T Stojkovic

Hôpital La Pitié Salpêtrière (Groupe Hospitalier "La Pitié Salpêtrière - Charles Foix"), Lutetia Parisorum, Île-de-France, France

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Publications (217)807.09 Total impact

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    ABSTRACT: This was a retrospective study to assess the diagnostic value of the non-ischaemic forearm exercise test in detecting McArdle's disease. The study is a retrospective diagnostic study over 15 years (1999-2013) on a referred sample of patients suffering from exercise intolerance and various muscle complaints, generally with elevated creatine kinase (CK). In all, 1226 patients underwent the non-ischaemic forearm exercise test. Blood lactate, ammonia and CK levels were analyzed. DNA analyses and/or muscle biopsies were assessed to confirm the diagnosis of McArdle's disease. The results of 60 volunteers were used to compare with the results of study subjects. In this cohort, 40 patients were finally diagnosed with McArdle's disease. Absolute values of lactate and ammonia rise were used to discriminate all McArdle patients from healthy patients. A sensitivity and specificity of respectively 100% and 99.7% were calculated. The 24-h CK level showed no significant difference from the CK level at the day of the test and confirms the safety of the test. This study has formally assessed the diagnostic value of the non-ischaemic forearm exercise test in the detection of McArdle's disease. Very high sensitivity and specificity were observed. Furthermore, the test is easy to set up and to perform, it is non-traumatic and cost effective. It may circumvent a muscle biopsy in McArdle patients presenting the most common mutations. Hence, it is a perfect and safe screening instrument to detect patients with McArdle's disease. Glycogen storage disease type III patients, however, may show similar patterns to McArdle patients. © 2015 EAN.
    European Journal of Neurology 03/2015; DOI:10.1111/ene.12685 · 3.85 Impact Factor
  • La Revue de Médecine Interne 12/2014; 35. DOI:10.1016/j.revmed.2014.10.028 · 1.32 Impact Factor
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    ABSTRACT: Mutations in one of the 3 genes encoding collagen VI (COLVI) are responsible for a group of heterogeneous phenotypes of which Bethlem myopathy (BM) represents the milder end of the spectrum. Genotype-phenotype correlations and long-term follow-up description in BM remain scarce. We retrospectively evaluated the long-term clinical evolution, and genotype-phenotype correlations in 35 genetically identified BM patients (23 index cases). Nineteen patients showed a typical clinical picture with contractures, proximal weakness and slow disease progression while 11 presented a more severe evolution. Five patients showed an atypical presentation, namely a limb girdle muscle weakness in 2 and a congenital myopathy pattern with either no contractures, or only limited to ankles, in 3 of them. Pathogenic COL6A1-3 mutations were mostly missense or in frame exon-skipping resulting in substitutions or deletions. Twenty one different mutations were identified including 12novel ones. The mode of inheritance was, autosomal dominant in 83% of the index patients (including 17% (N=4) with a de novo mutation), recessive in 13%, and undetermined in one patient. Skipping of exon 14 of COL6A1 was found in 35% of index cases and was mostly associated with a severe clinical evolution. Missense mutations were detected in 39% of index cases and associated with milder forms of the disease. Long-term follow-up identified important phenotypic variability in this cohort of 35 BM patients. However, worsening of the functional disability appeared typically after the age of 40 in 47% of our patients, and was frequently associated with COL6A1 exon 14 skipping. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Journal of Neurology Neurosurgery & Psychiatry 12/2014; DOI:10.1136/jnnp-2013-307245 · 5.58 Impact Factor
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    ABSTRACT: Background Charcot-Marie-Tooth type 1A disease (CMT1A) is a rare orphan inherited neuropathy caused by an autosomal dominant duplication of a gene encoding for the structural myelin protein PMP22, which induces abnormal Schwann cell differentiation and dysmyelination, eventually leading to axonal suffering then loss and muscle wasting. We favour the idea that diseases can be more efficiently treated when targeting multiple disease-relevant pathways. In CMT1A patients, we therefore tested the potential of PXT3003, a low-dose combination of three already approved compounds (baclofen, naltrexone and sorbitol). Our study conceptually builds on preclinical experiments highlighting a pleiotropic mechanism of action that includes downregulation of PMP22. The primary objective was to assess safety and tolerability of PXT3003. The secondary objective aimed at an exploratory analysis of efficacy of PXT3003 in CMT1A, to be used for designing next clinical development stages (Phase 2b/3).Methods80 adult patients with mild-to-moderate CMT1A received in double-blind for 1 year Placebo or one of the three increasing doses of PXT3003 tested, in four equal groups. Safety and tolerability were assessed with the incidence of related adverse events. Efficacy was assessed using the Charcot-Marie-Tooth Neuropathy Score (CMTNS) and the Overall Neuropathy Limitations Scale (ONLS) as main endpoints, as well as various clinical and electrophysiological outcomes.ResultsThis trial confirmed the safety and tolerability of PXT3003. The highest dose (HD) showed consistent evidence of improvement beyond stabilization. CMTNS and ONLS, with a significant improvement of respectively of 8% (0.4% - 16.2%) and 12.1% (2% - 23.2%) in the HD group versus the pool of all other groups, appear to be the most sensitive clinical endpoints to treatment despite their quasi-stability over one year under Placebo. Patients who did not deteriorate over one year were significantly more frequent in the HD group.Conclusions These results confirm that PXT3003 deserves further investigation in adults and could greatly benefit CMT1A-diagnosed children, usually less affected than adults.Trial registrationEudraCT Number: 2010-023097-40. ClinicalTrials.gov Identifier: NCT01401257. The Committee for Orphan Medicinal Products issued in February 2014 a positive opinion on the application for orphan designation for PXT3003 (EMA/OD/193/13).
    Orphanet Journal of Rare Diseases 12/2014; 9(1):199. DOI:10.1186/s13023-014-0199-0 · 3.96 Impact Factor
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    ABSTRACT: Collagen VI-related dystrophies and myopathies (COL6-RD) are a group of disorders that form a wide phenotypic spectrum, ranging from severe Ullrich congenital muscular dystrophy (UCMD), intermediate phenotypes, to the milder Bethlem myopathy (BM). Both inter- and intra-familial variable expressivity are commonly observed. We present clinical, immunohistochemical, and genetic data on four COL6-RD families with marked inter-generational phenotypic heterogeneity. This variable expression seemingly masquerades as anticipation is due to parental mosaicism for a dominant mutation, with subsequent full inheritance and penetrance of the mutation in the heterozygous offspring. We also present an additional 5th simplex patient identified as a mosaic carrier. Parental mosaicism was confirmed in the four families through quantitative analysis of the ratio of mutant versus wild-type allele (COL6A1, COL6A2 and COL6A3) in genomic DNA (gDNA) from various tissues; including blood, saliva, and dermal fibroblasts. Consistent with somatic mosaicism, parental samples had lower ratios of mutant versus wild-type allele compared to the fully heterozygote offspring. However, there was notable variability of the mutant allele levels between tissues tested, ranging from 16% (saliva) to 43% (fibroblasts) in one mosaic father. This is the first report demonstrating mosaicism as a cause of intra-familial/inter-generational variability of COL6-RD, and suggests that sporadic and parental mosaicism may be more common than previously suspected.This article is protected by copyright. All rights reserved
    Human Mutation 09/2014; DOI:10.1002/humu.22691 · 5.05 Impact Factor
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    ABSTRACT: Diseases due to mutations of POLG gene, encoding the mitochondrial DNA polymerase, are reputed to have very diverse clinical presentations and have been proposed to cause up to 25% adult mitochondrial diseases. Our objective was the evaluation of the specificity and sensitivity of the signs encountered with POLG mutations.
    Journal of Neurology Neurosurgery & Psychiatry 08/2014; DOI:10.1136/jnnp-2013-306799 · 5.58 Impact Factor
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    ABSTRACT: Axonal Charcot-Marie-Tooth disease (CMT) is genetically heterogeneous, with 11 genes identified. Axonal CMT has most frequently been associated with mutations in the MFN2 gene (CMT2A).
    JAMA Neurology 06/2014; 71(8). DOI:10.1001/jamaneurol.2014.629 · 7.01 Impact Factor
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    Revue Neurologique 06/2014; DOI:10.1016/j.neurol.2014.04.002 · 0.60 Impact Factor
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    ABSTRACT: To clarify the phenotypic spectrum and incidence of TRPV4 mutations in patients with inherited axonal neuropathies. We screened for TRPV4 mutations in 169 French unrelated patients with inherited axonal peripheral neuropathy. Ninety-five patients had dominant Charcot-Marie-Tooth type 2 (CMT2) disease, and 74 patients, including 39 patients with distal hereditary motor neuropathy, 14 with congenital spinal muscular atrophy and arthrogryposis, 13 with CMT2, and 8 with scapuloperoneal spinal muscular atrophy, presented with additional vocal cord paralysis and/or skeletal dysplasia. No deleterious TRPV4 mutation was identified in the 95 patients with "pure" CMT2 (0/95). In contrast, 12 of 74 patients (16%) with neuropathy and vocal cord paralysis and/or skeletal dysplasia presented pathogenic TRPV4 mutations, including 7 patients with distal hereditary motor neuropathy, 2 with scapuloperoneal spinal muscular atrophy, 2 with congenital spinal muscular atrophy and arthrogryposis, and one with CMT2. Investigation of affected relatives allowed us to study 17 patients. All patients had childhood-onset motor neuropathy and showed a variety of associated findings, including foot deformities (100% of cases), kyphoscoliosis (100%), elevated serum creatine kinase levels (100%), vocal cord paralysis (94%), scapular winging (53%), respiratory insufficiency (29%), hearing loss (24%), skeletal dysplasia (18%), and arthrogryposis (12%). Eight missense mutations were observed in these 12 families, including 2 previously unreported. Six mutations were de novo events, and 2 asymptomatic carriers were identified. With 16% of patients affected in our series, this study demonstrates that TRPV4 mutations are a major cause of inherited axonal neuropathy associated with a large spectrum of additional features.
    Neurology 04/2014; 82(21). DOI:10.1212/WNL.0000000000000450 · 8.30 Impact Factor
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    ABSTRACT: We conducted a prospective multinational study of muscle pathology using magnetic resonance imaging (MRI) in patients with limb-girdle muscular dystrophy 2I (LGMD2I). Thirty eight adult ambulant LGMD2I patients (19 male; 19 female) with genetically identical mutations (c.826C>A) in the fukutin-related protein (FKRP) gene were recruited. In each patient, T1-weighted (T1w) imaging was assessed by qualitative grading for 15 individual lower limb muscles and quantitative Dixon imaging was analysed on 14 individual lower limb muscles by region of interest analysis. We described the pattern and appearance of muscle pathology and gender differences, not previously reported for LGMD2I. Diffuse fat infiltration of the gastrocnemii muscles was demonstrated in females, whereas in males fat infiltration was more prominent in the medial than the lateral gastrocnemius (p = 0.05). In the anterior thigh of males, in contrast to females, median fat infiltration in the vastus medialis muscle (45.7%) exceeded that in the vastus lateralis muscle (11.2%) (p<0.005). MRI is non-invasive, objective and does not rely on patient effort compared to clinical and physical measures that are currently employed. We demonstrated (i) that the quantitative Dixon technique is an objective quantitative marker of disease and (ii) new observations of gender specific patterns of muscle involvement in LGMD2I.
    PLoS ONE 02/2014; 9(2):e90377. DOI:10.1371/journal.pone.0090377 · 3.53 Impact Factor
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    ABSTRACT: Congenital disorders of glycosylation are genetic syndromes that result in impaired glycoprotein production. We evaluated patients who had a novel recessive disorder of glycosylation, with a range of clinical manifestations that included hepatopathy, bifid uvula, malignant hyperthermia, hypogonadotropic hypogonadism, growth retardation, hypoglycemia, myopathy, dilated cardiomyopathy, and cardiac arrest. Homozygosity mapping followed by whole-exome sequencing was used to identify a mutation in the gene for phosphoglucomutase 1 (PGM1) in two siblings. Sequencing identified additional mutations in 15 other families. Phosphoglucomutase 1 enzyme activity was assayed on cell extracts. Analyses of glycosylation efficiency and quantitative studies of sugar metabolites were performed. Galactose supplementation in fibroblast cultures and dietary supplementation in the patients were studied to determine the effect on glycosylation. Phosphoglucomutase 1 enzyme activity was markedly diminished in all patients. Mass spectrometry of transferrin showed a loss of complete N-glycans and the presence of truncated glycans lacking galactose. Fibroblasts supplemented with galactose showed restoration of protein glycosylation and no evidence of glycogen accumulation. Dietary supplementation with galactose in six patients resulted in changes suggestive of clinical improvement. A new screening test showed good discrimination between patients and controls. Phosphoglucomutase 1 deficiency, previously identified as a glycogenosis, is also a congenital disorder of glycosylation. Supplementation with galactose leads to biochemical improvement in indexes of glycosylation in cells and patients, and supplementation with complex carbohydrates stabilizes blood glucose. A new screening test has been developed but has not yet been validated. (Funded by the Netherlands Organization for Scientific Research and others.).
    New England Journal of Medicine 02/2014; 370(6):533-42. DOI:10.1056/NEJMoa1206605 · 54.42 Impact Factor
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    ABSTRACT: Double-seronegative myasthenia gravis (dSN-MG, without detectable AChR and MuSK antibodies) presents a serious gap in MG diagnosis and understanding. Recently, autoantibodies against the low-density lipoprotein receptor-related protein 4 (LRP4) have been identified in several dSN-MG sera, but with dramatic frequency variation (∼2-50%). We have developed a cell based assay (CBA) based on human LRP4 expressing HEK293 cells, for the reliable and efficient detection of LRP4 antibodies. We have screened about 800 MG patient sera from 10 countries for LRP4 antibodies. The overall frequency of LRP4-MG in the dSN-MG group (635 patients) was 18.7% but with variations among different populations (range 7-32.7%). Interestingly, we also identified double positive sera: 8/107 anti-AChR positive and 10/67 anti-MuSK positive sera also had detectable LRP4 antibodies, predominantly originating from only two of the participating groups. No LRP4 antibodies were identified in sera from 56 healthy controls tested, while 4/110 from patients with other neuroimmune diseases were positive. The clinical data, when available, for the LRP4-MG patients were then studied. At disease onset symptoms were mild (81% had MGFA grade I or II), with some identified thymic changes (32% hyperplasia, none with thymoma). On the other hand, double positive patients (AChR/LRP4-MG and MuSK/LRP4-MG) had more severe symptoms at onset compared with any single positive MG subgroup. Contrary to MuSK-MG, 27% of ocular dSN-MG patients were LRP4 antibody positive. Similarly, contrary to MuSK antibodies, which are predominantly of the IgG4 subtype, LRP4 antibodies were predominantly of the IgG1 and IgG2 subtypes. The prevalence was higher in women than in men (female/male ratio 2.5/1), with an average disease onset at ages 33.4 for females and 41.9 for males. Overall, the response of LRP4-MG patients to treatment was similar to published responses of AChR-MG rather than to MuSK-MG patients.
    Journal of Autoimmunity 12/2013; DOI:10.1016/j.jaut.2013.12.004 · 7.02 Impact Factor
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    ABSTRACT: About 40% of responders to treatment for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) remain treatment dependent and have a relapse if treatment is interrupted. To look for factors associated with treatment dependence or successful withdrawal in CIDP patients. We retrospectively studied 70 responder CIDP patients comprising 34 patients who remained treatment dependent (treatment-dependent group) and 36 patients whose treatment could be discontinued (treatment withdrawal group). Clinical, biological, electrophysiological and therapeutic features were compared between these groups. A multifocal deficit was more frequent in the treatment-dependent group (35%) than in the treatment withdrawal group (8%) (p<0.01). The most frequent effective treatment was intravenous immunoglobulin (IVIG) for the treatment-dependent group (79%). In this group, more patients were resistant to corticosteroids in first-line therapy (93%) than in the treatment withdrawal group (40%) (p=0.002). The delay to effective treatment was significantly shorter for the treatment withdrawal group than for the treatment-dependent group (mean 11.1 vs 31.2 months; p<0.01). The rate of successful withdrawal was lower with IVIG (29%) than with corticosteroids (83%) (p<0.001). When compared with the treatment withdrawal group, the treatment-dependent group was more frequently responsive to IVIG, more frequently resistant to corticosteroids in first-line treatment, had a longer delay to effective treatment and was more likely to present a multifocal deficit. The rate of successful withdrawal seems to be higher with corticosteroids, but a prospective study with a long-term follow-up is needed to confirm these features.
    Journal of neurology, neurosurgery, and psychiatry 12/2013; 85(8). DOI:10.1136/jnnp-2013-306105 · 4.87 Impact Factor
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    ABSTRACT: IntroductionSensory chronic inflammatory demyelinating polyneuropathy (CIDP) can be difficult to diagnose. Methods We report 22 patients with chronic sensory polyneuropathy with 1 clinical sign atypical for chronic idiopathic axonal polyneuropathy (CIAP) but no electrodiagnostic criteria for CIDP. ResultsClinical signs atypical for CIAP were: sensory ataxia (59%), generalized areflexia (36%), cranial nerve involvement (32%), rapid upper limb involvement (40%), and age at onset 55 years (50%). Additional features were: normal sensory nerve action potentials (36%), abnormal radial/normal sural pattern (23%), abnormal somatosensory evoked potentials (SSEPs) (100%), elevated cerebrospinal fluid (CSF) protein (73%), and demyelinating features in 5/7 nerve biopsies. Over 90% of patients responded to immunotherapy. We conclude that all patients had sensory CIDP. Conclusions Sensory CIDP patients can be misdiagnosed as having CIAP. If atypical clinical/electrophysiologic features are present, we recommend performing SSEPs and CSF examination. Nerve biopsy should be restricted to disabled patients if other examinations are inconclusive.
    Muscle & Nerve 11/2013; 48(5). DOI:10.1002/mus.23821 · 2.31 Impact Factor
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    ABSTRACT: Heterogeneous clinical presentation and gender differences were reported in Charcot-Marie-Tooth disease type 1A (CMT1A). This report examined demographic and clinical data collected during a randomised controlled trial, to describe the clinical spectrum of a large and well-defined cohort of CMT1A patients. Among the 189 symptomatic patients screened, three patients (1.6%) reported first symptoms in the upper limbs, which may be misleading when establishing the clinical diagnosis. The quality of life (QoL) of patients was significantly deteriorated compared to the standard population, and slightly better compared to multiple sclerosis patients. According to the literature, patients reported several disorders which may be associated with CMT1A, including auditory dysfunction (7.9%), Carpal Tunnel Syndrome (CTS) (7.9%) or sleep apnoea (4.2%). Compared to available data, we reported more patients with CTS and fewer patients with sleep apnoea. Women were more affected by CTS than men (11% and 2.8%, respectively). Women also reported an earlier onset of symptoms than men (8.6±9.5years and 13.1±14years, respectively), higher deterioration of their QoL and higher disability of their upper limb, assessed by Overall Neuropathy Limitation Scale (p=0.023). This information will be useful for better understanding of this disease and for designing future clinical studies.
    Journal of the neurological sciences 10/2013; 336(1-2). DOI:10.1016/j.jns.2013.10.029 · 2.32 Impact Factor
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    ABSTRACT: In patients with myotonic dystrophy type 1 (DM1), the mechanisms underlying sudden cardiac death, which occurs in up to 1/3 of patients, are unclear. To study the potential role of Brugada syndrome in ventricular tachyarrhythmias and sudden death in DM1 patients. We screened 914 adult patients included in the DM1 Heart Registry during 2000-2009 for the presence of type 1 Brugada pattern on electrocardiogram (ECG). We also performed direct sequencing of SCN5A in patients with Brugada pattern. Further, we analysed SCN5A splicing on ventricular myocardial specimens harvested during cardiac transplantation in a 45-year-old patient with DM1 and three controls with inherited dilated cardiomyopathy. A type 1 Brugada pattern was present on the ECG of seven of 914 patients (0.8%), including five with a history of sustained ventricular tachyarrhythmia or sudden death, who fulfilled the criteria for Brugada syndrome. SCN5A sequencing was normal in all patients. Ventricular myocardial specimen analysis displayed abnormal splicing of SCN5A exon 6, characterized by over-expression of the 'neonatal' isoform, called exon 6A, in the patient with DM1, but not from the controls. Our findings suggest a potential implication of Brugada syndrome in sudden death in DM1, which may be related to missplicing of SCN5A. Our findings provide a new insight into the pathophysiology of heart disease in DM1. Number NCT01136330.
    Archives of cardiovascular diseases 10/2013; 106(12). DOI:10.1016/j.acvd.2013.08.003 · 1.66 Impact Factor
  • Neuromuscular Disorders 10/2013; 23(9-10):831-832. DOI:10.1016/j.nmd.2013.06.668 · 3.13 Impact Factor
  • Neuromuscular Disorders 10/2013; 23(9-10):765-766. DOI:10.1016/j.nmd.2013.06.459 · 3.13 Impact Factor
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    ABSTRACT: To provide a detailed phenotypical description of seronegative patients with generalized myasthenia gravis and antibodies to clustered acetylcholine receptors (AChRs) and to assess their frequency amongst a French seronegative generalized myasthenia gravis (SNMG) population. A French SNMG database was created and the sera from the 37 patients included in it were analysed by immunofluorescence of cell-based assays using cotransfection of AChR subunit genes together with rapsyn to densely cluster the AChRs. Sixteen per cent (n = 6) of the SNMG patients were found to have antibodies to clustered AChR. They presented either with early onset MG and thymic hyperplasia, late onset MG and thymic involution, or thymoma associated MG. They responded well to cholinesterase inhibitors and immunosuppressants. Patients with antibodies to clustered AChR account for a significant proportion of SNMG patients and resemble patients with AChR antibodies detected by standard radio-immunoprecipitation.
    European Journal of Neurology 09/2013; DOI:10.1111/ene.12270 · 3.85 Impact Factor
  • B Eymard, A Ferreiro, R Ben Yaou, T Stojkovic
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    ABSTRACT: Muscle diseases may have various clinical manifestations including muscle weakness, atrophy or hypertrophy and joint contractures. A spectrum of non-muscular manifestations (cardiac, respiratory, cutaneous, central and peripheral nervous system…) may be associated. Few of these features are specific. Limb joint contractures or spine rigidity, when prevailing over muscle weakness in ambulant patients, are of high diagnostic value for diagnosis orientation. Within this context, among several disorders, four groups of diseases should systematically come to mind including the collagen VI-related myopathies, the Emery-Dreifuss muscular dystrophies, the SEPN1 and FHL1 related myopathies. More rarely other genetic or acquired myopathies may present with marked contractures. Diagnostic work-up should include a comprehensive assessment including family history, neurological, cardiologic and respiratory evaluations. Paraclinical investigations should minimally include muscle imaging and electromyography. Muscle and skin biopsies as well as protein and molecular analyses usually help to reach a precise diagnosis. We will first describe the main muscle and neuromuscular junction diseases where contractures are typically a prominent symptom of high diagnostic value for diagnosis orientation. In the following chapters, we will present clues for the diagnostic strategy and the main measures to be taken when, at the end of the diagnostic work-up, no definite muscular disease has been identified.
    Revue Neurologique 09/2013; DOI:10.1016/j.neurol.2013.07.005 · 0.60 Impact Factor

Publication Stats

2k Citations
807.09 Total Impact Points


  • 2008–2014
    • Hôpital La Pitié Salpêtrière (Groupe Hospitalier "La Pitié Salpêtrière - Charles Foix")
      • Service de Biochimie Métabolique
      Lutetia Parisorum, Île-de-France, France
  • 2013
    • Polytech Paris-UPMC
      Lutetia Parisorum, Île-de-France, France
  • 2011–2013
    • Pierre and Marie Curie University - Paris 6
      • Institut de myologie
      Lutetia Parisorum, Île-de-France, France
    • Hôpitaux Universitaires La Pitié salpêtrière - Charles Foix
      Lutetia Parisorum, Île-de-France, France
  • 2012
    • Assistance Publique – Hôpitaux de Paris
      Lutetia Parisorum, Île-de-France, France
  • 1999–2012
    • University of Lille Nord de France
      Lille, Nord-Pas-de-Calais, France
  • 2010
    • Institute of Myology
      Lutetia Parisorum, Île-de-France, France
    • Hôpital Universitaire des Enfants Reine Fabiola
      Bruxelles, Brussels Capital Region, Belgium
  • 2009
    • Unité Inserm U1077
      Caen, Lower Normandy, France
    • University of Tunis El Manar
      Tunis-Ville, Tūnis, Tunisia
  • 2000–2009
    • Centre Hospitalier Régional Universitaire de Lille
      • • Division of Neurology
      • • Urology Service
      Lille, Nord-Pas-de-Calais, France
  • 2007
    • Centre Hospitalier de Valenciennes
      Valenciennes, Nord-Pas-de-Calais, France
  • 2005
    • Université du Droit et de la Santé Lille 2
      Lille, Nord-Pas-de-Calais, France
  • 2004
    • CHRU de Strasbourg
      Strasburg, Alsace, France
  • 2002
    • Centre Hospitalier de Lens
      Lens, Nord-Pas-de-Calais, France