F Tabaraud

Publications (57)106.1 Total impact

• Article: Alzheimer CSF biomarkers in routine clinical setting.

  F Tabaraud, J P Leman, A M Milor, J M Roussie, G Barrière, M Tartary, F Boutros-Toni, M Rigaud
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  ABSTRACT: Our work was aimed to evaluate Alzheimer's disease diagnosis improvement using cerebrospinal fluid biomarkers (CSF) in neurological daily practice. For this purpose, 150 patients clinically and neurochemically classified as having AD or cognitive impairment with or without other dementia type were included in the study. The following CSF peptides were studied, blindly to the clinical diagnosis: beta-amyloid(1-42) peptide (Aβ(1-42)), Tau (T-tau), threonine-181 hyperphosphorylated tau protein (P-tau(181)), and beta-amyloid(1-40) peptide (Aβ(1-40)). From these measurements, Innotest® Amyloid Tau Index (IATI) was calculated for each patient. This assessment allowed to separate 83 biochemical profiles of AD and 67 non-Alzheimer's disease (non-AD), both AD and non-AD categories match with clinical data amounting to 73% and 90%, respectively. Among mild cognitive impairment (MCI) patients, CSF biomarkers led to discriminate those who are likely to be AD. We devoted a special section to Aβ(1-40) which is not a routine parameter but can help to confirm a pathological amyloid process as Aβ(1-42)/Aβ(1-40) ratio underlining the real decline of the Aβ(1-42). The interest of biomarkers and their ability to solve awkward cases were carefully noticed all the more when a discrepancy between clinical and CSF biological data was involved. The final proposed algorithm allowed to identify pathogenic forms of AD according to the prevailing role of hyperphosphorylated tau or amyloid beta peptide.
  Acta Neurologica Scandinavica 09/2011; 125(6):416-23. · 2.47 Impact Factor
• Article: Atypical electrophysiologic findings in chronic inflammatory demyelinating polyneuropathy (CIDP)--diagnosis confirmed by nerve biopsy.

  S Boukhris, L Magy, R Kabore, T Mabrouk, Y Li, P Sindou, F Tabaraud, Jean-Michel Vallat
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  ABSTRACT: 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. Over a period of 3 years, we classified 44 patients into two categories: those presenting the strict AAN and/or INCAT criteria and those who we regarded as cases of CIDP not meeting these criteria. All patients benefited from one or more clinical and electrophysiological examination. 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, teasing and electron microscopic examination. Out of 44 patients, 36 fulfilled the INCAT or AAN criteria. In eight other patients, the diagnosis of CIDP was suspected on clinical and EMG examinations and confirmed by nerve biopsy. In these cases, the electrophysiological exploration showed some abnormalities such as multiple A waves in four out of eight patients or an abnormal pattern of the sensory responses of the median and sural nerves in four out of eight patients that were more indicative of an initial demyelinating process. Six of our patients received immunomodulatory treatment, and five responded favorably.
  Neurophysiologie Clinique/Clinical Neurophysiology 05/2004; 34(2):71-9. · 1.98 Impact Factor
• Article: Influence of propofol concentrations on multipulse transcranial motor evoked potentials.

  N Nathan, F Tabaraud, F Lacroix, D Mouliès, X Viviand, A Lansade, G Terrier, P Feiss
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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.
  BJA British Journal of Anaesthesia 10/2003; 91(4):493-7. · 4.24 Impact Factor
• Article: [Glycogenesis due to adult phosphorylase kinase deficiency].

  P Couratier, L Magy, C Baussan, M-T Antonini, J-F Martaille, F Tabaraud, J-M Vallat
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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.
  Revue Neurologique 08/2003; 159(6-7 Pt 1):681-4. · 0.49 Impact Factor
• Article: Interferon beta-1a as an investigational treatment for CIDP.

  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.
  Neurology 04/2003; 60(8 Suppl 3):S23-8. · 8.31 Impact Factor
• Article: [Chronic inflammatory demyelinating neuropathies and their variants]

  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.
  Revue Neurologique 01/2003; 158(123):27-31. · 0.49 Impact Factor
• Article: [Chronic polyradiculoneuritis and its frontiers].

  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.
  Revue Neurologique 01/2003; 158(12 Pt 2):S27-31. · 0.49 Impact Factor
• Article: [Myelin-axon: a married couple].

  J M Vallat, F Tabaraud, L Magy, P Couratier
  Revue Neurologique 10/2002; 158(8-9):782-3. · 0.49 Impact Factor
• Article: [Ventricular tachycardia by branch to branch re-entry. Familial case with Steinert's disease].

  A Lagrange, P Lagrange, S Boveda, E Espaliat, J P Penot, P Defaye, T Arentz, F Tabaraud, P Virot, P Blanc
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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.
  Archives des maladies du coeur et des vaisseaux 07/2000; 93(6):743-9. · 0.40 Impact Factor
• Article: Myelin widenings and MGUS-IgA: an immunoelectron microscopic study.

  J M Vallat, F Tabaraud, P Sindou, P M Preux, A Vandenberghe, A Steck
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  ABSTRACT: A few studies have reported a variety of nonspecific histological lesions in patients with IgA monoclonal gammopathies and polyneuropathy. In our case, using electron microscopy, we observed widenings of the myelin lamellae identical to those commonly described in IgM neuropathies with anti-myelin-associated glycoprotein activity. Using immunoelectron microscopy, we demonstrated a direct involvement of IgA in myelin lesions. The search for a direct link between monoclonal dysglobulinemia, regardless of type, and polyneuropathy is important and may influence treatment.
  Annals of Neurology 07/2000; 47(6):808-11. · 11.09 Impact Factor
• Article: [Bilateral phrenic involvement disclosing Parsonage Turner syndrome].

  E Petit, F Devière, F Tabaraud, T Truong, J M Vallat, P Couratier
  Revue Neurologique 05/2000; 156(4):403-4. · 0.49 Impact Factor
• Article: [Cranial nerve palsies in a multifocal demyelinating neuropathy with persistent nerve block associated with hemorrhagic ulcerative colitis].

  P Couratier, C T Truong, M Khalil, P M Preux, F Tabaraud, J M Vallat
  Revue Neurologique 03/2000; 156(2):179. · 0.49 Impact Factor
• Article: Is the morning peak of acute myocardial infarction's onset due to sleep-related breathing disorders? A prospective study.

  V Aboyans, C Cassat, P Lacroix, P Tapie, F Tabaraud, F Pesteil, F Bertin, M Laskar, P Virot
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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.
  Cardiology 02/2000; 94(3):188-92. · 1.71 Impact Factor
• Article: Demyelinating X-linked Charcot-Marie-Tooth disease: unusual electrophysiological findings.

  F Tabaraud, E Lagrange, P Sindou, A Vandenberghe, N Levy, J M Vallat
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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.
  Muscle & Nerve 11/1999; 22(10):1442-7. · 2.37 Impact Factor
• Article: Demyelinating X‐linked Charcot–Marie–Tooth disease: Unusual electrophysiological findings

  F. Tabaraud MD, E. Lagrange MD, P. Sindou PhD, A. Vandenberghe PhD, PhD N. Levy MD, J.M. Vallat MD, F. Tabaraud, E. Lagrange, P. Sindou, A. Vandenberghe, N. Levy, J.M. Vallat
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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
  Muscle & Nerve 09/1999; 22(10):1442 - 1447. · 2.37 Impact Factor
• Article: Ultrastructural protein zero expression in Charcot-Marie-Tooth type 1B disease.

  P Sindou, J M Vallat, F Chapon, J J Archelos, F Tabaraud, T Anani, K G Braund, T Maisonobe, J J Hauw, A Vandenberghe
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  ABSTRACT: Charcot-Marie-Tooth type 1B (CMT 1B) disease, an inherited demyelinating peripheral neuropathy, results from different point mutations located in the P0 gene on chromosome 1 q21-23. We have quantified, at the ultrastructural level, the immunocytochemical expression of the P0 protein in two unrelated CMT 1B patients with mutations (Ser 78 to Leu and Asn 122 to Ser) located in two different exons in the extracellular domain of the protein. A twofold decrease in P0 expression was observed in compact myelin in each case, compared with age-matched controls. The severity of the phenotypes showed no direct relationship to the levels of P0 protein expression in these 2 patients.
  Muscle & Nerve 02/1999; 22(1):99-104. · 2.37 Impact Factor
• Article: Electroencephalographic and polygraphic features of 24-hour recordings in sleeping sickness and healthy African subjects.

  P Tapie, A Buguet, F Tabaraud, P Bogui, F Doua, J Bert
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  ABSTRACT: Electroencephalographic (EEG) and polygraphic features were analysed in six healthy control subjects and eight patients suffering from sleeping sickness meningoencephalitis in order to determine possible functional relationships. One patient was disqualified because of intermittent metabolic disease. Twenty-four h polygraphic recordings-EEG, electrooculography (EOG), electromyography (EMG), nasal and buccal air flow, chest respiratory movements-were performed continuously both on paper and on cassette tapes. Tapes were played back on paper (paper speed: 15 mm/s). Traces were analyzed for normal and pathologic features, and transient activation phases and paroxysmal hypnopompic hypersynchrony events were counted. During wakefulness, slow theta and delta waves occurred in four patients, but alpha reactivity was present. During sleep, normal features were seen. However, transient activation phases were decreased in the patients. During slow-wave sleep, four patients presented predominantly monophasic frontal delta bursts along with paroxysmal hypnopompic hypersynchrony events. In conclusion, in sleeping sickness patients, although dampened, the waking process remains responsive and slows down only during the late stage of meningoencephalitis.
  Journal of Clinical Neurophysiology 08/1996; 13(4):339-44. · 1.45 Impact Factor
• Article: Ultrastructural PMP22 expression in inherited demyelinating neuropathies.

  J M Vallat, P Sindou, P M Preux, F Tabaraud, A M Milor, P Couratier, E LeGuern, A Brice
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  ABSTRACT: Charcot-Marie-Tooth type 1A (CMT-1A) disease results from a duplication of the PMP22 gene on chromosome 17p11.2. A deletion of the same region causes hereditary neuropathy with liability to pressure palsies (HNPP). We examined the expression of PMP22 in sural nerve biopsies from 2 unrelated patients with CMT-1A, 2 unrelated patients with HNPP, and control patients. The ultrastructural immunocytochemical quantitative analysis of cases of CMT-1A and HNPP showed, respectively, an elevated and reduced expression of PMP22 level compared with controls.
  Annals of Neurology 07/1996; 39(6):813-7. · 11.09 Impact Factor
• Article: Survival prediction in sporadic amyotrophic lateral sclerosis. Age and clinical form at onset are independent risk factors.

  P M Preux, P Couratier, F Boutros-Toni, J Y Salle, F Tabaraud, P Bernet-Bernady, J M Vallat, M Dumas
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  ABSTRACT: Amyotrophic lateral sclerosis is a progressive neurological disease of unknown etiology and fatal outcome. Patient management can be aided by careful assessment of prognostic factors. A prospective study of 158 patients was carried out to examine the prognostic significance of age and clinical form at onset. The overall 5-year survival rate was 14.7%. The higher the age was at first symptoms, the worse the prognosis. The bulbar and common forms had a worse prognosis than the pseudo-polyneuritic forms. After adjustment for age, the clinical form at onset remained a prognostic factor. In a multivariate analysis using the Cox model, these two factors remained independent despite the later onset of the bulbar forms. In view of the discrepancies between the different published studies, the evaluation of the survival of an individual patient is of doubtful value.
  Neuroepidemiology 02/1996; 15(3):153-60. · 2.31 Impact Factor
• Article: Non-Hodgkin malignant lymphomas and peripheral neuropathies--13 cases.

  J M Vallat, H A De Mascarel, D Bordessoule, M O Jauberteau, F Tabaraud, A Gelot, A V Vallat
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  ABSTRACT: Non-Hodgkin's malignant lymphomas (NHML) are malignant lymphoid proliferations which may be of B or T cell type. Thirteen observations of an association between peripheral neuropathy and B type NHML are reported. None of the cases had evidence of meningeal propagation or neurotoxicity from chemotherapy. The NHML were classified according to the Working Formulation and Kiel classifications. The various mechanisms of peripheral neuropathy in these cases were split into four broad groups. Group I consisted of four cases in which the peripheral nerve lesions were directly linked to a propagation of malignant cells into the peripheral nervous system; this was revealed by autopsy and/or nerve biopsy. Malignant B cell proliferation was demonstrated in three out of four of these cases by immunolabelling of the infiltrates. Group II included three patients whose serum contained a monoclonal immunoglobulin (IgM) with antimyelin activity, and two who had pathological IgM deposits in endoneurial connective tissue. Group III comprised two cases. The immune dysfunction of the NHML was responsible for a Guillain-Barré syndrome in one, and for a chronic inflammatory demyelinating polyneuropathy in the other. Group IV included two patients in whom the mechanism of the peripheral neuropathy, although almost certainly directly related to the NHML, could not be determined beyond doubt. The peripheral neuropathy might have been a result of a paraneoplasic process or, possibly, an undetected lymphomatous invasion of nervous tissue. All these cases of clinically diverse peripheral neuropathy, which either occurred before the discovery of the haemopathy or arose as complications of it, are discussed along with similar observations reported in the literature. Immunolabelling of lymphomatous proliferations and nerves is now of considerable value for classifying and indicating the exact aetiology of the peripheral neuropathy. It can also detect pathogenic consequences of any associated monoclonal dysglobulinemia. In any event, a direct link between the peripheral neuropathy and NHML represents an indication for intensification of specific chemotherapy, which in some of our patients led to significant regression of the peripheral neuropathy. Nonetheless, in some cases, the link between peripheral neuropathy and NHML could not be established with certainty. Long-term follow-up is essential in such cases. The present results show the importance of a case by case study of patients with NHML and peripheral neuropathy.
  Brain 11/1995; 118 ( Pt 5):1233-45. · 9.46 Impact Factor