients. Cerebellar atrophy appeared in all instances. The progressivity and severity of ataxia varied greatly, but no patients had the typical inexorable ataxic course that characterizes other childhood-onset recessive ataxias. The ataxia was frequently associated with other neurological signs. Importantly, stroke-like episodes contributed to significant deterioration of the neurological status in two patients. Ubidecarenone therapy markedly improved the movement disorders, including ataxia, in two other patients. The 7 novel ADCK3 mutations found in the 10 new patients were two missense and five truncating mutations. There was no apparent correlation between the genotype and the phenotype. Our series reveals that the clinical spectrum of ARCA2 encompasses a range of ataxic phenotypes. On one end, it may manifest as a pure ataxia with very slow progressivity and, on the other end, as a severe infantile encephalopathy with cerebellar atrophy. The phenotype of most patients, however, lies in between. It is characterized by a very slowly progressive or apparently stable ataxia associated with other signs of central nervous system involvement. We suggest undergoing the molecular analysis of ADCK3 in patients with this phenotype and in those with cerebellar atrophy and a stroke-like episode. The diagnosis of patients with a severe ARCA2 phenotype may also be performed on the basis of biological data, i.e. low ubiquinone level or functional evidence of ubiquinone deficiency. This diagnosis is crucial since the neurological status of some patients may be improved by ubiquinone therapy.

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 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.

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.

Presence of intracranial artery calcification is associated with mortality and vascular events in patients with ischemic stroke after hospital discharge: a cohort study.

BACKGROUND AND PURPOSE: Although intracranial artery calcification (IAC) has been reported to be a risk factor for ischemic stroke, the prognostic implications of IAC in stroke outcome are unknown. The purpose of this study was to determine the association between IAC and risk of vascular events and death in patients with stroke after hospital discharge. METHODS: All patients with ischemic stroke over a 1-year period were included (n=302). IAC, assessed by multidetector CT, was defined as hyperdense foci (peak density>130 Hounsfield units) and assessed in the 7 major cerebral arteries. The IAC scores ranged from 0 (no calcification) to 7. Follow-up information on major clinical events (including fatal or nonfatal ischemic stroke, cardiac and peripheral artery events, and all-cause death) was obtained by means of a structured phone interview. RESULTS: IAC was present in 260 patients (83%). With a mean follow-up of 773±223 days, 88 major clinical events occurred in 67 patients (22%): 45 new ischemic vascular events (ischemic stroke: n=22; cardiac event: n=15; peripheral artery event: n=8) and 43 deaths from any cause. Patients with the highest IAC scores had significantly higher rates of death and vascular events than those with the lowest IAC scores (log rank test, P=0.029). In the Cox proportional hazards regression model, the IAC score was significantly associated with major clinical events (hazard ratio, 1.34; 95% CI, 1.11-1.61; P=0.002). CONCLUSIONS: In patients with ischemic stroke, IAC detection may constitute a simple marker of a high risk of future major clinical events.

Is the Montreal Cognitive Assessment superior to the Mini-Mental State Examination to detect poststroke cognitive impairment? A study with neuropsychological evaluation.

BACKGROUND AND PURPOSE: A screening test is required to improve the diagnosis of poststroke cognitive impairment. The Montreal Cognitive Assessment (MoCA), a newly designed screening test, has been found to be more sensitive than Mini-Mental State Examination (MMSE), but its clinical value has not been established by means of a comprehensive neuropsychological battery. This study was designed to assess the value of MoCA and MMSE to detect poststroke cognitive impairment determined by a neuropsychological battery. METHODS: Both screening tests and a neuropsychological battery were administered during the acute phase in 95 patients referred for recent infarct or hemorrhage. Raw MMSE and MoCA scores were used with published cutoffs and new cutoff scores for MMSE and MoCA were also computed after adjustment for age and education. RESULTS: Using raw scores, MoCA was more frequently impaired (P=0.0001) than MMSE. MoCA showed good sensitivity (sensitivity, 0.94) but moderate specificity (specificity, 0.42; positive predictive value, 0.77; negative predictive value, 0.76), whereas an inverse profile was observed for MMSE (sensitivity, 0.66; specificity, 0.97; positive predictive value, 0.98; negative predictive value, 0.58). Adjusted scores with new cutoffs (MMSE(adj) ≤24, MoCA(adj) ≤20) provided good sensitivity and very good specificity for both tests (MMSE(adj): sensitivity, 0.7, specificity, 0.97, positive predictive value, 0.98, negative predictive value, 0.61; MoCA(adj): sensitivity, 0.67, specificity, 0.9, positive predictive value, 0.93, negative predictive value, 0.57). On receiver operating characteristic curve analysis, areas under the curve of all scores were >0.88. CONCLUSIONS: The previously reported high sensitivity of MoCA is associated with low specificity. Both screening tests are moderately sensitive to acute poststroke cognitive impairment. This study provides indications for the diagnosis of poststroke cognitive impairment.

Central neuropathic pain after cerebral venous thrombosis is not so uncommon: an observational study.

Central neuropathic pain (CNP) after stroke has not been studied in sufficient detail and published studies have only included patients with cerebral artery infarct or hemorrhage. This study evaluates the prevalence and factors associated with CNP after cerebral venous (and sinus) thrombosis (CVT). This observational study included all patients admitted to our stroke unit for CVT between January 2002 and December 2007. Clinical data for each patient were collected prospectively and were combined with retrospective review of neuroradiological imaging. CVT patients were systematically examined at the outpatient clinic at 6 months, 12 months, and annually thereafter, and information on long-term functional outcome, including the presence of CNP, were obtained by open-ended questions. A standardized CNP assessment was performed during the last outpatient visit and was based on the patient's interview and clinical examination. Pain characteristics were assessed by the DN4-questionnaire. CNP was considered when the patient met the following criteria: painful area within the area of sensory abnormalities and follow-up MRI showing brain parenchymal lesion. Among the 43 patients admitted for CVT, seven (16%) developed CNP during the first year of follow-up. Standardized CNP assessment was performed 24.9 ± 11.6 months after CVT: eight patients (19%) suffered from CNP. Initial motor deficit (87 vs. 17%, p < 0.001), initial sensory deficit (62 vs. 20%, p = 0.03), cerebral infarction (75 vs. 23%, p = 0.009), right-sided lesion on initial MRI (62 vs. 17%, p = 0.017), thalamic (37 vs. 0%, p = 0.005) and basal ganglia involvement (25 vs. 0%, p = 0.03) and vein of Galen occlusion (25 vs. 0%) were significantly associated with CNP. Despite several methodological limitations, CNP after CVT seems to be frequent, accounting for one-fifth of all cases of CVT. Some clinical and radiological factors might contribute to the development of CNP.