F Tabaraud

University of Limoges, Limages, Limousin, France

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Publications (82)93.42 Total impact

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    ABSTRACT: Objectives. – Numerous sets of electrophysiological criteria of chronic inflammatory demyelinating polyneuropathy (CIDP) have been proposed, among which the criteria established by an ad hoc subcommittee of the American Academy of Neurology (AAN) in 1991 (Neurology 41 (1991) 617) are the most widely used. As they seemed rather restrictive, the Inflammatory Neuropathy Cause and Treatment (INCAT) group (Ann. Neurol. 50 (2001) 195) proposed modifications of these electrophysiological criteria. However, even using these criteria, some cases of CIDP may not be recognized. In such cases, nerve biopsy has proven useful for confirmation of the diagnosis by demonstrating specific abnormalities. The objective of the study was to determine the profile of electrophysiological abnormalities in patients with atypical electrophysiologic criteria of CIDP and the diagnostic value of multiple A waves and a low median to sural amplitude ratio.
    Full-text · Article · May 2004 · Neurophysiologie Clinique/Clinical Neurophysiology
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    ABSTRACT: Motor evoked potentials can be affected by propofol anaesthesia. We studied how increasing target concentrations of propofol altered transcranial motor evoked potentials (tcMEP) during scoliosis surgery. Fifteen patients undergoing surgery for scoliosis were anaesthetized with remifentanil and propofol without nitrous oxide or neuromuscular blocking agents (BIS<60). tcMEP were elicited by transcranial electric multipulse stimulation of the motor cortex and recording of compound action potentials from the anterior tibialis muscle. tcMEP were obtained before surgery with propofol target values set from 4 to 8 mg litre(-1), and then during surgery. Arterial propofol concentrations were measured for each tcMEP recording. Before surgery, increasing propofol reduced tcMEP amplitude in a dose-dependent manner, with no effect on latency. During surgery, at equivalent propofol concentrations, tcMEP were not statistically different from those obtained before surgery. In all except one patient, tcMEP signals were present during the entire procedure. In this patient the loss of tcMEP was unfortunately related to an anterior spinal cord lesion, which was confirmed by a wake-up test. We found that, although propofol had a dose-dependent effect on tcMEP amplitude, anaesthesia could be maintained with remifentanil and propofol to allow recording and interpretation of tcMEP signals.
    Preview · Article · Oct 2003 · BJA British Journal of Anaesthesia
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    ABSTRACT: A 42-year-old man presented exercise-induced muscle pain without myogloburia since the age of 12 years. Histochemistry and electronmicroscopy of a muscle biopsy revealed subsarcolemmal and inter-myofibrillar accumulation of glycogen. Exercise on a bicycle ergometer produced a normal raise of lactate. Biochemical study showed a partial defect in phosphorylase activity.
    No preview · Article · Aug 2003 · Revue Neurologique
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    ABSTRACT: The diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) relies primarily on clinical and electrophysiologic examination, but the nerve biopsy findings may be supportive, especially in atypical cases. In order to define the usefulness of nerve biopsy in this disease, we retrospectively studied 44 consecutive patients whom we classified as having CIDP on pathological grounds. We found that 8 of these 44 patients had pathological findings indicative of CIDP but did not meet any of the usually accepted electrophysiological criteria for its diagnosis. Among these eight patients, five responded favorably to conventional therapy. All of these eight patients had an electrophysiological pattern of generalized axonopathy with additional subtle findings suggestive of demyelination that prompted us to perform a nerve biopsy. Our data suggest that a significant number of patients with unrecognized CIDP are erroneously classified as having chronic idiopathic axonal polyneuropathy. CIDP should be suspected if the electrophysiological examination displays subtle abnormalities suggestive of demyelination, even in the presence of a prominent axonal pattern. Nerve biopsy in these patients may reveal abnormalities suggestive of CIDP and guide therapeutic options.
    No preview · Article · May 2003 · Muscle & Nerve
  • J-M Vallat · A.F. Hahn · J-M Léger · D P Cros · L Magy · F Tabaraud · P Bouche · P-M Preux
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    ABSTRACT: A prospective, multicenter, open-label study was conducted to determine the safety and efficacy of intramuscular (IM) interferon beta-1a (IFNbeta-1a) (Avonex) for treatment of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Eligible patients received IM IFNbeta-1a 30 microg once weekly for 6 months. Safety and tolerability were evaluated by reporting of adverse events, measurement of vital signs, and results of blood chemistry, hematology, and urinalysis. The primary efficacy end points were changed from baseline to month 6 on a quantitative Neurologic Disability Score (NDS), a clinical grading (CG) scale, and grip strength (GS) measures. Electrophysiologic measurements were performed at baseline and month 6. A total of 20 treatment-resistant patients with CIDP were enrolled in the study. The tolerability of IFNbeta-1a in patients with CIDP was similar to that seen with its use in MS. There were no serious adverse events, and no patients discontinued treatment due to adverse events. Seven patients (35%) showed clinical improvement, 10 (50%) had stable disease, and 3 (15%) continued to deteriorate. Significant improvements from baseline were observed in NDS in both the intent-to-treat and per protocol analyses (p=0.0005). For CG, significant improvement from baseline was observed in the per protocol analysis (p<0.05) but not in the intent-to-treat analysis. There was no significant effect of treatment on GS. Clinical improvement was not dependent on age, gender, clinical form of CIDP, or duration of symptoms. Electrophysiologic data showed improvements in mean median, ulnar, and tibial motor nerve potential areas. There was no correlation between clinical improvement and electrophysiologic data. The promising results of this study, especially given the refractory nature of the patient population, suggest that a larger placebo-controlled study should be performed to further evaluate the efficacy of IM IFNbeta-1a for the treatment of CIDP.
    No preview · Article · Apr 2003 · Neurology
  • S Blaise · J-M Vallat · F Tabaraud · J-M Bonnetblanc
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    ABSTRACT: Schnitzler's syndrome is a rare etiology of chronic urticaria. The disease is characterized by the association of chronic urticaria, intermittent chronic fever, bone pain, osteosclerotic bone lesions and IgM monoclonal gammapathy. More than fifty patients with this syndrome have been reported since Schnitzler reported the first case in 1974, but neuropathies are seen only in a few cases. Our patient developed, eight years after the diagnosis of Schnitzler'syndrome, a peripheral sensitive neuropathy. Anti-myelin-associated glycoprotein antibodies were not significant. A nerve biopsy specimen has revealed aspecific demyelinization. Direct and indirect immunofluorescence were negative. We conclused is that our patient presented chronic inflammatory demyelinating polyneuropathy. We found one published case of Schnitzler's syndrome and myelin-associated glycoprotein reactive peripheral neuropathy. The diagnosis of chronic inflammatory demyelinating polyneuropathy is a diagnosis of elimination. It is not the most common neuropathy associated with monoclonal gammapathy. To the best of our knowledge, it is the first case of Schnitzler's syndrome with this type of neuropathy. But there are some descriptions of chronic inflammatory demyelinating polyneuropathy presenting autoantibody activity against a myelin component, up to two years after the diagnosis of IgM monoclonal gammapathy.
    No preview · Article · Apr 2003 · Annales de Dermatologie et de Vénéréologie
  • Jean-Michel Vallat · François Tabaraud · Laurent Magy · Philippe Couratier
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    ABSTRACT: The objective of the study was to define how could be helpful a nerve biopsy for identification of atypical cases of chronic inflammatory demyelinating polyneuropathy (CIDP). An ad hoc committee in 1991 defined the clinical, electrophysiological and pathological criteria for diagnosis of CIDP. In common with other authors, we regard the rather specific electrophysiological criteria as being too restrictive, and we think that a significant number of patients may therefore not benefit from effective treatment or be excluded from therapeutic trials. The Inflammatory Neuropathy Cause and Treatment (INCAT) group (2001) has proposed new electrophysiological criteria of CIDP, which are more sensitive and do not loose any specificity. Over a period of three years (January 1999 to December 2001), we classified 44 patients into two categories: those presenting the strict criteria of the ad hoc committee and those who we regarded as cases of CIDP who did not meet these strict criteria. All these patients benefited from one or more clinical and electrophysiological examinations; extensive biological workup and genetic study when appropriate excluded other causes of neuropathy. Nerve biopsies were taken from all patients and samples were included in paraffin and epon for systematic light and electron microscopic examination. Out of 44 patients, 24 fulfilled the INCAT electrophysiological criteria with only 12 of these cases fulfilling the criteria of the ad hoc committee. Eight patients did not fulfill any of the widely accepted electrophysiological criteria of CIDP. However, study of nerve biopsies of these eight patients revealed histological features characteristic of CIDP according to histological criteria (AAN-1991). Among these patients, six have been treated and five responded favorably to conventional treatments for CIDP. Without information from the nerve biopsy, these patients would not have been treated effectively because their electrophysiological profile was indicative of axonal impairment interpreted erroneously as primary.
    No preview · Article · Feb 2003 · Bulletin de l'Académie nationale de médecine
  • J.-M. Vallat · F. Tabaraud · L. Magy · F. Macian
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    ABSTRACT: The Chronic Inflammatory Demyelinating Polyradiculoneuropathies (CIDP) constitute a syndrome whose incidence is difficult to evaluate, and is probably underestimated. In the course of this presentation, we deliberately restricted discussion to issues raised in recent years concerning the extent of this syndrome. We discuss diagnostic criteria, especially electrophysiological ones. As the criteria proposed by the ad hoc committee of the American Academy of Neurology in 1991 have been questioned due to lack of sensitivity, new ones have been proposed recently. We briefly discuss the different types of chronic dysimmune demyelinating neuropathy: not only the CIDP, but also the Lewis and Sumner syndrome or multifocal inflammatory demyelinating neuropathy and the multiple conduction block neuropathies. At last, we point out the consistent finding of axonal involvement in the course of a chronic demyelinating neuropathy; over time, it can become predominant, which may make diagnosis difficult by suggesting a chronic axonal neuropathy that may be assumed to be primary. Consideration of these points may help clinicians recognize more chronic dysimmune neuropathies, for which immunosuppressive therapy has been found to be effective.
    No preview · Article · Jan 2003 · Revue Neurologique
  • J M Vallat · F Tabaraud · L Magy · F Macian
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    ABSTRACT: The Chronic Inflammatory Demyelinating Polyradiculoneuropathies (CIDP) constitute a syndrome whose incidence is difficult to evaluate, and is probably underestimated. In the course of this presentation, we deliberately restricted discussion to issues raised in recent years concerning the extent of this syndrome. We discuss diagnostic criteria, especially electrophysiological ones. As the criteria proposed by the ad hoc committee of the American Academy of Neurology in 1991 have been questioned due to lack of sensitivity, new ones have been proposed recently. We briefly discuss the different types of chronic dysimmune demyelinating neuropathy: not only the CIDP, but also the Lewis and Sumner syndrome or multifocal inflammatory demyelinating neuropathy and the multiple conduction block neuropathies. At last, we point out the consistent finding of axonal involvement in the course of a chronic demyelinating neuropathy; over time, it can become pre-dominant, which may make diagnosis difficult by suggesting a chronic axonal neuropathy that may be assumed to be primary. Consideration of these points may help clinicians recognize more chronic dysimmune neuropathies, for which immunosuppressive therapy has been found to be effective.
    No preview · Article · Jan 2003 · Revue Neurologique
  • J M Vallat · F Tabaraud · L Magy · P Couratier

    No preview · Article · Oct 2002 · Revue Neurologique

  • No preview · Article · Sep 2001
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    ABSTRACT: Ventricular tachycardia by branch to branch reentry is a rare arrhythmia. It occurs in cardiomyopathies associated with conduction defects. During tachycardia a His potential precedes each QRS complex which usually has a left bundle branch block appearance. The authors report two familial cases of ventricular branch to branch tachycardia (son and mother) without cardiomyopathy. The diagnosis of Steinert's disease was made post-mortem in these two patients. In cases of branch to branch ventricular tachycardia, the diagnosis of myotonic dystrophy should be excluded. Conversely, endocavitary electrophysiological investigation with ventricular stimulation should be proposed for symptomatic patients (dizzy spells, syncope) to diagnose branch to branch ventricular tachycardia, even in cases with conduction defects which could also explain the symptoms.
    No preview · Article · Jul 2000 · Archives des maladies du coeur et des vaisseaux
  • E Petit · F Devière · F Tabaraud · T Truong · J M Vallat · P Couratier

    No preview · Article · May 2000 · Revue Neurologique
  • P Couratier · C T Truong · M Khalil · P M Preux · F Tabaraud · J M Vallat

    No preview · Article · Mar 2000 · Revue Neurologique
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    ABSTRACT: Many studies have shown that the risk of experiencing a myocardial infarction (MI) is increased during the first hours of the morning. Sleep apnea syndrome (SAS) is associated with an enhanced adrenergic activity, prolonged a few hours after awakening. We aimed at assessing whether sleep breathing disorders could be a culprit for the morning excess rate of MI. We studied 40 middle-aged men admitted for an acute MI. An overnight polysomnographic study was performed 37.4 +/- 9.4 days after the MI. The prevalence of SAS was high (30%). The prevalence of SAS was significantly higher in patients with the MI onset during the morning. The circadian pattern was significantly different in patients with or without SAS: those with SAS presented an important peak of MI onset during the period between 06.00 and 11.59 h. None of them had their MI during the period between 24.00 and 05.59 h. This different nyctohemeral pattern underlines the potential role of sleep breathing disorders as a trigger of MI.
    No preview · Article · Feb 2000 · Cardiology
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    ABSTRACT: X-linked Charcot–Marie–Tooth disease (CMT-X) is caused by mutations of connexin-32 (Cx-32), which encodes a gap-junction protein. Whether the neuropathy is primarily demyelinative or axonal remains to be established. We report findings of prominent demyelination in a 71-year-old woman with late-onset disease. Electrophysiological studies revealed a nonuniform slowing of motor conduction velocities and dispersion of compound action potentials indicative of a demyelinating process which was confirmed by nerve biopsy. Such electrophysiological features are unusual in hereditary neuropathies and are more commonly found with acquired chronic demyelinating neuropathies. A systematic search confirmed the molecular genomic diagnosis of CMT-X, illustrating the value of such tests in sporadic cases. Severity of clinical symptoms and signs may vary with age and sex of the patient. The pathology of CMT-X in other reported cases has been variably interpreted as axonal, demyelinating, or showing both features. Our observations emphasize the demyelinative nature. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1442–1447, 1999
    Full-text · Article · Oct 1999 · Muscle & Nerve
  • P. Bernet-Bernady · M. Tuillas · F. Tabaraud · P. Tapie

    No preview · Article · May 1998 · Neurophysiologie Clinique/Clinical Neurophysiology
  • Source
    JY Salle · JM Zola · F Tabaraud · JC Daviet · S Guinvarc'h · M Munoz · P Dudognon

    Full-text · Article · Dec 1997 · Annales de Réadaptation et de Médecine Physique

  • No preview · Article · Sep 1997
  • JM Zola · JY Salle · F Tabaraud · J Hugon · JM Vallat · M Dumas

    No preview · Article · Apr 1997 · Neurophysiologie Clinique/Clinical Neurophysiology

Publication Stats

855 Citations
93.42 Total Impact Points

Institutions

  • 1990-2003
    • University of Limoges
      • Institut d'Epidémiologie Neurologique et de Neurologie Tropicale (IENT)
      Limages, Limousin, France
  • 1996
    • Institut de France
      Lutetia Parisorum, Île-de-France, France
  • 1995
    • Centre Hospitalier de Cahors
      Cahors, Midi-Pyrénées, France
  • 1985-1992
    • Centre Hospitalier Universitaire de Limoges
      • Department of Neurology
      Limages, Limousin, France