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

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

  • [Show abstract] [Hide abstract]
    ABSTRACT: To assess long-term safety and efficacy of fingolimod in patients with relapsing-remitting multiple sclerosis (RRMS). Patients completing FTY720 Research Evaluating Effects of Daily Oral Therapy in MS (FREEDOMS) were eligible for this dose-blinded, parallel-group extension study, continuing fingolimod 0.5 mg/day or 1.25 mg/day, or switching from placebo to either dose, randomized 1:1. Efficacy variables included annualized relapse rate (ARR), brain volume loss (BVL), and confirmed disability progression (CDP). Between-group analyses were conducted in the intent-to-treat (ITT) population from FREEDOMS baseline to end of study. Within-group analyses compared years 0-2 (FREEDOMS) and years 2-4 (extension) in the extension ITT population. Of 1,272 patients (FREEDOMS ITT population), 1,033 were eligible, and 920 enrolled in the extension study (continuous-fingolimod: 0.5 mg [n = 331], 1.25 mg [n = 289]; placebo-fingolimod: 0.5 mg [n = 155], 1.25 mg [n = 145]); 916 formed the extension ITT population (n = 330; n = 287; n = 154; n = 145) and 773 (84%) completed. In the continuous-fingolimod groups, ARR was lower (p < 0.0001), BVL was reduced (p < 0.05), and proportionately more patients were free from 3-month CDP (p < 0.05) than in a group comprising all placebo-fingolimod patients. Within each placebo-fingolimod group, ARR was lower (p < 0.001, both) and BVL was reduced after switching (p < 0.01, placebo-fingolimod 0.5 mg). Rates and types of adverse events were similar across groups; no new safety issues were reported. Efficacy benefits of fingolimod during FREEDOMS were sustained during the extension; ARR and BVL were reduced after switching. This study provides Class IV evidence that long-term fingolimod treatment is well-tolerated and reduces relapse rates, disability progression, and MRI effects in patients with RRMS. © 2015 American Academy of Neurology.
    Neurology 03/2015; DOI:10.1212/WNL.0000000000001462
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    ABSTRACT: To test if TIA/stroke electronic decision support in primary care improves management. Multicenter, single-blind, parallel-group, cluster randomized, controlled trial comparing TIA/stroke electronic decision support guided management with usual care. Main outcomes were guideline adherence and 90-day stroke risk. Secondary outcomes were cerebrovascular/vascular/death/adverse events, cost, and user feedback. Main analysis was logistic regression with a normal random effect for clusters using a generalized linear mixed model. Twenty-nine clinics were randomized to intervention, 27 to control, recruiting 172 and 119 eligible patients. More intervention patients received guideline-adherent care (131/172; 76.2%) than control patients (49/119; 41.2%) (adjusted odds ratio [OR] 4.57; 95% confidence interval [CI] 2.39-8.71; p < 0.001). Ninety-day stroke occurred in 2/172 (1.2%) intervention and 5/119 (4.2%) control patients (OR 0.27; 95% CI 0.05-1.41; p = 0.098). Ninety-day TIA or stroke occurrence was lower in the intervention group, 4/172 (2.3%) compared to 10/119 (8.5%) control (adjusted OR 0.26; 95% CI 0.70-0.97; p = 0.045). Fewer vascular events/deaths occurred in intervention, 6/172 (3.5%), than in control patients, 14/119 (11.9%) (adjusted OR 0.27; 95% CI 0.09-0.78; p = 0.016). Treatment cost ratio of 0.65 (95% CI 0.47-0.91; p = 0.013) favored the intervention without increased adverse events. Clinician feedback was positive. Primary care use of the TIA/stroke electronic decision support tool improves guideline adherence, safely reduces treatment cost, achieves positive user feedback, and may reduce cerebrovascular and vascular event risk following TIA/stroke. This study provides Class II evidence that a primary care electronic decision support tool improves guideline adherence and might reduce 90-day stroke risk. © 2015 American Academy of Neurology.
    Neurology 03/2015; DOI:10.1212/WNL.0000000000001472
  • Neurology 03/2015; DOI:10.1212/WNL.0000000000001504
  • Neurology 03/2015; DOI:10.1212/WNL.0000000000001470
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    ABSTRACT: To use in vivo neuroimaging and postmortem neuropathologic analysis in C9orf72 repeat expansion patients to investigate the hypothesis that C9orf72 promoter hypermethylation is neuroprotective and regionally selective. Twenty patients with a C9orf72 repeat expansion participating in a high-resolution MRI scan and a clinical examination and a subset of patients (n = 11) were followed longitudinally with these measures. Gray matter (GM) density was related to C9orf72 promoter hypermethylation using permutation-based testing. Regional neuronal loss was measured in an independent autopsy series (n = 35) of C9orf72 repeat expansion patients. GM analysis revealed that hippocampus, frontal cortex, and thalamus are associated with hypermethylation and thus appear to be relatively protected from mutant C9orf72. Neuropathologic analysis demonstrated an association between reduced neuronal loss and hypermethylation in hippocampus and frontal cortex. Longitudinal neuroimaging revealed that hypermethylation is associated with reduced longitudinal decline in GM regions protected by hypermethylation and longitudinal neuropsychological assessment demonstrated that longitudinal decline in verbal recall is protected by hypermethylation. These cross-sectional and longitudinal neuroimaging studies, along with neuropathologic validation studies, provide converging evidence for neuroprotective properties of C9orf72 promoter hypermethylation. These findings converge with prior postmortem studies suggesting that C9orf72 promoter hypermethylation may be a neuroprotective target for drug discovery. © 2015 American Academy of Neurology.
    Neurology 03/2015; DOI:10.1212/WNL.0000000000001495
  • Neurology 03/2015; DOI:10.1212/WNL.0000000000001480
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    ABSTRACT: We tested the value of measuring modularity, a graph theory metric indexing the relative extent of integration and segregation of distributed functional brain networks, for predicting individual differences in response to cognitive training in patients with brain injury. Patients with acquired brain injury (n = 11) participated in 5 weeks of cognitive training and a comparison condition (brief education) in a crossover intervention study design. We quantified the measure of functional brain network organization, modularity, from functional connectivity networks during a state of tonic attention regulation measured during fMRI scanning before the intervention conditions. We examined the relationship of baseline modularity with pre- to posttraining changes in neuropsychological measures of attention and executive control. The modularity of brain network organization at baseline predicted improvement in attention and executive function after cognitive training, but not after the comparison intervention. Individuals with higher baseline modularity exhibited greater improvements with cognitive training, suggesting that a more modular baseline network state may contribute to greater adaptation in response to cognitive training. Brain network properties such as modularity provide valuable information for understanding mechanisms that influence rehabilitation of cognitive function after brain injury, and may contribute to the discovery of clinically relevant biomarkers that could guide rehabilitation efforts. © 2015 American Academy of Neurology.
    Neurology 03/2015; DOI:10.1212/WNL.0000000000001476
  • Neurology 03/2015; DOI:10.1212/WNL.0000000000001452
  • Neurology 03/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this study was to investigate whether the resting-state coactivation of the hypothalamus, both ipsilateral and contralateral to the headache side, and the salience network (SN) was altered in patients with cluster headache (CH) in the headache attack remission state in the cluster period, and to reveal possible pathogenesis of CH attacks and gain further insight into the pathophysiology of CH. Resting-state fMRI scans of 21 patients with CH were obtained (13 with right-sided headache and 8 with left-sided headache) and 21 age- and sex-matched normal controls. The resting-state fMRI data were analyzed using independent component analysis to identify the group differences of hypothalamic-SN coactivation between the patients with CH and healthy controls. Decreased functional coactivation was detected between the hypothalamus, both ipsilateral and contralateral to the headache side, and the SN both in patients with right-sided CH and in those with left-sided CH. Our findings suggest that the decreased hypothalamus-SN coactivation may have a role in CH attacks by the defective central pathway of pain control and autonomic nervous system dysregulation. This helps to gain additional insight into the pathophysiologic basis of CH and the nature of the brain dysfunction in CH. © 2015 American Academy of Neurology.
    Neurology 03/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this study was to investigate whether the resting-state coactivation of the hypothalamus, both ipsilateral and contralateral to the headache side, and the salience network (SN) was altered in patients with cluster headache (CH) in the headache attack remission state in the cluster period, and to reveal possible pathogenesis of CH attacks and gain further insight into the pathophysiology of CH. Resting-state fMRI scans of 21 patients with CH were obtained (13 with right-sided headache and 8 with left-sided headache) and 21 age- and sex-matched normal controls. The resting-state fMRI data were analyzed using independent component analysis to identify the group differences of hypothalamic-SN coactivation between the patients with CH and healthy controls. Decreased functional coactivation was detected between the hypothalamus, both ipsilateral and contralateral to the headache side, and the SN both in patients with right-sided CH and in those with left-sided CH. Our findings suggest that the decreased hypothalamus-SN coactivation may have a role in CH attacks by the defective central pathway of pain control and autonomic nervous system dysregulation. This helps to gain additional insight into the pathophysiologic basis of CH and the nature of the brain dysfunction in CH. © 2015 American Academy of Neurology.
    Neurology 03/2015;
  • Neurology 01/2015; 84(4):437.
  • Neurology 01/2015; 84(2). DOI:10.1212/WNL.0000000000001119
  • Source
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    ABSTRACT: Immunoglobulin G4-related disease (IgG4-RD) is a novel clinical entity characterized by elevated serum IgG4 levels and histopathologic features of storiform fibrosis, obliterative phlebitis, tissue eosinophilia, and infiltration of IgG4-positive plasma cells. Although it can involve almost any organ, IgG4-RD rarely involves the nervous system. The principal neurologic manifestations include hypophysitis and hypertrophic pachymeningitis (HP). In some patients, previously known idiopathic HP may in fact be IgG4-related.
    Neurology 12/2014; DOI:10.1212/NXI.0000000000000041
  • Neurology 11/2014; 83:e197-e198. DOI:10.1212/WNL.0000000000001032