Neurology (Neurology)

Publisher: American Academy of Neurology, American Academy of Neurology

Journal description

Current impact factor: 8.30

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 8.303
2012 Impact Factor 8.249
2011 Impact Factor 8.312
2010 Impact Factor 8.017
2009 Impact Factor 8.172
2008 Impact Factor 7.043
2007 Impact Factor 6.014
2006 Impact Factor 5.69
2005 Impact Factor 4.947
2004 Impact Factor 5.973
2003 Impact Factor 5.678
2002 Impact Factor 5.34
2001 Impact Factor 5.212
2000 Impact Factor 4.781
1999 Impact Factor 5.232
1998 Impact Factor 4.972
1997 Impact Factor 4.526
1996 Impact Factor 4.612
1995 Impact Factor 4.633
1994 Impact Factor 4.347
1993 Impact Factor 3.99
1992 Impact Factor 4.355

Impact factor over time

Impact factor
Year

Additional details

5-year impact 8.40
Cited half-life 9.00
Immediacy index 1.82
Eigenfactor 0.13
Article influence 2.91
Other titles Neurology (Online), Neurology, Neurology online
ISSN 1526-632X
OCLC 40802116
Material type Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

American Academy of Neurology

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • NIH, Wellcome Trust, HHMI, CIHR, MRC, BBSRC, NERC, ESRC and STFC authors will on their behalf have the Publisher's version/PDF deposited in PubMed Central for release 12 months embargo after publication
    • If required by institutional policy, Publisher's version/PDF deposited available in PubMed Central may be deposited in institutional repository12 months embargo after publication
    • Publisher last reviewed on 09/04/2014
  • Classification
    ​ white

Publications in this journal

  • Liping Liu · Ka Sing Lawrence Wong · Xinyi Leng · Yuehua Pu · Yilong Wang · Jing Jing · Xinying Zou · Yuesong Pan · Anxin Wang · Xia Meng · Chunxue Wang · Xingquan Zhao · Yannie Soo · S. Claiborne Johnston · Yongjun Wang · For the CHANCE Investigators
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: We aimed to investigate whether the efficacy and safety of clopidogrel plus aspirin vs aspirin alone were consistent between patients with and without intracranial arterial stenosis (ICAS), in the Clopidogrel in High-Risk Patients with Acute Non-disabling Cerebrovascular Events (CHANCE) trial. Methods: We assessed the interaction of the treatment effects of the 2 antiplatelet therapies among patients with and without ICAS, identified by magnetic resonance angiography (MRA) in CHANCE (ClinicalTrials.gov identifier NCT00979589). Results: Overall, 1,089 patients with MRA images available in CHANCE were included in this subanalysis, 608 patients (55.8%) with ICAS and 481 (44.2%) without. Patients with ICAS had higher rates of recurrent stroke (12.5% vs 5.4%; p < 0.0001) at 90 days than those without. But there was no statistically significant treatment by presence of ICAS interaction on either the primary outcome of any stroke (hazard ratio for clopidogrel plus aspirin vs aspirin alone: 0.79 [0.47–1.32] vs 1.12 [0.56–2.25]; interaction p = 0.522) or the safety outcome of any bleeding event (interaction p = 0.277). Conclusions: The results indicated higher rate of recurrent stroke in minor stroke or high-risk TIA patients with ICAS than in those without. However, there was no significant difference in the response to the 2 antiplatelet therapies between patients with and without ICAS in the CHANCE trial. Classification of evidence: This study provides Class II evidence that for patients with acute minor stroke or TIA with and without ICAS identified by MRA, clopidogrel plus aspirin is not significantly different than aspirin alone in preventing recurrent stroke.
    Neurology 09/2015;
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    ABSTRACT: To describe characteristics of young children with arterial ischemic stroke (AIS) and bilateral cerebral arteriopathies. Retrospective review of clinical features, course, and outcome. Neuroimaging was analyzed for infarct pattern, cerebrovascular diagnosis (anatomic/Childhood Arterial Ischemic Stroke Standardized Classification and Diagnostic Evaluation [CASCADE] criteria), and disease progression. In the 31 children (median age, 18 months), presentations included acute hemiparesis (n = 23) and focal seizures (n = 12). Seven had systemic arterial disease; 13 had cardiac abnormalities. Twenty had recurrent AIS or transient ischemic attack (after median of 3 months); 16 had >1 recurrence. Median modified Rankin Scale score was 3, with motor impairments in 20, cognitive impairments in 11, and seizures in 7. At presentation, 17 had old and acute infarcts. Twenty-five had high signal in white matter. A total of 13/23 reimaged patients accrued further infarcts over a median of 39 months. Arteriopathy involved the carotid circulation bilaterally in all; 6 had posterior circulation and 11 had extracranial involvement. Arteriopathy distribution was symmetric in 24/31. CASCADE categories were 3A in 19, 3B in 5, 3C in 5, and 7 in 2. After a median of 35 months, 14 had had progression of arteriopathy. Patients categorized as CASCADE 3A (moyamoya) had significantly shorter time to recurrence than other groups. Young children with bilateral cerebral arteriopathies (particularly meeting criteria for CASCADE 3A) have a malignant course, with frequent recurrent events, progressive disease, and poor outcomes. Current classifications are limited in characterizing disease in many cases. Symmetric involvement suggests these arteriopathies may be developmentally determined, while systemic involvement suggests potential genetic etiology. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001969
  • Neurology 08/2015; DOI:10.1212/WNL.0000000000001978
  • Neurology 08/2015; DOI:10.1212/WNL.0000000000001984
  • Neurology 08/2015; DOI:10.1212/WNL.0000000000001973
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    ABSTRACT: To determine incidence and early predictors of generalized tonic-clonic seizures (GTCs) in children with childhood absence epilepsy (CAE). Occurrence of GTCs was determined in 446 children with CAE who participated in a randomized clinical trial comparing ethosuximide, lamotrigine, and valproate as initial therapy for CAE. As of June 2014, the cohort had been followed for a median of 7.0 years since enrollment and 12% (53) have experienced at least one GTC. The median time to develop GTCs from initial therapy was 4.7 years. The median age at first GTC was 13.1 years. Fifteen (28%) were not on medications at the time of their first GTC. On univariate analysis, older age at enrollment was associated with a higher risk of GTCs (p = -0.0009), as was the duration of the shortest burst on the baseline EEG (p = 0.037). Failure to respond to initial treatment (p < 0.001) but not treatment assignment was associated with a higher rate of GTCs. Among patients initially assigned to ethosuximide, 94% (15/16) with GTCs experienced initial therapy failure (p < 0.0001). A similar but more modest effect was noted in those initially treated with valproate (p = 0.017) and not seen in those initially treated with lamotrigine. The occurrence of GTCs in a well-characterized cohort of children with CAE appears lower than previously reported. GTCs tend to occur late in the course of the disorder. Children initially treated with ethosuximide who are responders have a particularly low risk of developing subsequent GTCs. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001971
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    ABSTRACT: To characterize the natural history and neuropathologic basis of unawareness of memory loss in late-life dementia. Analyses are based on 2,092 older persons from 3 longitudinal clinical-pathologic cohort studies who had no memory or cognitive impairment at baseline. Annual evaluations included clinical classification of dementia plus self-rating and performance testing of memory. At death, there was a uniform neuropathologic examination to quantify 7 dementia-related pathologies. In the full group, memory ratings were modestly correlated with memory performance (intercepts r = 0.26, p < 0.001; slopes r = 0.23, p < 001) and so we regressed each person's memory performance on their memory ratings, and the residuals provided longitudinal indicators of memory awareness. In a subset of 239 persons who developed dementia, episodic memory awareness was stable until a mean of 2.6 years before dementia onset (95% credible interval -2.7, -1.6); thereafter, memory awareness declined rapidly (mean annual change -0.32, 95% credible interval -0.37, -0.28). Older age at baseline was associated with later onset of memory unawareness. In a subset of 385 persons who died and underwent neuropathologic examination, transactive response DNA-binding protein 43 (TDP-43) pathology, tau tangles, and gross cerebral infarcts were related to decline in memory awareness. In the absence of these pathologies, no decline in memory awareness was evident. Results were similar in subgroups with and without dementia. Awareness of memory impairment typically begins to decline about 2-3 years before dementia onset and is associated with postmortem evidence of TDP-43 pathology, tangles, and gross cerebral infarcts. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001935
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    ABSTRACT: To determine the association of lipoprotein-associated phospholipase A2 (Lp-PLA2) measured in the acute period and the short-term risk of recurrent vascular events in patients with TIA or minor stroke. We measured Lp-PLA2 activity (Lp-PLA2-A) in a subset of 3,201 participants enrolled in the CHANCE (Clopidogrel in High-Risk Patients with Acute Non-disabling Cerebrovascular Events) trial. Participants with TIA or minor stroke were enrolled within 24 hours of symptom onset and randomized to single or dual antiplatelet therapy. In the current analysis, the primary outcome was defined as the composite of ischemic stroke, myocardial infarction, or death within 90 days. The composite endpoint occurred in 299 of 3,021 participants (9.9%). The population average Lp-PLA2-A level was 209 ± 59 nmol/min/mL (95% confidence interval [CI] 207-211). Older age, male sex, and current smoking were associated with higher Lp-PLA2-A levels. Lp-PLA2-A was significantly associated with the primary endpoint (adjusted hazard ratio 1.07, 95% CI 1.01-1.13 for every 30 nmol/min/mL increase). Similar results were seen for ischemic stroke alone. Adjustment for low-density lipoprotein cholesterol attenuated the association between Lp-PLA2-A and the primary endpoint (adjusted hazard ratio 1.04, 95% CI 0.97-1.11 for every 30 nmol/min/mL increase). Higher levels of Lp-PLA2-A in the acute period are associated with increased short-term risk of recurrent vascular events. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001938
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    ABSTRACT: To describe (1) the predictability of frequent emergency department (ED) use (a marker of inadequate disease control and/or poor access to care), and (2) the demographics, comorbidities, and use of health services of frequent ED users, among people with epilepsy. We obtained demographics, comorbidities, and 2 years of encounter data for 8,041 people with epilepsy from a health information exchange in New York City. Using a retrospective cohort design, we explored bivariate relationships between baseline characteristics (year 1) and subsequent frequent ED use (year 2). We then built, evaluated, and compared predictive models to identify frequent ED users (≥4 visits year 2), using multiple techniques (logistic regression, lasso, elastic net, CART [classification and regression trees], Random Forests, AdaBoost, support vector machines). We selected a final model based on performance and simplicity. People with epilepsy who, in year 1, were adults (rather than children or seniors), male, Manhattan residents, frequent users of health services, users of multiple health systems, or had medical, neurologic, or psychiatric comorbidities, were more likely to frequently use the ED in year 2. Predictive techniques identified frequent ED visitors with good positive predictive value (approximately 70%) but poor sensitivity (approximately 20%). A simple strategy, selecting individuals with 11+ ED visits in year 1, performed as well as more sophisticated models. People with epilepsy with 11+ ED visits in a year are at highest risk of continued frequent ED use and may benefit from targeted intervention to avoid preventable ED visits. Future work should focus on improving the sensitivity of predictions. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001944
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    ABSTRACT: In a longitudinal follow-up study, we compared the clinical features and motor progression of patients with Parkinson disease (PD) who are carriers of the leucine-rich repeat kinase 2 (LRRK2) gene risk variants with patients who are noncarriers. We prospectively evaluated a cohort of patients with PD for their clinical characteristics, disease severity, and LRRK2 genotype. Carriers of risk variants (G2385R, R1628P, S1647T) and noncarriers were classified separately. A longitudinal, linear mixed model analysis of motor score progression was performed to compare motor progression between the 2 groups. Motor score progression was defined as the difference between Unified Parkinson's Disease Rating Scale motor score at baseline and follow-up scores. A total of 184 patients (122 risk variant carriers and 62 noncarriers) were evaluated and followed up for up to 6.5 years. No differences in demographics and baseline disease characteristics were found. In the longitudinal, linear mixed model analysis, risk variant carriers experienced greater rate of motor progression than noncarriers after 4 years from the date of diagnosis (p ≤ 0.018). PD LRRK2 risk variant carriers showed greater motor progression after 4 years of disease duration compared with noncarrier patients, suggesting that these risk variants may facilitate neurodegeneration with increasing disease duration. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001953
  • Neurology 08/2015; DOI:10.1212/WNL.0000000000001956
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    ABSTRACT: We aimed to perform an observational study of age at loss of independent ambulation (LoA) and side-effect profiles associated with different glucocorticoid corticosteroid (GC) regimens in Duchenne muscular dystrophy (DMD). We studied 340 participants in the Cooperative International Neuromuscular Research Group Duchenne Natural History Study (CINRG-DNHS). LoA was defined as continuous wheelchair use. Effects of prednisone or prednisolone (PRED)/deflazacort (DFZ), administration frequency, and dose were analyzed by time-varying Cox regression. Side-effect frequencies were compared using χ(2) test. Participants treated ≥1 year while ambulatory (n = 252/340) showed a 3-year median delay in LoA (p < 0.001). Fourteen different regimens were observed. Nondaily treatment was common for PRED (37%) and rare for DFZ (3%). DFZ was associated with later LoA than PRED (hazard ratio 0.294 ± 0.053 vs 0.490 ± 0.08, p = 0.003; 2-year difference in median LoA with daily administration, p < 0.001). Average dose was lower for daily PRED (0.56 mg/kg/d, 75% of recommended) than daily DFZ (0.75 mg/kg/d, 83% of recommended, p < 0.001). DFZ showed higher frequencies of growth delay (p < 0.001), cushingoid appearance (p = 0.002), and cataracts (p < 0.001), but not weight gain. Use of DFZ was associated with later LoA and increased frequency of side effects. Differences in standards of care and dosing complicate interpretation of this finding, but stratification by PRED/DFZ might be considered in clinical trials. This study emphasizes the necessity of a randomized, blinded trial of GC regimens in DMD. This study provides Class IV evidence that GCs are effective in delaying LoA in patients with DMD. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001950
  • Neurology 08/2015; 85(8):737-8. DOI:10.1212/WNL.0000000000001872
  • Neurology 08/2015; 85(8):735-6. DOI:10.1212/WNL.0000000000001873
  • Neurology 08/2015; 85(8):e66-8. DOI:10.1212/WNL.0000000000001921
  • Neurology 08/2015; 85(8):e64-5. DOI:10.1212/WNL.0000000000001868
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    ABSTRACT: To evaluate the response to salbutamol and ephedrine in the treatment of congenital myasthenic syndromes due to CHRNE mutations causing severe acetylcholine receptor (AChR) deficiency. A cohort study of 6 patients with severe AChR deficiency, symptomatic despite optimal therapy with anticholinesterase and 3,4-diaminopyridine, were analyzed for their response to the addition of salbutamol or ephedrine to their medication. Baseline quantitative myasthenia gravis (QMG) (severity) scores were worse than 15 of 39. Patients were assessed in clinic with QMG and mobility scores. Pretreatment and 6- to 8-month follow-up scores were evaluated. All 6 patients tolerated treatment well and reported no side effects. There was a strong positive response to treatment over the 6- to 8-month assessment period with significant improvement in QMG (p = 0.027) and mobility scores. The analysis of subcomponents of the QMG score revealed marked improvement in upper (p = 0.028) and lower (p = 0.028) limb raise times. All patients reported enhanced activities of daily living at 6 to 8 months. Oral salbutamol and ephedrine appear to be effective treatments in severe cases of AChR deficiency on pyridostigmine. They are well tolerated and improvement in strength can be dramatic. This study provides Class IV evidence that salbutamol or ephedrine improves muscle strength in patients with congenital myasthenia from severe AChR deficiency. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001952
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    ABSTRACT: We used a prospective clinical trial to examine the risks conferred by metabolic syndrome (METS) and diabetes mellitus (DM) to recurrent strokes in the Secondary Prevention of Small Subcortical Strokes (SPS3) study cohort. The SPS3 trial enrolled 3,020 patients with lacunar strokes. Participants were stratified into groups of METS only, DM only, both, or neither using American Heart Association/National Heart, Lung, and Blood Institute and World Health Organization guidelines. Annualized event rates of strokes, myocardial infarction (MI), and all-cause mortality were calculated, and hazard ratios (HRs) referencing the "neither" group were computed, controlling for significantly associated baseline characteristics. Among 2,999 participants, 25% had METS only, 6% had DM only, 32% had both conditions, and 37% had neither. Over a median of 3.8 years of follow-up, there were 274 recurrent strokes (240 ischemic, 34 hemorrhagic) and 74 MIs; among the 240 ischemic strokes, 134 (56%) were lacunar. The rates of any recurrent stroke (HR 1.7, 95% confidence interval [CI] 1.3-2.3) or lacunar stroke (HR 2.4, 95% CI 1.5-3.7) were significantly higher for those with concurrent METS and DM compared with those who had neither. Risk of incident MI was higher in participants with DM (HR 2.8, 95% CI 1.1-7.0) or concurrent DM and METS (HR 2.6, 95% CI 1.4-4.9). METS and DM were significant comorbid conditions in lacunar stroke patients and they were associated with stroke recurrence. In patients with lacunar infarcts, a vigilant approach to prevent development of DM in those with METS may be a potential strategy to reduce recurrent strokes. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001933
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    ABSTRACT: To assess the clinical and immunologic findings in children with voltage-gated potassium channel (VGKC)-complex antibodies (Abs). Thirty-nine of 363 sera, referred from 2 pediatric centers from 2007 to 2013, had been reported positive (>100 pM) for VGKC-complex Abs. Medical records were reviewed retrospectively and the patients' condition was independently classified as inflammatory (n = 159) or noninflammatory (n = 204). Positive sera (>100 pM) were tested/retested for the VGKC-complex Ab-positive complex proteins LGI1 and CASPR2, screened for binding to live hippocampal neurons, and 12 high-titer sera (>400 pM) tested by radioimmunoassay for binding to VGKC Kv1 subunits with or without intracellular postsynaptic density proteins. VGKC-complex Abs were found in 39 children, including 20% of encephalopathies and 7.6% of other conditions (p = 0.001). Thirty children had inflammatory conditions and 9 had noninflammatory etiologies but titers >400 pM (n = 12) were found only in inflammatory diseases (p < 0.0001). Four sera, including from 2 children with coexisting NMDA receptor Abs and one with Guillain-Barré syndrome and Abs to both LGI1 and CASPR2, bound to hippocampal neurons. None of the sera bound detectably to VGKC Kv1 subunits on live HEK cells, but 4 of 12 >400 pM sera immunoprecipitated VGKC Kv1 subunits, with or without postsynaptic densities, extracted from transfected cells. Positive VGKC-complex Abs cannot be taken to indicate a specific clinical syndrome in children, but appear to be a nonspecific biomarker of inflammatory neurologic diseases, particularly of encephalopathy. Some of the Abs may bind to intracellular epitopes on the VGKC subunits, or to the intracellular interacting proteins, but in many the targets remain undefined. © 2015 American Academy of Neurology.
    Neurology 08/2015; DOI:10.1212/WNL.0000000000001922