Revue Neurologique Journal Impact Factor & Information

Publisher: Société Française de Neurologie, Elsevier Masson

Journal description

Au service de l'actualité neurologique. La Revue Neurologique publie des mises au point, des mémoires originaux, des brèves communications, des lettres de l'Editeur... en neurologie, neurochirurgie, neurophysiologie, neuropathologie, neurologie expérimentale et autres disciplines associées. Tribune des équipes francophones et internationales. Organe de diffusion de la recherche francophone et internationale, elle publie des articles scientifiques qui vous permettent de vous tenir informé des grandes acquisitions en neurologie clinique et en neurosciences. Un renouveau éditorial. Soucieuse de maintenir sa place parmi les différents outils de travail des neurologues, la Revue Neurologique maintient une ligne éditoriale de qualité pour répondre aux exigences de ses lecteurs. Soutenue par un Comité Editorial chargé de susciter la soumission d'articles d'équipes de premier rang, la rédaction a mis au point une partie de formation post-universitaire avec un grand nombre de rubriques tres variées

Current impact factor: 0.66

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 0.663
2013 Impact Factor 0.601
2012 Impact Factor 0.51
2011 Impact Factor 0.488
2010 Impact Factor 0.528
2009 Impact Factor 0.605
2008 Impact Factor 0.508
2007 Impact Factor 0.448
2006 Impact Factor 0.501
2005 Impact Factor 0.443
2004 Impact Factor 0.434
2003 Impact Factor 0.456
2002 Impact Factor 0.468
2001 Impact Factor 0.598
2000 Impact Factor 0.692
1999 Impact Factor 1.013
1998 Impact Factor 1.45
1997 Impact Factor 1.11

Impact factor over time

Impact factor

Additional details

5-year impact 0.50
Cited half-life >10.0
Immediacy index 0.17
Eigenfactor 0.00
Article influence 0.14
Website Revue Neurologique website
ISSN 0035-3787
OCLC 163811705
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Elsevier Masson

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 01/05/2015
    • 'Elsevier Masson' is an imprint of 'Elsevier'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Even prior to the introduction of criteria defining the radiologically isolated syndrome (RIS), longitudinal clinical data from individuals with incidentally identified T2 lesions suggestive of multiple sclerosis (MS) were described. Healthy individuals who do not exhibit signs of neurological dysfunction may have a brain MRI performed for a reason other than suspicion of MS that reveals unexpected anomalies highly suggestive of demyelinating plaques given their size, location, and morphology. These healthy subjects lack a history or symptomatology suggestive of MS and fulfill formal criteria for RIS, a recently described MS subtype that shares the phenotype of at-risk individuals for future demyelinating events. A formal description of RIS was first introduced in 2009 by Okuda et al., and defines a cohort of individuals who are at risk for future demyelinating events. European or North American observational studies have found that up to 30-45% of patients presenting with RIS will present with neurological symptoms, either acute or progressive. The median time to clinical conversion differs between studies. It was 2.3 years for a series of French patients and 5.4 years for an American cohort. Most patients who developed clinical symptoms had prior radiological progression. The presence of asymptomatic lesions in the cervical cord indicated an increased risk of progression, either to relapsing or to progressive MS. The consortium studying the epidemiology of RIS worldwide (RISC) presented their first retrospective cohort last year. Data were available for 451 RIS subjects (F: 354 [78.5%]). The mean age at RIS diagnosis was 37.2 years with a mean clinical follow-up time of 4.4 years. The observed 5-year conversion rate to the first clinical event was 34%. Of the converters within this time period, 9.6% fulfilled criteria for primary progressive MS. In the multivariate model, age, sex (male), and lesions within the cervical or thoracic spinal cord were identified as significant predictors for the development of a first clinical event. Cognitive impairment is observed in RIS patients, and two studies demonstrated a significant proportion of patients with cognitive decline compared with healthy controls. Despite progress into the characterization of RIS subjects and into our understanding of risk factors for initial symptom development, the natural course of such cases and risk-profiles for a seminal neurological event, from prospectively acquired data, remain unclear. A prospective study is mandatory to increase our knowledge about these asymptomatic patients and individual therapeutic initiatives cannot be undertaken until a prospective clinical study demonstrates the benefit of introducing a disease modifying treatment for this very early stage of a chronic demyelinating disease.
    Revue Neurologique 09/2015; DOI:10.1016/j.neurol.2015.05.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Parkinson's disease (PD) is a progressive neurodegenerative disorder whose etiology, besides a minority of genetic cases, is still largely unknown. Animal models have contributed to elucidate PD etiology and pathogenesis, as well as its cellular and molecular mechanisms, leading to the general hypothesis that this neurological disorder is due to complex interactions between environmental and genetic factors. However, the full understanding of PD is still very far from being achieved, and new potential treatments need to be tested to further improve patients' quality of life and, possibly, slow down the neurodegenerative process. In this context, animal models of PD are required to address all these issues. "Classic" models are based on neurotoxins that selectively target catecholaminergic neurons (such as 6-hydroxydopamine, 1-methyl-1,2,3,6-tetrahydropiridine, agricultural pesticides, etc.), while more recent models employ genetic manipulations that either introduce mutations similar to those find in familial cases of PD (α-synuclein, DJ-1, PINK1, Parkin, etc.) or selectively disrupt nigrostriatal neurons (MitoPark, Pitx3, Nurr1, etc.). Each one of these models has its own advantages and limitations, thus some are better suited for studying PD pathogenesis, while others are more pertinent to test therapeutic treatments. Here, we provide a critical and updated review of the most used PD models.
    Revue Neurologique 09/2015; DOI:10.1016/j.neurol.2015.07.011
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the absence of a specific test for the diagnosis of multiple sclerosis (MS), cerebrospinal fluid analysis (CSF) remains discussed. There are robust evidences which demonstrated that an early diagnosis of MS must be done, due to the availability of disease-modifying drugs that could influence the natural history of the disease. However, several arguments can be put forward to assert that CSF analysis is not useful for the diagnosis of MS and thus should not be realized in a systematic way. First, MRI remains the most sensitive and specific marker to validate dissemination in space and in time and CSF analysis is not recommended by the 2010 McDonald criteria. The second argument is related to the low sensitivity and specificity of abnormalities detected in CSF analysis to confirm the diagnosis of MS. Moreover, there is currently no evidence that the presence of oligoclonal bands could represent a surrogate marker on an individual prognostic way. Furthermore, lumbar puncture could be traumatic, may entail some infrequent risks and represents unnecessary expense. Thus, there are strong reasons to not recommend systematic CSF examination to diagnose MS.
    Revue Neurologique 09/2015; DOI:10.1016/j.neurol.2015.05.006
  • [Show abstract] [Hide abstract]
    ABSTRACT: Myofibrillar myopathies (MFM) have been described in the mid-1990s as a group of diseases sharing common histological features, including an abnormal accumulation of intrasarcoplasmic proteins, the presence of vacuoles and a disorganization of the intermyofibrillar network beginning at the Z-disk. The boundaries of this concept are still uncertain, and whereas six genes (DES, CRYAB, LDB3/ZASP, MYOT, FLNC and BAG3) are now classically considered as responsible for MFM, other entities such as FHL1 myopathy or Hereditary Myopathy with Early Respiratory Failure linked to mutations of titin can now as well be included in this group. The diagnosis of MFM is not always easy; as histological lesions can be focal, and muscle biopsy may be disappointing; this has led to a growing importance of muscle imaging, and the selectivity of muscle involvement has now been described in several disorders. Due to the rarity of these myopathies, if some clinical patterns (such as distal myopathy associated with cardiomyopathy due to desmin mutations) are now well known, surprises remain possible and should lead to systematic testing of the known genes in case of a typical histological presentation. In this paper, we aim at reviewing the data acquired on the six main genes listed above as well as presenting the experience from two French reference centres, Paris and Marseilles. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 09/2015; DOI:10.1016/j.neurol.2015.06.002
  • Revue Neurologique 09/2015; DOI:10.1016/j.neurol.2015.06.007
  • Revue Neurologique 09/2015; DOI:10.1016/j.neurol.2015.07.010
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.07.009
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.06.009
  • [Show abstract] [Hide abstract]
    ABSTRACT: Headaches are a common reason for consultation with a prevalence of 30%. Few data exist for military personnel, including in situations of war operations. The main objective of this work was to measure the evolution of the impact of headache in such a context. Two hundred and one personnel deployed in the Kaïa military field hospital in Afghanistan were recruited. A questionnaire designed to recognize headaches, supported by two quality of life scales (MIDAS and HIT-6) and a stress questionnaire were filled out before departure and upon return from missions. Sixty-three patients with headache were initially identified, of whom 52 remained symptomatic during the mission. The average total score of MIDAS before departure was 4days and fell to 1.4days upon return, with a mean measured change of 3.3days. For HIT-6, the mean total score was 51.2points initially and 51.9points at the end of the mission with a mean change of-0.3points. Nine patients without headache initially became symptomatic: MIDAS and HIT-6 were not affected. Thus, the impact of headache in the particular context of presence in a theater of operations was low: improved MIDAS score and the lack of influence on the HIT-6 score are underlined. Copyright © 2015. Published by Elsevier Masson SAS.
    Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.05.002
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.06.003
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.07.003
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.07.001
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.05.004
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.05.003
  • Revue Neurologique 08/2015; DOI:10.1016/j.neurol.2015.04.011