Neurology (Neurology)

Publisher: American Academy of Neurology, American Academy of Neurology

Current impact factor: 8.29

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 8.286
2013 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

Additional details

5-year impact 8.35
Cited half-life 9.90
Immediacy index 1.79
Eigenfactor 0.12
Article influence 2.99
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

Publications in this journal

  • Daniel M Hartung · Dennis N Bourdette · Sharia Ahmed · Ruth H Whitham

    No preview · Article · Feb 2016 · Neurology
  • Brian E Rittenhouse

    No preview · Article · Feb 2016 · Neurology
  • Daniel M Hartung · Dennis N Bourdette · Ruth H Whitham

    No preview · Article · Feb 2016 · Neurology
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    ABSTRACT: Objective: To analyze the spectrum and mechanisms of cutaneous adverse events (AEs) in patients with multiple sclerosis treated with daclizumab high-yield process (DAC-HYP). Methods: A total of 31 participants in an institutional review board-approved open-label phase I study of DAC-HYP (NCT01143441) were prospectively evaluated over 42 months for development of cutaneous AEs. Participants provided written informed consent. Fifteen participants were naive to anti-CD25 therapy (cohort B), while 16 had received daclizumab (Zenapax; Hoffmann-La Roche) IV for 4-9 years (mean 5.8 years) prior to enrollment (cohort A). Immunohistochemistry was performed on pretreatment and posttreatment skin biopsies of normal-appearing skin (cohort B only) and on lesional biopsies in participants presenting with rash (both cohorts). Results: Cutaneous AEs occurred in 77% of patients, the majority presenting with patches of eczema requiring no treatment. Moderate to severe rash developed in 6 participants (19%) and required discontinuation of DAC-HYP in 4 (13%). More severe rashes presented psoriasiform phenotype, but lesional biopsies lacked features of either psoriasis or drug hypersensitivity eruptions. Instead, irrespective of clinical severity, lesional biopsies showed nonspecific features of eczematous dermatitis, but with prominent CD56+ lymphocytic infiltrates. Pretreatment and posttreatment biopsies of normal-appearing skin demonstrated no histopathologic changes. Conclusions: Observed cutaneous AEs are likely related to the immunomodulatory effects DAC-HYP exerts on innate lymphoid cells, including natural killer cells. Vigilance and timely management of skin reactions may prevent treatment discontinuation in participants with severe rash.
    No preview · Article · Feb 2016 · Neurology
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    ABSTRACT: Objective: To investigate the histopathologic substrate of microbleeds detected on 7T postmortem MRI in autopsy cases with severe cerebral amyloid angiopathy (CAA) and Alzheimer pathology. Methods: Five decedents (mean age at death 79.6 ± 5.7 years) with documented severe CAA and Alzheimer pathology on standard neuropathologic examination were selected from a local database. Formalin-fixed coronal brain slices were scanned at 7T MRI, including high-resolution T2- and T2*-weighted sequences. Representative microbleeds from each case were sampled for histopathologic analysis, including the presence of blood, blood breakdown products, and markers of ischemic tissue injury. Results: On MRI, we identified >300 cortical and 4 subcortical microbleeds. Two out of 15 sampled cortical microbleeds corresponded histologically to erythrocytes (suggestive of recent hemorrhages), 4 to vasculopathies (fibrinoid necrosis in 3 and a cavernoma) without substantial parenchymal tissue injury, and 9 to accumulations of iron-positive siderophages without erythrocytes (suggestive of old hemorrhages) combined with mild to moderate degrees of chronic ischemic tissue injury. Conclusions: This study provides evidence for heterogeneous pathologic substrates and possibly different pathophysiologic mechanisms underlying MRI-observed cortical microbleeds in the context of advanced CAA and Alzheimer disease.
    No preview · Article · Feb 2016 · Neurology

  • No preview · Article · Feb 2016 · Neurology

  • No preview · Article · Feb 2016 · Neurology

  • No preview · Article · Feb 2016 · Neurology
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    ABSTRACT: Objective: We report the clinical and serologic features of Japanese patients with chronic inflammatory demyelinating polyneuropathy (CIDP) displaying anti-neurofascin-155 (NF155) immunoglobulin G4 (IgG4) antibodies. Methods: In sera from 533 patients with CIDP, anti-NF155 IgG4 antibodies were detected by ELISA. Binding of IgG antibodies to central and peripheral nerves was tested. Results: Anti-NF155 IgG4 antibodies were identified in 38 patients (7%) with CIDP, but not in disease controls or normal participants. These patients were younger at onset as compared to 100 anti-NF155-negative patients with CIDP. Twenty-eight patients (74%) presented with sensory ataxia, 16 (42%) showed tremor, 5 (13%) presented with cerebellar ataxia associated with nystagmus, 3 (8%) had demyelinating lesions in the CNS, and 20 of 25 (80%) had poor response to IV immunoglobulin. The clinical features of the antibody-positive patients were statistically more frequent as compared to negative patients with CIDP (n = 100). Anti-NF155 IgG antibodies targeted similarly central and peripheral paranodes. Conclusion: Anti-NF155 IgG4 antibodies were associated with a subgroup of patients with CIDP showing a younger age at onset, ataxia, tremor, CNS demyelination, and a poor response to IV immunoglobulin. The autoantibodies may serve as a biomarker to improve patients' diagnosis and guide treatments.
    No preview · Article · Feb 2016 · Neurology
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    ABSTRACT: Objective: Using a single patient case study, we aimed to look at the interaction between full face transplantation and subsequent somatosensory representation in the cortex. Methods: We present a patient with full face transplantation who has recovered primary sensory modalities. The patient also has facial sensations such as touch perception in sensory examinations of the hands and fingers. Results: fMRI findings show interactions between the cortical representations of the face and hand. Conclusion: This phenomenon is one of the well-known referred sensations and reveals how face transplantation relates to cortical plasticity.
    No preview · Article · Feb 2016 · Neurology
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    ABSTRACT: Objective: To evaluate whether headache exacerbation associated with IV dihydroergotamine (DHE) infusion predicts medium-term headache outcome in patients with chronic migraine. Methods: This was a retrospective chart review study of the UCSF Headache Center's use of IV DHE for chronic migraine from 2008 to 2012. Medium-term headache outcome was assessed at 6-week follow-up. Univariate and multivariate logistic regression models were used to assess for predictors of outcome. Results: Patients with chronic migraine (n = 274) were treated with a course of IV DHE. Of 214 with 6-week follow-up, 78% had medium-term headache benefit. In a univariate logistic regression model, headache exacerbation with DHE was associated with lower odds of a positive medium-term headache outcome (odds ratio [OR] 0.43, 95% confidence interval [CI] 0.20-0.91). However, in the multivariate logistic regression model, headache exacerbation was no longer an independent predictor of treatment outcome (OR 0.65, 95% CI 0.28-1.51). Factors that independently predicted outcome were nausea (OR 0.12, 95% CI 0.02-1.00, p = 0.05), age (OR 1.68 for each decade increase in age, 95% CI 1.24-2.28), and medication overuse (OR 0.42, 95% CI 0.18-0.97). Conclusions: After controlling for nausea and other factors, headache exacerbation with DHE infusions is not an independent predictor of poor headache outcome and clinicians should not interpret its presence as a reason to stop treatment. The focus of management should be on controlling nausea as it is the most important modifiable factor in achieving a good headache outcome with an inpatient course of IV DHE for chronic migraine.
    No preview · Article · Feb 2016 · Neurology

  • No preview · Article · Feb 2016 · Neurology

  • No preview · Article · Feb 2016 · Neurology

  • No preview · Article · Feb 2016 · Neurology
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    ABSTRACT: Stroke-like migraine attacks after radiation therapy (SMART) syndrome is characterized by transient, focal neurologic symptoms occurring years after radiation,1 with focal or regional cortical thickening and gadolinium enhancement on MRI in the area of brain exposed to radiation. The pathophysiology of the syndrome is not well-understood. We present 2 patients with recurrent attacks of SMART syndrome with increased cerebral blood volume in affected regions and abnormal vascular reactivity on transcranial Doppler ultrasound, suggesting a potential mechanism.
    No preview · Article · Jan 2016 · Neurology

  • No preview · Article · Jan 2016 · Neurology
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    ABSTRACT: Objective: To examine risk factors for REM sleep behavior disorder (RBD) in a large-scale community-based study. Methods: This community-based study included 12,784 Chinese adults (10,556 men and 2,228 women, aged 24 years or older) who were free of Parkinson disease and dementia in 2012. Probable RBD (pRBD) status was determined by a validated questionnaire (Chinese RBD questionnaire-Hong Kong) in 2012. Potential risk factors-including age, sex, smoking, socioeconomic status, physical activity, obesity, consumption of tea (surrogate for caffeine intake) and alcohol, serum concentrations of lipids and glucose, and chronic disease status-were assessed in 2006. Logistic regression was used to calculate odds ratios and 95% confidence intervals and to test differences in prevalence of pRBD across exposures. Results: Prevalence of pRBD was 5.9% in men and 4.1% in women. In the fully adjusted model, risk factors that were significantly associated with a higher risk of having pRBD included lower education level, coal mining and other blue collar occupation, lower physical activity level, diabetes or prediabetes, lower body mass index, head injury, higher low-density lipoprotein level, and chronic olfactory and taste dysfunction. In sensitivity analyses, restricting to pRBD cases with symptom onset within 1 year or excluding coal miners or those with history of head injury generated similar results. Conclusion: We found several potential risk factors for pRBD, including socioeconomic status, head injury, olfactory and taste dysfunction, and various cardiovascular risk factors. Future prospective studies to establish the temporal relationship between these potential risk factors and RBD are warranted.
    No preview · Article · Jan 2016 · Neurology
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    ABSTRACT: Objectives: We tested whether brain-derived neurotrophic factor (BDNF) gene expression levels are associated with cognitive decline in older adults. Methods: Five hundred thirty-five older participants underwent annual cognitive assessments and brain autopsy at death. BDNF gene expression was measured in the dorsolateral prefrontal cortex. Linear mixed models were used to examine whether BDNF expression was associated with cognitive decline adjusting for age, sex, and education. An interaction term was added to determine whether this association varied with clinical diagnosis proximate to death (no cognitive impairment, mild cognitive impairment, or dementia). Finally, we examined the extent to which the association of Alzheimer disease (AD) pathology with cognitive decline varied by BDNF expression. Results: Higher brain BDNF expression was associated with slower cognitive decline (p < 0.001); cognitive decline was about 50% slower with the 90th percentile BDNF expression vs 10th. This association was strongest in individuals with dementia. The level of BDNF expression was lower in individuals with pathologic AD (p = 0.006), but was not associated with macroscopic infarcts, Lewy body disease, or hippocampal sclerosis. BDNF expression remained associated with cognitive decline in a model adjusting for age, sex, education, and neuropathologies (p < 0.001). Furthermore, the effect of AD pathology on cognitive decline varied by BDNF expression such that the effect was strongest for high levels of AD pathology (p = 0.015); thus, in individuals with high AD pathology (90th percentile), cognitive decline was about 40% slower with the 90th percentile BDNF expression vs 10th. Conclusions: Higher brain BDNF expression is associated with slower cognitive decline and may also reduce the deleterious effects of AD pathology on cognitive decline.
    No preview · Article · Jan 2016 · Neurology
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    ABSTRACT: Objective: To compare motor symptoms, cognition, mood, and behavior 3 years after deep brain stimulation (DBS) of the globus pallidus pars interna (GPi) and subthalamic nucleus (STN) in advanced Parkinson disease (PD). Methods: Patients with PD eligible for DBS were randomized to bilateral GPi DBS and bilateral STN DBS (1:1). The primary outcome measures were (1) improvement in motor symptoms in off-drug phase measured with the Unified Parkinson Disease Rating Scale (UPDRS) and (2) a composite score for cognitive, mood, and behavioral effects, and inability to complete follow-up at 36 months after surgery. Results: Of the 128 patients enrolled, 90 were able to complete the 3-year follow-up. We found significantly more improvement of motor symptoms after STN DBS (median [interquartile range (IQR)] at 3 years, GPi 33 [23-41], STN 28 [20-36], p = 0.04). No between-group differences were observed on the composite score (GPi 83%, STN 86%). Secondary outcomes showed larger improvement in off-drug functioning in the AMC Linear Disability Scale score after STN DBS (mean ± SD, GPi 65.2 ± 20.1, STN 72.6 ± 18.0, p = 0.05). Medication was reduced more after STN DBS (median levodopa equivalent dose [IQR] at 3 years, GPi 1,060 [657-1,860], STN 605 [411-875], p < 0.001). No differences in adverse effects were recorded, apart from more reoperations to a different target after GPi DBS (GPi n = 8, STN n = 1). Conclusions: Off-drug phase motor symptoms and functioning improve more after STN DBS than after GPi DBS. No between-group differences were observed on a composite score for cognition, mood, and behavior, and the inability to participate in follow-up. Classification of evidence: This study provides Class II evidence that STN DBS provides more off-phase motor improvement than GPi DBS, but with a similar risk for cognitive, mood, and behavioral complications.
    No preview · Article · Jan 2016 · Neurology