P Vermersch

University of Lille Nord de France, Lille, Nord-Pas-de-Calais, France

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Publications (334)1200.08 Total impact

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    ABSTRACT: Background Patients who develop relapsing-remitting multiple sclerosis (MS) present with a first clinical demyelinating event. In this double-blind, multicentre, randomised, phase 3 study we investigated the effect of oral cladribine on conversion to clinically definite MS in patients with a first clinical demyelinating event, when given at the same doses shown to be effective in relapsing-remitting MS. Methods Between Oct 21, 2008, and Oct 11, 2010, we recruited patients aged 18–55 years, inclusive, from 160 hospitals, private clinics, or treatment centres in 34 countries. Eligible patients had a first clinical demyelinating event within 75 days before screening, at least two clinically silent lesions of at least 3 mm on a T2-weighted brain MRI scan, and an Expanded Disability Status Scale score of 5·0 or lower. Patients with a first clinical demyelinating event ≤75 days before screening were randomly assigned (1:1:1) to receive cladribine tablets at cumulative doses of 5·25 mg/kg or 3·5 mg/kg or placebo. Randomisation was done with a central web-based randomisation system and was stratified by geographic region. Masking was maintained using a two-physician model. The primary endpoint of this 96-week study was time to conversion to clinically definite MS according to the Poser criteria. This study is registered with ClinicalTrials.gov, number NCT00725985. Findings Of 903 participants assessed for eligibility, 616 patients received cladribine 5·25 mg/kg (n=204), cladribine 3·5 mg/kg (n=206), or placebo (n=206). At trial termination on Oct 25, 2011, cladribine was associated with a risk reduction versus placebo for time to conversion to clinically definite MS (hazard ratio [HR] for 5·25 mg/kg=0·38, 95% CI 0·25–0·58, p<0·0001; HR for 3·5 mg/kg=0·33, 0·21–0·51, p<0·0001). Adverse events were reported in 165 (81%) patients in the cladribine 5·25 mg/kg group, 168 (82%) patients in the cladribine 3·5 mg/kg group, and 162 (79%) patients in the placebo group. We noted no increase in risk of adverse events with active treatment versus placebo apart from lymphopenia, which was a severe event in 10 (5%) patients in the 5·25 mg/kg group and four (2%) patients in the 3·5 mg/kg group. Interpretation Both doses of cladribine significantly delayed MS diagnosis compared with placebo. The safety profile of cladribine was similar to that noted in a trial in patients with relapsing-remitting MS. Further research could clarify the potential effects of oral cladribine treatment in the early stages of MS. Funding Merck Serono SA Geneva, a subsidiary of Merck KGaA, Darmstadt, Germany.
    01/2014;
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    ABSTRACT: Encephalitis with anti-N-methyl-D-aspartate receptor antibodies (anti-NMDAR-Ab) is a rapid-onset encephalitis including psychosis, seizures, various movement disorders and autonomic system disturbances. We report a very unusual case of extensive myelitis associated with anti-NMDAR-Ab. MRI also revealed a hyperintense T2 lesion, non-suggestive of MS, which progressively extended, associated with periventricular gadolinium enhancement visualized on brain MRI. Ophthalmological evaluation showed subclinical right optic neuritis. The absence of anti-AQP4 antibody argued against neuromyelitis optica spectrum disorder. A slight psychomotor slowing prompted us to search for various causes of autoimmune encephalitis. Anti-NMDAR-Ab was found in cerebrospinal fluid. In patients with extensive myelitis who are seronegative for anti-AQP4 antibodies, and after other classical causes have been excluded, the hypothesis of atypical anti-NMDAR-Ab encephalitis should also be considered.
    BMC Neurology 12/2013; 13(1):211. · 2.56 Impact Factor
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    ABSTRACT: BACKGROUND AND PURPOSE:Therapeutic strategies for patients with MS partly rely on contrast-enhanced MR imaging. Our aim was to assess the diagnostic performance of 3D turbo spin-echo MR imaging with variable refocusing flip angles at 3T for the detection of enhanced inflammatory lesions in patients with multiple sclerosis.MATERIALS AND METHODS:Fifty-six patients with MS were prospectively investigated by using postcontrast T1-weighted axial 2D spin-echo and 3D TSE MR images. The order in which both sequences were performed was randomized. Axial reformats from 3D T1 TSE were generated to match the 2D spin-echo images. The reference standard was defined by using clinical data and all MR images available. Three separate sets of MR images (2D spin-echo images, axial reformats, and multiplanar images from 3D TSE sequences) were examined in a blinded fashion by 2 neuroradiologists separately for the detection of enhanced MS lesions. Image artifacts and contrast were evaluated.RESULTS:No artifacts related to vascular pulsation were observed on 3D TSE images, whereas image artifacts were demonstrated on 2D spin-echo images in 41 patients. One hundred twelve enhanced MS lesions were identified in 19 patients. Sixty-four lesions were correctly diagnosed by using 2D spin-echo images; 90, by using 3D TSE axial reformatted views; and 106, by using multiplanar analysis of the 3D TSE sequence. Multiplanar analysis was 94.7% sensitive and 100% specific for the diagnosis of patients with at least 1 enhanced lesion. Contrast of enhanced MS lesions was significantly improved by using the 3D TSE sequence (P < .011).CONCLUSIONS:The 3D TSE sequence with multiplanar analysis is a useful tool for the detection of enhanced MS lesions.
    American Journal of Neuroradiology 11/2013; · 3.17 Impact Factor
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    ABSTRACT: Cavitary white matter changes are mainly described in leukodystrophies and especially in vanishing white matter disease. Large cavitary lesions are not typical for multiple sclerosis (MS). We studied MS patients with large cavitary brain lesions. Patient characteristics, disease onset/duration/subtype, expanded disability status scale (EDSS), mini mental state (MMS), vanishing white matter disease genetic analysis, and MRI characteristics of the cavitary lesions were analyzed. Twenty patients were analyzed (6 men and 14 women). Mean age at disease onset was 37.6 (range 17-58). Mean disease duration was 10 years (range 2-20). Five patients had initial relapsing-remitting MS and nine patients had primary-progressive MS. Mean EDSS was 5.5 (range 2-8). Mean MMS was 20/30. Vanishing white matter disease genetic analysis was performed and negative in seven patients. Inferior corpus callosum lesions were seen in all patients with available sagittal FLAIR sequences. Cavitary lesions were strictly supratentorial, and located inside the diffuse leukoencephalopathy, with often a posterior predominance. MS patients with large cavitary lesions seem to represent a MS subgroup, predominantly women, with relatively late disease onset, predominantly primary-progressive type, relatively high EDSS scores, and severe cognitive dysfunction.
    Revue Neurologique 10/2013; · 0.51 Impact Factor
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    ABSTRACT: In previous studies, teriflunomide significantly reduced the annualised relapse rate (ARR) and disability progression. This phase 3, rater-blinded study (NCT00883337) compared teriflunomide with interferon-beta-1a (IFNβ-1a). Patients with relapsing multiple sclerosis were randomised (1:1:1) to oral teriflunomide 7-or 14mg, or subcutaneous IFNβ-1a 44µg. The primary composite endpoint was time to failure, defined as first occurrence of confirmed relapse or permanent treatment discontinuation for any cause. Secondary endpoints included ARR, Fatigue Impact Scale (FIS) and Treatment Satisfaction Questionnaire for Medication (TSQM). The study was completed 48 weeks after the last patient was randomised. Some 324 patients were randomised (IFNβ-1a: 104; teriflunomide 7 mg: 109; teriflunomide 14 mg: 111). No difference in time to failure was observed. There was no difference in ARR between teriflunomide 14 mg and IFNβ-1a, but ARR was significantly higher with teriflunomide 7 mg. FIS scores indicated more frequent fatigue with IFNβ-1a, though differences were only significant with teriflunomide 7 mg. TSQM scores were significantly higher with teriflunomide. There were no unexpected safety findings. Effects on time to failure were comparable between teriflunomide and IFNβ-1a. There was no difference between teriflunomide 14 mg and IFNβ-1a on ARR, though ARR was higher with teriflunomide 7 mg. The teriflunomide safety profile was consistent with previous studies.
    Multiple Sclerosis 10/2013; · 4.47 Impact Factor
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    ABSTRACT: The objectives of this study were to evaluate the rate of JC virus (JCV) seroconversion/seroreversion in a French cohort of multiple sclerosis (MS) patients receiving natalizumab (NTZ), describe the characteristics of this population, identify risk factors for JCV seropositivity and analyse the additional value of quantitative JCV serology results in this context. MS patients from two French MS centres, whose JCV serological status in 2011 while receiving NTZ was known (n=357; first-generation enzyme-linked immunosorbent assay (ELISA) test (Gen1)), were proposed for inclusion in this study. We evaluated the rate of JCV seroconversion over a period of one year with a second-generation ELISA test (Gen2; n=303) and analysed the quantitative results. Multivariate analysis was performed to identify risk factors for JCV seropositivity. Among the patients with Gen2 JCV serology (n=303) that had been JCV-seronegative one year before (n=165), the rate of JCV seroconversion was 26.67% (44/165). We observed a higher proportion of anti-JCV antibody seroconverters (14.5%) than expected (≤3%) but also increasing index values of anti-JCV antibody over time. Our data suggest that JCV reactivation occurs during NTZ therapy and leads to an increase in the anti-JCV antibodies titre, thus making them more easily detectable by the second-generation ELISA test.
    Multiple Sclerosis 09/2013; · 4.47 Impact Factor
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    ABSTRACT: To find biomarkers identifying patients at risk for the development of progressive multifocal leukoencephalopathy (PML) during natalizumab treatment. Patients were recruited from 10 European and US cohorts. Of 289 patients with multiple sclerosis (MS), 224 had been treated with natalizumab (18-80 months), 21 received other immune-modulatory treatments, and 28 were untreated. We had access to samples from 16 natalizumab PML patients. Eight of these patients had given blood before the diagnosis of PML. We also analyzed non-natalizumab-treated patients who developed PML (n = 10) and age- and sex-matched healthy donors (n = 31). All flow cytometric assessments were done on previously cryopreserved, viable peripheral blood mononuclear cells. The percentage of l-selectin-expressing CD4+ T cells was significantly lower in patients treated long-term with natalizumab (40.2%) when compared with patients not receiving natalizumab treatment (47.2%; p = 0.016) or healthy controls (61.0%; p < 0.0001). An unusually low percentage (9-fold lower; 4.6%) was highly correlated with the risk of developing PML in the patient group with available pre-PML samples when compared with non-PML natalizumab-treated patients (p ≤ 0.0001). Samples were gathered between 4 and 26 months before PML diagnosis. The cell-based assessment of the percentage of l-selectin-expressing CD4 T cells could provide an urgently needed biomarker for individual PML risk assessment.
    Neurology 08/2013; · 8.25 Impact Factor
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    ABSTRACT: BACKGROUND: Neuromyelitis optica (NMO) is an inflammatory disease associated with optic neuritis and myelitis. Recently, several studies showed that optical coherence tomography (OCT) could be an interesting method for the evaluation of disease severity; however, to date there are no studies with a longitudinal follow-up of visual function in NMO. The aim of this study was to assess the ability of OCT to evaluate the progression of visual dysfunction in NMO. PATIENTS AND METHODS: A group of 30 NMO patients (thus, 60 eyes), comprised of 20 women and 10 men with a mean age of 43.7 +/- 12.3 years, were prospectively evaluated clinically and by a whole neuro-ophthalmological work-up, including: visual acuity (VA), fundoscopy, visual evoked potential (VEP), visual field (VF) and optical coherence tomography (OCT). All patients were tested at baseline (after a mean disease duration of 6.1 years) and after a mean time of follow-up of 18 months (range: 12-36 months). RESULTS: Mean VA was similar at the two evaluation times (0.77 +/- 0.36 versus 0.77 +/- 0.35). The mean VF defect decreased slightly, but the difference was not significant (-5.9 +/- 1.3 dB versus -5.3 +/- 1.3 dB). In contrast, the mean retinal thickness seen on OCT decreased from 87.4 +/- 23.3 µm to 79.7 +/- 22.4 µm (p = 0.006). These modifications were only observed in eyes with a past or a recent history of optic neuritis (-15.1 µm; p < 0.001) and not in eyes without any history of optic neuritis (-2.4 µm; not significant). Also, they occurred independently of the occurrence of relapses (n = 13) and especially optic neuritis episodes; however, the number of optic neuritis episodes was low (n = 5). CONCLUSION: OCT seems to be a more sensitive test than VA or VF for monitoring ophthalmological function in NMO and it seems to be helpful for the detection of infra-clinical episodes in patients with a past history of optic neuritis. Our results suggest that this easily performed technique should be used in the follow-up of NMO, but complementary studies are warranted to confirm its interest at an individual level.
    Multiple Sclerosis 02/2013; · 4.47 Impact Factor
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    ABSTRACT: In clinical practice natalizumab is typically used in patients who have experienced breakthrough disease during treatment with interferon beta (IFNβ) or glatiramer acetate. In these patients it is important to reduce disease activity as quickly as possible. In a phase II study, differences between natalizumab and placebo in MRI outcomes reflecting inflammatory activity were evident after the first infusion and maintained through a 6-month period, suggesting a rapid onset of natalizumab treatment effects. To explore how soon after natalizumab initiation clinical effects become apparent, annualized relapse rates per 3-month period and time to first relapse were analyzed in the phase III AFFIRM study (natalizumab vs. placebo) and in the multinational Tysabri(®) Observational Program (TOP). In AFFIRM, natalizumab reduced the annualized relapse rate within 3 months of treatment initiation compared with placebo in the overall population (0.30 vs. 0.71; p < 0.0001) and in patients with highly active disease (0.30 vs. 0.94; p = 0.0039). The low annualized relapse rate was maintained throughout the 2-year study period, and the risk of relapse in AFFIRM patients treated with natalizumab was reduced [hazard ratio against placebo 0.42 (95 % CI 0.34-0.52); p < 0.0001]. Rapid reductions in annualized relapse rate also occurred in TOP (baseline 1.99 vs. 0-3 months 0.26; p < 0.0001). Natalizumab resulted in rapid, sustained reductions in disease activity in both AFFIRM and in clinical practice. This decrease in disease activity occurred within the first 3 months of treatment even in patients with more active disease.
    Journal of Neurology 01/2013; · 3.58 Impact Factor
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    ABSTRACT: Introduction Cavitary white matter changes are mainly described in leukodystrophies and especially in vanishing white matter disease. Large cavitary lesions are not typical for multiple sclerosis (MS). Methods We studied MS patients with large cavitary brain lesions. Patient characteristics, disease onset/duration/subtype, expanded disability status scale (EDSS), mini mental state (MMS), vanishing white matter disease genetic analysis, and MRI characteristics of the cavitary lesions were analyzed. Results Twenty patients were analyzed (6 men and 14 women). Mean age at disease onset was 37.6 (range 17–58). Mean disease duration was 10 years (range 2–20). Five patients had initial relapsing-remitting MS and nine patients had primary-progressive MS. Mean EDSS was 5.5 (range 2–8). Mean MMS was 20/30. Vanishing white matter disease genetic analysis was performed and negative in seven patients. Inferior corpus callosum lesions were seen in all patients with available sagittal FLAIR sequences. Cavitary lesions were strictly supratentorial, and located inside the diffuse leukoencephalopathy, with often a posterior predominance. Conclusion MS patients with large cavitary lesions seem to represent a MS subgroup, predominantly women, with relatively late disease onset, predominantly primary-progressive type, relatively high EDSS scores, and severe cognitive dysfunction.
    Revue Neurologique 01/2013; · 0.51 Impact Factor
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    ABSTRACT: OBJECTIVE: In Assessment of OraL Laquinimod in PrEventing ProGRession in Multiple SclerOsis (ALLEGRO), a phase III study in relapsing-remitting multiple sclerosis (RRMS), oral laquinimod slowed disability and brain atrophy progression, suggesting laquinimod may reduce tissue damage in MS. MRI techniques sensitive to the most destructive aspects of the disease were used to further investigate laquinimod's potential effects on inflammation and neurodegeneration. METHODS: 1106 RRMS patients were randomised 1:1 to receive once-daily oral laquinimod (0.6 mg) or placebo for 24 months. White matter (WM), grey matter (GM) and thalamic fractions were derived at months 0, 12 and 24. Also assessed were evolution of gadolinium-enhancing and/or new T2 lesions into permanent black holes (PBH); magnetisation transfer ratio (MTR) of normal-appearing brain tissue (NABT), WM, GM and T2 lesions; and N-acetylaspartate/creatine (NAA/Cr) levels in WM. RESULTS: Compared with placebo, laquinimod-treated patients showed lower rates of WM at months 12 and 24 (p=0.004 and p=0.035) and GM (p=0.004) atrophy at month 12 and a trend for less GM atrophy at month 24 (p=0.078). Laquinimod also slowed thalamic atrophy at month 12 (p=0.005) and month 24 (p=0.003) and reduced the number of PBH at 12 and 24 months evolving from active lesions (all p<0.05). By month 24, MTR decreased significantly in NABT (p=0.015), WM (p=0.011) and GM (p=0.034) in placebo-treated patients, but not in laquinimod-treated patients. WM NAA/Cr tended to increase with laquinimod and decrease with placebo at 24 months (p=0.179). CONCLUSIONS: Oral laquinimod may reduce (at least in the initial phase of treatment) some of the more destructive pathological processes in RRMS patients. TRIAL REGISTRATION: The ALLEGRO trial identifier number with clinicaltrials.gov is NCT00509145. KEYWORDS: MRI, Multiple Sclerosis
    Journal of neurology, neurosurgery, and psychiatry 01/2013; · 4.87 Impact Factor
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    ABSTRACT: We herein provide a comprehensive assessment of magnetic resonance imaging (MRI) outcomes from CLARITY, a 96-week, double-blind study demonstrating significant clinical and MRI improvements in patients with relapsing-remitting multiple sclerosis (RRMS) treated with cladribine tablets. Patients with RRMS were randomized 1:1:1 to annual short-course therapy with cladribine tablets cumulative dose 3.5 or 5.25 mg/kg or placebo. MRI endpoints included mean number of T1 gadolinium-enhancing (Gd+), active T2 and combined unique (CU) lesions/patient/scan. MRI-measured disease activity was significantly reduced in both cladribine tablets groups versus placebo. The proportion of patients with no active lesions at study end was: T1 Gd+ lesions: 86.8 and 91.0 versus 48.3 % (p < 0.001); active T2 lesions: 61.7 and 62.5 versus 28.4 % (p < 0.001); CU lesions: 59.6 and 60.7 versus 26.1 % (p < 0.001). Clinically meaningful and significant reductions in active lesion counts and increases in proportions of active lesion-free patients were achieved consistently in cladribine tablet groups when data were stratified by baseline disease characteristics. For example, the percentage of patients who remained lesion-free over the study was significantly greater in cladribine tablet groups than in the placebo group for all lesion types regardless of relapse category at baseline (p < 0.001 for all analyses of patients with ≤1 or 2 relapses; p ≤ 0.022 for analyses of patients with ≥3 relapses). MRI-measured disease activity was greatly reduced by both doses of cladribine tablets, with consistent effect across clinically relevant patient populations. These findings add to our scientific understanding of the neurological impact of this therapeutic modality in patients with RRMS.
    Journal of Neurology 12/2012; · 3.58 Impact Factor
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    ABSTRACT: BACKGROUND: Mutations of the peripheral myelin protein-22 (PMP22) gene are the most common cause of inherited disease of the peripheral nervous system (PNS), with its deletion resulting in hereditary neuropathy with liability to pressure palsies (HNPP), and its duplication inducing Charcot-Marie-Tooth 1A (CMT1A) disease. Although mainly expressed in the PNS, PMP22 mRNA and protein are also present in the central nervous system (CNS). OBJECTIVE: To investigate whether patients with PMP22 mutations present with CNS abnormalities. METHODS: Fifteen patients with HNPP and 15 patients with CMT1A disease were prospectively included and their brain MRI and neuropsychological assessment were compared with those of healthy subjects. We evaluated, in particular, the volumes of grey and white matter (GM and WM) and looked for metabolic changes using spectroscopy, and abnormal architecture using fractional anisotropy (FA) measurement. A post mortem examination of the CNS of a patient with PMP22 gene duplication was also performed. RESULTS: We found a decrease in the volume of WM in 70% of patients, a reduced creatine level in WM in 28% and a cognitive impairment in 70%. FA was significantly altered in several areas of WM, including the columns of the fornix. The results for WM volume, creatine level in WM and cognitive testing showed that 47% of patients (patients with HNPP and those with CMT1A) presented with at least two abnormal results. Pathological examination of the brain of a patient with PMP22 gene duplication showed diffuse hypomyelination sparing the U fibres. CONCLUSIONS: This study demonstrates that altered PMP22 gene expression induces significant CNS alterations in patients with HNPP and CMT1A, including cerebral WM abnormalities and cognitive impairment.
    Journal of neurology, neurosurgery, and psychiatry 12/2012; · 4.87 Impact Factor
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    ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disease, which primarily affects skin and joints. Peripheral neurologic syndrome and central nervous system (CNS) manifestations are common in lupus patients but are not always attributable to lupus itself. A classification, published in 1999 by the American College of Rheumatology (ACR) research committee, described 12 CNS syndromes and seven peripheral neurologic syndromes compatible with “neuropsychiatric systemic lupus erythematosus” (NPSLE). Despite this consensus, studies which have been published since 1999 have reported a prevalence of NPSLE varying from 20 to 97 %, which shows the diagnosis difficulty and the heterogeneity of neuropsychiatric manifestations in SLE. In order to understand the limits of this classification, we propose in this first part an exhaustive review of publications describing neuropsychiatric manifestations according to the ACR 1999 classification. We also detail case definitions, prevalence and risk factors, clinical characteristics and diagnosis of each lupus-related psychiatric and CNS manifestation.
    La Revue de Médecine Interne. 09/2012; 33(9):491–502.
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    ABSTRACT: Neurological and psychiatric manifestations of systemic lupus erythematosus are a heterogenous set of clinical manifestations grouped under the term of “neuropsychiatric systemic lupus erythematosus”. The classification of these manifestations published in 1999 has harmonized the definitions cases used in the studies but did not help the clinician to positively identify a specific manifestation of lupus or a neurological or psychiatric event occurred independently of the disease. Published cases series help us to identify neurological or psychiatric manifestations of lupus but modern diagnosis tools contribution have to be evaluated in order to optimize diagnosis management of such manifestations and to distinguish specific events related to lupus and independent manifestations. In this second part of our literature review about neuropsychiatric lupus, we propose to identify arguments, which could be in favor of lupus responsibility in front of a neurological or psychiatric event, and immunosuppressive treatments which are recommended.
    La Revue de Médecine Interne. 09/2012; 33(9):503–513.
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    ABSTRACT: BACKGROUND AND PURPOSE:DTI is a promising technique for imaging of the spinal cord, but the technique has susceptibility-induced artifacts. We evaluated a pulse-triggered DTI sequence with an rFOV technique and coronal acquisition for the assessment of the cervical spinal cord in patients with myelitis at 3T.MATERIALS AND METHODS:A rFOV acquisition was established by a noncoplanar application of the excitation and the refocusing pulse in conjunction with outer volume suppression. The DTI sequence was performed in the coronal plane in 12 healthy volunteers and 40 consecutive patients with myelitis. Probabilistic tractography of the posterior and lateral funiculi was performed from the C1 to C7 levels. FA, MD, aD, rD, and ratios of aD and rD were measured.RESULTS:In healthy volunteers, mean DTI indices within the whole-fiber pathways were the following: FA = 0.61, MD = 1.17 × 10(-3) mm(2)/s, aD = 1.96 × 10(-3) mm(2)/s, rD = 0.77 × 10(-3) mm(2)/s, and ratios of aD and rD = 2.5. Comparison of healthy controls and patients with myelitis identified statistically significant differences for all DTI parameters. Different patterns of myelitis, including spinal cord atrophy and active inflammatory lesions, were recognized. There was a significant correlation between clinical severity and DTI parameters.CONCLUSIONS:The present work introduces a new approach for DTI of the cervical spinal cord at 3T, enabling a quantitative follow-up of patients with myelitis.
    American Journal of Neuroradiology 08/2012; · 3.17 Impact Factor
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    ABSTRACT: Natalizumab-associated progressive multifocal leukoencephalopathy (N-PML) in multiple sclerosis (MS) is due to CNS infection by the opportunistic JC virus (JCV). As of December 2011, 193 confirmed cases of N-PML have been observed, giving rise to an overall risk of approximately 0.202%.(1) N-PML pathogenesis remains partially elusive although risk factors have now been clearly delineated.(2) In patients with prior JCV infection detected by serum anti-JCV antibodies,(3) duration of therapy and prior use of immunosuppressants (IS) increase the risk of N-PML. The clinical outcome of patients with MS who developed N-PML was highly variable, ranging from asymptomatic case(4) to varying degrees of neurologic disability or even death.(5) It was also observed in real-life setting that the earlier N-PML was diagnosed and treated, the better was the clinical outcome.(5) Clinical vigilance is now considered as the established cornerstone of PML risk-management algorithm.(2).
    Neurology 08/2012; 79(10):1067-9. · 8.25 Impact Factor
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    ABSTRACT: The impact of autoimmunity on malaria-infection evolution reported by various works has led us to compare reactive patterns of self-dependent systemic IgG from 54 patients aged less than 15 years old to those from 46 subjects older than 15 years. These subjects were divided into 34 Plasmodium falciparum asymptomatic carriers (ACs), 30 cases of uncomplicated malaria (UM), and 36 patients suffering from cerebral malaria (CM) living in the same endemic area. The reactivity of the plasma antibodies against human brain tissue extract was assessed by western blotting. Comparative analysis of reactive bands (linear discriminant analysis, LDA) revealed the existence of patterns that distinguish, among the more susceptible subjects aged less than 15 years old, the different clinical forms. In contrast, in less susceptible subjects aged more than 15 years old, the patterns are homogenous and do not allow the separation of these clinical forms. This self-reactive repertoire might be witnessed as an imprint of the clinical tolerance acquired during the years of living in endemic areas. The singularity of this profile under the age of 15 years might have a prognostic value.
    Bulletin de la Société de pathologie exotique 08/2012; 105(4):276-83.
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    ABSTRACT: Inherited diseases of cobalamin (cbl) intracellular metabolism are very rare disorders affecting the synthesis of adenosylcobalamin or methylcobalamin. Methylcobalamin deficiency is generally characterized by homocystinuria and hypomethioninemia in the absence of methylmalonic aciduria (figure e-1 on the Neurology® Web site at www.neurology.org). We report one of the oldest known patients with cblG disease (deficiency of methionine synthase).
    Neurology 07/2012; 79(4):386-8. · 8.25 Impact Factor
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    ABSTRACT: Neurology® 2012;79:104-105.
    Neurology 07/2012; 79(1):104-5. · 8.25 Impact Factor

Publication Stats

4k Citations
1,200.08 Total Impact Points

Institutions

  • 1992–2014
    • University of Lille Nord de France
      Lille, Nord-Pas-de-Calais, France
  • 2010–2013
    • University of Strasbourg
      Strasburg, Alsace, France
    • Centre hospitalier Gustave Dron
      Tourcoing, Nord-Pas-de-Calais, France
  • 2012
    • University of Liège
      Luik, Walloon Region, Belgium
    • Centre Hospitalier Universitaire Rouen
      Rouen, Upper Normandy, France
  • 1990–2012
    • Centre Hospitalier Régional Universitaire de Lille
      • • Division of Neurology
      • • Urology Service
      Lille, Nord-Pas-de-Calais, France
  • 2002–2011
    • Université du Droit et de la Santé Lille 2
      Lille, Nord-Pas-de-Calais, France
  • 1998–2011
    • CHRU de Strasbourg
      Strasburg, Alsace, France
  • 1988–2011
    • Lille Catholic University
      Lille, Nord-Pas-de-Calais, France
  • 2007
    • Thomas Jefferson University
      Philadelphia, Pennsylvania, United States
    • Centre Hospitalier de Valenciennes
      Valenciennes, Nord-Pas-de-Calais, France
  • 2004
    • Université Charles-de-Gaulle Lille 3
      Lille, Nord-Pas-de-Calais, France
  • 1992–1997
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 1995
    • Centre Hospitalier Universitaire de Rennes
      Roazhon, Brittany, France