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: 0.60

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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
Year

Additional details

5-year impact 0.50
Cited half-life 0.00
Immediacy index 0.15
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
    • On authors personal or authors institutions server
    • Published source must be acknowledged
    • Must link to journal home page
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'Elsevier Masson' is an imprint of 'Elsevier'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to evaluate the impact, on a regional scale (Franche-Comté), of 3 National Alzheimer care plans, particularly concerning the development of the offer of care management by clinicians as well as the panel of diagnoses concerned. Data on sociodemographic, neuropsychological and diagnostic characteristics were retrieved from the RAPID regional database between 1st January 2003 and 31st December 2012. These analyses focused exclusively on patients who had an initial consultation (n=12,017) during the same period. The existence of a previously established health network capable of carrying out governmental health plans has produced an effective interface between regional administrative structures responsible for the implementation of these plans and health professionals responsible for carrying out them out. This network study, the use of a battery of tests and a common software database have enabled the development of patient care management throughout the Franche-Comté region. It also showed the diversification of diagnoses mentioned over the past years as well as changes in clinical practices on how to address the issue of cognitive impairment. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 07/2015; DOI:10.1016/j.neurol.2015.04.008
  • Revue Neurologique 07/2015; DOI:10.1016/j.neurol.2015.04.007
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    ABSTRACT: An intronic GGGGCC repeat expansion in c9orf72 gene has been identified as the most common genetic cause of frontotemporal lobar dementia (FTLD), amyotrophic lateral sclerosis (ALS) and FTLD-ALS. The discovery of c9orf72 gene has led to important scientific progresses and has considerably changed our clinical practice over the last few years. This paper summarizes the common and less typical phenotypes associated with c9orf72 expansion, the complex pathological pattern characterized by p62/dipeptide repeat aggregates, as well as the pathological mechanisms by which the expansion might produce neurodegeneration implicating loss-of-function, RNA toxicity, RNA-binding protein sequestration and accumulation of dipeptide repeats. We also discuss the recommendations and limits for genetic testing and counseling in clinical practice. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.04.004
  • Revue Neurologique 05/2015; DOI:10.1016/j.neurol.2015.04.001
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    ABSTRACT: Primary brain tumors comprise a large group of malignant and non-malignant tumors including heterogeneous entities with various biological and clinical behaviors. Up till recently, diagnosis of brain cancers, that drives treatment decision-making, was based on integration of clinical, radiological and pathological features of patients and tumors. Over the last years, practical neuro-oncology has entered an era of molecular-based personalized medicine. Indeed, molecular features of tumors provide critical information to physicians for daily clinical management of patients and for design of relevant clinical research. Sporadic gliomas or glial tumors are the most common primary brain tumors in adults. Recently, their medical management has been revolutionized by molecular data. Indeed, optimal therapeutic management of grade III glioma patients now requires assessment of chromosome arms 1p/19q copy number and IDH mutational statuses as predictive and prognostic biomarkers. Indeed, two large phase III clinical trials have demonstrated that early chemotherapy plus radiotherapy, versus radiotherapy alone, doubles median overall survival of patients suffering from 1p/19q co-deleted and/or IDH mutated anaplastic oligodendroglial tumor. Interestingly, both biomarkers have been identified in a large proportion of WHO grade II gliomas. Their clinical value, in this population, is under investigation through multiple phase III clinical trials. In sporadic WHO grade I gliomas, and specifically in pilocytic astrocytomas, MAPK signaling pathway activation is a frequent event, mainly due to genetic alterations involving BRAF gene. This characteristic opens new therapeutic perspectives using MAPK signaling pathway inhibitors. Finally, in the most aggressive gliomas, WHO grade IV gliomas, two critical biomarkers have been identified: (i) MGMT promoter methylation associated with longer survival and better response to chemotherapy and (ii) IDH mutations predicting better prognosis. Although, further studies are needed, MGMT promoter methylation will undoubtedly be transferred soon to clinical practice. Molecular characteristics are beginning to be valuable and indispensable in neuro-oncology for better management of brain tumors patients. The near future will be marked by identification of novel molecular biomarkers and their validation for clinical practice. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.04.002
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    ABSTRACT: Pharmacogenetics aims to identify the underlying genetic factors participating in the variability of drug response. Indeed, genetic variability at the DNA or RNA levels can directly or indirectly modify the pharmacokinetic or the pharmacodynamic parameters of a drug. The ultimate aim of pharmacogenetics is to move towards a personalised medicine by predicting responders and non-responders, adjusting the dose of the treatment, and identifying individuals at risk of adverse drug effects. A literature research was performed in which we reviewed all pharmacogenetic studies in neurological disorders including neurodegenerative diseases, multiple sclerosis, stroke and epilepsy. Several pharmacogenetic studies have been performed in neurology, bringing insights into the inter-individual drug response variability and in the pathophysiology of neurological diseases. The principal implications of these studies for the management of patients in clinical practice are discussed. Although several genetic factors have been identified in the modification of drug response in neurological disorders, most of them have a marginal predictive effect at the single gene level, suggesting mutagenic interactions as well as other factors related to drug interaction and disease subtypes. Most pharmacogenetic studies deserve further replication in independent populations and, ideally, in pharmacogenetic clinical trials to demonstrate their relevance in clinical practice. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.04.003
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    ABSTRACT: The benefit of the thrombectomy using stents retrievers in the acute stroke phase is now demonstrated when there is a proximal occlusion of an intracranial artery, whatever its mechanism. The place of the anticoagulants in the management of cervical artery dissections remains uncertain, while the benefit of the blood pressure control in the secondary prevention of deep and lobar intracerebral hemorrhages is critical. The development of cardiac MRI, prolonged cardiac monitoring and transcranial doppler seems to improve the diagnosis of cardio-embolic sources of stroke.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.04.005
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    ABSTRACT: The field of essential tremor (ET) genetics remains extremely challenging. The relative lack of progress in understanding the genetic etiology of ET, however, does not reflect the lack of a genetic contribution, but rather, the presence of substantial phenotypic and genotypic heterogeneity. A meticulous approach to phenotyping is important for genetic research in ET. The only tool for phenotyping is the clinical history and examination. There is currently no ET-specific serum or imaging biomarker or defining neuropathological feature (e.g., a protein aggregate specific to ET) that can be used for phenotyping, and there is considerable clinical overlap with other disorders such as Parkinson's disease (PD) and dystonia. These issues greatly complicate phenotyping; thus, in some studies, as many as 30–50% of cases labeled as “ET” have later been found to carry other diagnoses (e.g., dystonia, PD) rather than ET. A cursory approach to phenotyping (e.g., merely defining ET as an “action tremor”) is likely a major issue in some family studies of ET, and this as well as lack of standardized phenotyping across studies and patient centers is likely to be a major contributor to the relative lack of success of genome wide association studies (GWAS). To dissect the genetic architecture of ET, whole genome sequencing (WGS) in carefully characterized and well-phenotyped discovery and replication datasets of large case-control and familial cohorts will likely be of value. This will allow specific hypotheses about the mode of inheritance and genetic architecture to be tested. There are a number of approaches that still remain unexplored in ET genetics, including the contribution of copy number variants (CNVs), ‘uncommon’ moderate effect alleles, ‘rare’ variant large effect alleles (including Mendelian and complex/polygenic modes of inheritance), de novo and gonadal mosaicism, epigenetic changes and non-coding variation. Using these approaches is likely to yield new ET genes.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.02.015
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    ABSTRACT: Epilepsies have long remained refractory to gene identification due to several obstacles, including a highly variable inter- and intrafamilial expressivity of the phenotypes, a high frequency of phenocopies, and a huge genetic heterogeneity. Recent technological breakthroughs, such as array comparative genomic hybridization and next generation sequencing, have been leading, in the past few years, to the identification of an increasing number of genomic regions and genes in which mutations or copy-number variations cause various epileptic disorders, revealing an enormous diversity of pathophysiological mechanisms. The field that has undergone the most striking revolution is that of epileptic encephalopathies, for which most of causing genes have been discovered since the year 2012. Some examples are the continuous spike-and-waves during slow-wave sleep and Landau-Kleffner syndromes for which the recent discovery of the role of GRIN2A mutations has finally confirmed the genetic bases. These new technologies begin to be used for diagnostic applications, and the main challenge now resides in the interpretation of the huge mass of variants detected by these methods. The identification of causative mutations in epilepsies provides definitive confirmation of the clinical diagnosis, allows accurate genetic counselling, and sometimes permits the development of new appropriate and specific antiepileptic therapies. Future challenges include the identification of the genetic or environmental factors that modify the epileptic phenotypes caused by mutations in a given gene and the understanding of the role of somatic mutations in sporadic epilepsies. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.01.569
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    ABSTRACT: Huntington's disease was the first adult onset neurological disease for which presymptomatic genetic testing became possible. It served as a model for the approach which constituted a radical change in medical practice and provided an important framework for multi-step, multidisciplinary, counselling for at risk persons. We will review the historical context of guidelines and good clinical practices, the experiences of our team which covers more than 20 years of presymptomatic testing for Huntington's disease in France, and explore the impact of the new French legislation for the future of presymptomatic testing of diseases for which neither preventive measures nor curative treatments are yet available. Copyright © 2015. Published by Elsevier Masson SAS.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.02.016
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    ABSTRACT: Inborn errors of metabolism (IEM) are traditionally defined by enzymatic deficiencies or defects in proteins involved in cellular metabolism. Historically discovered and characterized in children, a growing number of IEM are described in adults, and especially in the field of neurology. In daily practice, it is important to recognize emergency situations as well as neurodegenerative diseases for which a metabolic disease is likely, especially when therapeutic interventions are available. Here, the goal is to provide simple clinical, imaging and biochemical tools that can first orientate towards and then confirm the diagnosis of IEM. General guidelines are presented to treat the most common IEM during metabolic crises - acute encephalopathies with increased plasma ammonia, lactate or homocystein, as well as rhabdomyolysis. Examples of therapeutic strategies currently applied to chronic neurometabolic diseases are also provided - GLUT1 deficiency, adrenoleukodystrophy, cerebrotendinous xanthomatosis, Niemann-Pick type C and Wilson disease. Genetic counseling is mandatory in some X-linked diseases - ornithine transcarbamylase deficiency and adrenoleukodystrophy - and recommended in maternally inherited mitochondrial diseases - mutations of mitochondrial DNA. Besides these practical considerations, the contribution of metabolism to the field of adult neurology and neurosciences is much greater: first, with the identification of blood biomarkers that are progressively changing our diagnostic strategies thanks to lipidomic approaches, as illustrated in the field of spastic paraplegia and atypical psychiatric presentations; and second, through the understanding of pathophysiological mechanisms involved in common neurological diseases thanks to the study of these rare diseases. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
    Revue Neurologique 05/2015; 171(6-7). DOI:10.1016/j.neurol.2015.02.018
  • Revue Neurologique 04/2015; 171. DOI:10.1016/j.neurol.2015.01.011
  • Revue Neurologique 04/2015; 171. DOI:10.1016/j.neurol.2015.01.028
  • Revue Neurologique 04/2015; 171. DOI:10.1016/j.neurol.2015.01.030
  • [Show abstract] [Hide abstract]
    ABSTRACT: Auteur correspondant. HIA Desgenettes, neurologie, 108, boulevard Pinel, 69275 Lyon, France.
    Revue Neurologique 04/2015; 171. DOI:10.1016/j.neurol.2015.01.052
  • Revue Neurologique 04/2015; 171. DOI:10.1016/j.neurol.2015.01.025
  • Revue Neurologique 04/2015; 171. DOI:10.1016/j.neurol.2015.01.021