Publications (26)115.98 Total impact
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Article: Paraneoplastic disorders of the peripheral nervous system.
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ABSTRACT: Paraneoplastic neurological syndromes are rare but can affect any part of the peripheral nervous system (PNS) including motor neurons, sensory ganglia, nerve roots, plexuses, cranial and peripheral nerves, and neuromuscular junctions. The type of cancer, lymphoma or solid tumour, is a determinant factor of the underlying mechanism. With solid tumour, antibodies directed to intracellular (anti-Hu or anti-CV2/CRMP5 antibodies) or surface antigens (anti-VGCC,or LGI1 and Caspr2 antibodies) have been identified while with lymphoma, the neuropathy is usually linked to a monoclonal gammopathy. This review discusses the different etiologies and mechanisms of paraneoplastic disorders of the PNS in patients emphasising their evaluation, diagnosis and treatment.La Presse Médicale 04/2013; · 0.67 Impact Factor -
Article: Treatment Options in Paraneoplastic Disorders of the Peripheral Nervous System.
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ABSTRACT: OPINION STATEMENT: Paraneoplastic disorders of the peripheral nervous system (PNS) are the most frequent manifestation of paraneoplasia. As with the central nervous system, two categories of immune mechanisms are distinguished. On one side, antibodies toward intracellular antigens (HuD and CV2-CRMP5) occur with subacute sensory neuronopathy or sensorimotor neuropathy probably depending on a T cell mediated disorder (group 1). On the other side, the Lambert-Eaton myasthenic syndrome (LEMS) and peripheral nerve hyperexcitability (PNH) occur with antibodies to cell membrane antigens, respectively, the voltage gated calcium channel and CASPR2 proteins, which are responsible for the disease (group 2). Treatment recommendation mostly depends on class IV studies. Three lines of therapeutics can be proposed, namely tumor, immunomodulatory and symptomatic treatments. Cancer treatment is crucial since an early tumor cure is the best way to stabilize patients in group 1 and improve those in group 2. This implies the use of an efficient strategy for cancer diagnosis. With group 2 symptomatic treatment including 3,4 diaminopyridine for LEMS and carbamazepine for PNH may suffice to obtain good quality remission. Immunomodulatory treatments like IVIg and plasma exchange, which have a well-established efficacy in antibody dependent diseases, may be used as second line treatments. Rituximab, for which there is only little evidence in this context, may be kept in a third line for severe refractory patients. With group 1 patients, who frequently develop an evolving and disabling disorder, bolus of methylprednisolone and or IVIg may be recommended while searching for and treating the tumor. If the tumor is not found and the patient deteriorates, monthly pulses of cyclophosphamide may stabilize the patients. Antidepressants and antiepileptic drugs efficacious in the treatment of neuropathic pain are to be used as symptomatic treatment when necessary. The choice is then based on the cost effectiveness and tolerance of these drugs.Current Treatment Options in Neurology 01/2013; · 1.29 Impact Factor -
Article: Trismus as the first symptom of amyotrophic lateral sclerosis.
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ABSTRACT: We report the case of a 75-year-old female who had a trismus as the first, long-lasting and, isolated symptom of ALS. We discuss also therapeutic possibilities.Amyotrophic Lateral Sclerosis 06/2012; 13(5):475-6. · 3.40 Impact Factor -
Article: The collapsin response mediator protein 5 onconeural protein is expressed in Schwann cells under axonal signals and regulates axon-Schwann cell interactions.
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ABSTRACT: Collapsin response mediator protein 5 (CRMP5) is one of the rare peripheral nerve antigens that is a target of autoantibodies in a paraneoplastic peripheral neuropathy. The pattern of axonal and myelin alterations suggests that CRMP5 is involved in axon-Schwann cell interaction. We examined CRMP5 expression and function in primary cultures of Schwann cells and neurons and at various developmental and regenerating stages of rat sciatic nerve and in CRMP5-deficient mice in vivo. Collapsin response mediator protein 5 was strongly expressed during postnatal development and regeneration and decreased with myelination. It was mainly expressed by immature Schwann cells and persisted in Remak cells in the adult; however, a subpopulation of Schwann cells that were induced to myelinate also expressed CRMP5. We identified 2 axonal molecular cues regulating CRMP5 expression: human neuregulin type 1, which induces CRMP5 expression in immature and premyelinating Schwann cells, and cyclic adenosine monophosphate, which inhibits CRMP5 expression when Schwann cells begin myelination. Collapsin response mediator protein 5-deficient mice showed abnormal Schwann process extension resulting in abnormal cell-axon segregation, indicating that CRMP5 is involved in the morphologic adaptation of Schwann cells to surround axons. These results demonstrate the importance of CRMP5 in axon-Schwann cell cooperation during development and regeneration.Journal of Neuropathology and Experimental Neurology 04/2012; 71(4):298-311. · 4.26 Impact Factor -
Article: Differential effect of oxidative or excitotoxic stress on the transcriptional profile of amyotrophic lateral sclerosis-linked mutant SOD1 cultured neurons.
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ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a progressive, lethal, degenerative disorder of motor neurons. The causes of most cases of ALS are as yet undefined. In a previous study, it was shown that N-methyl-D-aspartate (NMDA) and H(2)O(2) stimuli reduce neuronal survival in cortical neurons in culture (Boutahar et al., 2008). To identify variations in gene expression in response to these neurotoxins in transgenic vs. control cortical neurons cultures, both microarray and RT-PCR analysis were performed. High-density oligonucleotide microarrays showed changes in the expression of about 600 genes involved in protein degradation, neurotrophic factors pathway, cell cycle, inflammation, cytoskeleton, cell adhesion, transcription, or signalling. The most up-regulated genes following H(2)O(2) treatment were involved in cytoskeletal organization and axonal transport, such as ARAP2, KIF17, and DKK2, or in trophic factors pathways, such as insulin-like growth factor-binding protein 4 (IGFBP4), FGF17, and serpin2. The most down-regulated genes were involved in ion transport, such as TRPV1. After NMDA treatment, the most up-regulated genes were involved in protein degradation, such as ubiquitin-conjugating enzyme E2I and cathepsin H, and the most down-regulated genes were involved in ion transport, such as SCN7A. We conclude that these neurotoxins act through different transcriptional inductions, and these changes may reflect an adaptative cellular response to the cellular stress induced by the neurotoxins involved in ALS in the presence of mutant human SOD1.Journal of Neuroscience Research 06/2011; 89(9):1439-50. · 2.74 Impact Factor -
Article: Chorea and related movement disorders of paraneoplastic origin: the PNS EuroNetwork experience.
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ABSTRACT: Chorea and other movement disorders are rarely described as paraneoplastic. The aim of this study was to describe 13 patients with paraneoplastic chorea and dystonia collected by the members of the paraneoplastic neurological syndrome (PNS) EuroNetwork and to review 29 cases from the literature. We analyzed neurological symptoms, severity of the neurological syndrome, delay in neurological diagnosis, associated cancer, oncological and neurological treatments received, and outcome. Eleven (1.2%) out of 913 patients with PNS were identified in the EuroNetwork register. Two more patients not included in the register were added. The overall population consisted of 13 patients with a median age of 75 years (range 49-82 years). In most patients, the movement disorder was classical choreoathetosis with symmetric involvement of the trunk, neck, and limbs. A minority of patients presented unilateral chorea, dystonia, and orobuccal dyskinesia. Associated symptoms, as polyneuropathy, encephalitis, psychiatric disturbances, or visual defects, were often present. The movement disorder usually had a subacute course. The most frequently associated cancer was small cell lung cancer (SCLC). Lymphoma, bowel, or kidney cancers were also reported. CV2/CRMP5 was the most frequently associated antibody, followed by Hu. Hyperintense lesions of the basal ganglia on T2-weighted images were seldom observed. Response to cancer therapy was observed in a minority of patients, but survival was short (17 months). As in other neurological diseases, movement disorders should also be suspected as paraneoplastic when they develop subacutely in older patients (usually over 50) and often in the presence of other ancillary neurological symptoms.Journal of Neurology 05/2011; 258(11):2058-68. · 3.47 Impact Factor -
Article: Sensory and motor neuronopathy in a patient with the A382P TDP-43 mutation.
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ABSTRACT: Patients with TARDBP mutations have so far been classified as ALS, sometimes with frontal lobe dysfunction. A 66-year-old patient progressively developed a severe sensory disorder, followed by a motor disorder, which evolved over nine years. Symptoms started in the left hand and slowly involved the four limbs. Investigations were consistent with a mixed sensory and motor neuronopathy. A heterozygous change from an alanine to a proline at amino acid 382 was identified in exon 6 of the TARDPB gene (p.A382P). This case expands the phenotypic spectrum associated with mutations in the TARDBP gene and shows that sensory neurons can be severely damaged early in the course of the disease, following a propagating process, with an orderly progression from a focal starting point. A combination of severe sensory and motor neuronopathy is rarely encountered in clinical practice. The possibility of an A382P TDP-43 mutation should be considered in patients with such an association.Orphanet Journal of Rare Diseases 01/2011; 6:4. · 5.83 Impact Factor -
Article: Acute hemorrhagic leukoencephalopathy associated with influenza A (H1N1) virus.
Journal of Neurology 10/2010; 258(3):513-4. · 3.47 Impact Factor -
Article: Delayed onset of a second paraneoplastic neurological syndrome in eight patients.
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ABSTRACT: The occurrence of a second delayed paraneoplastic neurological syndrome (PNS), different from the first, in the same patient, is not well known. However, recognition of this possibility is important in the management of the patient with PNS. To describe eight patients who presented with two different PNS with a time delay of months to years. Retrospective analysis of eight patients, included in the European PNS database, with two different PNS that occurred months to years apart. The median delay between the two different PNS was 15 months. The antibody repertoire did not change between the two episodes. Anti-Hu was detected in five patients, and anti-CV2 and anti-Ri in one each. One patient did not present onconeural antibodies. Lung cancer was diagnosed in six patients. In five patients, the second PNS revealed a cancer relapse (n=4) or a second cancer (n=1) and in three it occurred without evidence of tumour recurrence. In these three patients, all with anti-Hu antibodies, the second episode consisted of a lower motor neuron disease. Median survival was not reached after a median follow-up of 5 years. A second PNS can reveal a cancer relapse but can also arise in its absence. The long survival of patients with a second PNS suggests that the immune response might be more effective in controlling the cancer.Journal of neurology, neurosurgery, and psychiatry 08/2010; 81(8):937-9. · 4.87 Impact Factor -
Article: Musty odour, mental retardation, and spastic paraplegia revealing phenylketonuria in adulthood.
Journal of Neurology 10/2009; 257(2):302-4. · 3.47 Impact Factor -
Article: The pattern and diagnostic criteria of sensory neuronopathy: a case-control study.
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ABSTRACT: Acquired sensory neuronopathies encompass a group of paraneoplastic, dysimmune, toxic or idiopathic disorders characterized by degeneration of peripheral sensory neurons in dorsal root ganglia. As dorsal root ganglia cannot easily be explored, the clinical diagnosis of these disorders may be difficult. The question as to whether there exists a common clinical pattern of sensory neuronopathies, allowing the establishment of validated and easy-to-use diagnostic criteria, has not yet been addressed. In this study, logistic regression was used to construct diagnostic criteria on a retrospective study population of 78 patients with sensory neuronopathies and 56 with other sensory neuropathies. For this, sensory neuronopathy was provisionally considered as unambiguous in 44 patients with paraneoplastic disorder or cisplatin treatment and likely in 34 with a dysimmune or idiopathic setting who may theoretically have another form of neuropathy. To test the homogeneity of the sensory neuronopathy population, likely candidates were compared with unambiguous cases and then the whole population was compared with the other sensory neuropathies population. Criteria accuracy was checked on 37 prospective patients referred for diagnosis of sensory neuropathy. In the study population, sensory neuronopathy showed a common clinical and electrophysiological pattern that was independent of the underlying cause, including unusual forms with only patchy sensory loss, mild electrical motor nerve abnormalities and predominant small fibre or isolated lower limb involvement. Logistic regression allowed the construction of a set of criteria that gave fair results with the following combination: ataxia in the lower or upper limbs + asymmetrical distribution + sensory loss not restricted to the lower limbs + at least one sensory action potential absent or three sensory action potentials <30% of the lower limit of normal in the upper limbs + less than two nerves with abnormal motor nerve conduction study in the lower limbs.Brain 07/2009; 132(Pt 7):1723-33. · 9.46 Impact Factor -
Article: In situ evidence of involvement of Schwann cells in ulcerative colitis: autocrine and paracrine signaling by A disintegrin and metalloprotease-17-mediated tumor necrosis factor alpha production.
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ABSTRACT: An increase in S100 protein-positive cells has been reported in inflammatory bowel diseases, mainly Crohn disease. These cells were interpreted as myeloid-derived dendritic cells, chiefly in follicular areas. We were prompted to assess the nature of these cells in interfollicular areas of inflamed colonic mucosa in ulcerative colitis and study their involvement in tumor necrosis factor alpha production, the main inflammatory cytokine in ulcerative colitis. The number and distribution of cells expressing S100 protein, nerve growth factor receptor, CD68, CD1a, CD83, and calretinin were studied in samples from 16 patients with active ulcerative colitis using simple and double immunohistochemistry. Then, the localization in S100 protein-positive cells of (1) tumor necrosis factor alpha, (2) its sheddase A disintegrin and metalloprotease-17, and (3) the receptors TNFR1 was assessed using double immunofluorescence followed by confocal microscopy. In active ulcerative colitis, there was an increased number in S100 protein-positive cells in interfollicular areas of colonic mucosa compared with quiescent ulcerative colitis, nonulcerative colitis, or normal mucosa. All S100 protein-positive cells ensheathed calretinin-positive axons, indicating their Schwann cell origin. No CD1a- or CD83-positive dendritic cells were detected. Double immunofluorescence studies showed that in normal colon, Schwann cells of the mucosa and submucosal plexuses weakly expressed A disintegrin and metalloprotease-17 but did not express tumor necrosis factor alpha. By contrast, in active ulcerative colitis, they expressed both A disintegrin and metalloprotease-17 and tumor necrosis factor alpha. Schwann cells as well as calretinin-positive axons strongly expressed TNFR1. This study shows (1) a Schwann cell proliferation in the inflamed colonic mucosa during active ulcerative colitis and (2) that Schwann cells produce tumor necrosis factor alpha. Tumor necrosis factor alpha is thus likely to stimulate Schwann cell proliferation through an autocrine/paracrine mechanism.Human pathology 05/2009; 40(8):1159-67. · 3.03 Impact Factor -
Article: [Paraneoplastic peripheral neuropathy due to solid cancers].
La Revue du praticien 12/2008; 58(17):1890-1. -
Article: Onco-neural antibodies and tumour type determine survival and neurological symptoms in paraneoplastic neurological syndromes with Hu or CV2/CRMP5 antibodies.
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ABSTRACT: Anti-Hu antibodies (Hu-Ab) and anti-CV2/CRMP5 antibodies (CV2/CRMP5-Ab) have been identified in association with paraneoplastic neurological disorders. However, it is not clear whether these antibodies are associated with specific neurological symptoms or are only markers of anti-cancer immune reaction. To address this question, 37 patients with CV2/CRMP5-Ab and 324 patients with Hu-Ab were compared. Whereas the age and sex ratio were the same between the two groups, the distribution of neurological symptoms was not. Patients with CV2/CRMP5-Ab presented more frequently cerebellar ataxia, chorea, uveo/retinal symptoms and myasthenic syndrome (Lambert-Eaton myasthenic syndrome LEMS or myasthenia gravis). They also had a better Rankin score. In contrast, dysautonomia, brainstem encephalitis and peripheral neuropathy were more frequent in patients with Hu-Ab. Limbic encephalitis occurred similarly in both groups. Small-cell lung cancer was the most frequently associated tumour in both groups of patients, while malignant thymoma was observed only in patients with CV2/CRMP5-Ab. In particular, patients with CV2/CRMP5-Ab and thymoma developed myasthenic syndrome more frequently, while patients with SCLC developed neuropathies more frequently. Chorea and myasthenic syndrome were only seen in patients with CV2/CRMP5-Ab. The median survival time was significantly longer in patients with CV2/CRMP5-Ab, and this effect was not dependent on the type of tumour. Interpretation: The data demonstrate that in patients with paraneoplastic neurological syndromes, the neurological symptoms and survival vary with both the type of associated onco-neural antibody and the type of tumour.Journal of neurology, neurosurgery, and psychiatry 11/2008; 80(4):412-6. · 4.87 Impact Factor -
Article: [Paraneoplastic neurological syndromes].
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ABSTRACT: The classic paraneoplastic neurological syndromes include Lambert-Eaton myasthenic syndrome, limbic encephalitis, sensory neuronopathy, intestinal pseudo-obstruction, subacute cerebellar degeneration, encephalomyelitis, and dermatomyositis. Approximately ten onconeural antibodies that recognize cancer and the nervous system have been described in paraneoplastic neurological syndromes. These antibodies appear to be important diagnostic tools, even though they may not always be present. Deciding whether a given neurological picture is definitely or possibly paraneoplastic depends on the clinical syndrome, any association with onconeural antibodies, and the time elapsed between onset of neurological symptoms and the discovery of the cancer. Diagnosis of a classic paraneoplastic neurological syndrome or the discovery of onconeural antibodies mandates an active and persistent search for cancer, using new techniques such as fluorodeoxyglucose positron emission tomography. In patients with one of these syndromes, the best treatment of the neurological disease is often the diagnosis and early treatment of the cancer.La Presse Médicale 10/2007; 36(10 Pt 2):1418-26. · 0.67 Impact Factor -
Article: Paraneoplastic neurological syndromes.
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ABSTRACT: Paraneoplastic neurological syndromes (PNS) can be defined as remote effects of cancer that are not caused by the tumor and its metastasis, or by infection, ischemia or metabolic disruptions. PNS are rare, affecting less than 1/10,000 patients with cancer. Only the Lambert-Eaton myasthenic syndrome is relatively frequent, occurring in about 1% of patients with small cell lung cancer. PNS can affect any part of the central and peripheral nervous system, the neuromuscular junction, and muscle. They can be isolated or occur in association. In most patients, the neurological disorder develops before the cancer becomes clinically overt and the patient is referred to the neurologist who has the charge of identifying a neurological disorder as paraneoplastic. PNS are usually severely disabling. The most common PNS are Lambert-Eaton myasthenic syndrome (LEMS), subacute cerebellar ataxia, limbic encephalitis (LE), opsoclonus-myoclonus (OM), retinopathies (cancer-associated retinopathy (CAR) and melanoma-associated retinopathy (MAR), Stiff-Person syndrome (SPS), chronic gastrointestinal pseudoobstruction (CGP), sensory neuronopathy (SSN), encephalomyelitis (EM) and dermatomyositis. PNS are caused by autoimmune processes triggered by the cancer and directed against antigens common to both the cancer and the nervous system, designated as onconeural antigens. Due to their high specificity (> 90%), the best way to diagnose a neurological disorder as paraneoplastic is to identify one of the well-characterized anti-onconeural protein antibodies in the patient's serum. In addition, as these antibodies are associated with a restricted range of cancers, they can guide the search for the underlying tumor at a stage when it is frequently not clinically overt. This is a critical point as, to date, the best way to stabilize PNS is to treat the cancer as soon as possible. Unfortunately, about one-third of patients do not have detectable antibodies and 5% to 10% have an atypical antibody that is not well-characterized. As PNS are believed to be immune-mediated, suppression of the immune response represents another treatment approach.Orphanet Journal of Rare Diseases 02/2007; 2:22. · 5.83 Impact Factor -
Article: Peripheral nervous system involvement in patients with cancer.
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ABSTRACT: Involvement of the peripheral nervous system (PNS) is common in patients with cancer and any part, including motor neurons, sensory ganglia, nerve roots, plexuses, cranial and peripheral nerves, and neuromuscular junctions, can be affected. Different mechanisms can initiate damage associated with cancer-related PNS disorders. These include tumour infiltration, toxicity of treatments, metabolic and nutritional perturbations, cachexia, virus infections, and paraneoplastic neurological syndromes. The type of cancer, lymphoma, or solid tumour is a further determinant of a PNS disorder. In this Review we discuss the different causes and mechanisms of disorders of the PNS in patients with cancer and we will focus on their assessment and diagnosis.The Lancet Neurology 02/2007; 6(1):75-86. · 23.46 Impact Factor -
Article: Prospective study of positional nystagmus in 100 consecutive patients.
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ABSTRACT: The purpose of this study was to investigate the various diagnoses of patients who present with positional nystagmus. Positional maneuvers were systematically performed in the plane of the posterior canal (PC; Dix-Hallpike maneuver) and the horizontal canal (HC; patients were rolled to either side in a supine position) on 490 consecutive patients essentially referred for vertigo and/or gait unsteadiness. One hundred patients (20%) presented positional nystagmus. This nystagmus had a peripheral origin in 83 patients, including 80 patients with benign paroxysmal positional vertigo (BPPV). In BPPV, the PC was involved in 61 patients, the HC in 18 patients (geotropic horizontal nystagmus in 11 and ageotropic in 7; changing from geotropic to ageotropic or the reverse in 4 patients), and both the PC and HC in 1 patient. There was evidence of central positional nystagmus in 12 patients, including positional downbeat nystagmus during the Dix-Hallpike maneuver in 7 patients with various neurologic disorders, and ageotropic horizontal nystagmus during the HC maneuver in 2 patients with, respectively, cerebellar ischemia and definite migrainous vertigo. The peripheral or central origin of the positional nystagmus could not be ascertained in 5 patients, including 1 patient with probable migrainous vertigo and another with possible anterior canal BPPV. A rotatory-upbeat nystagmus in the context of PC BPPV, a horizontal nystagmus, whether geotropic or ageotropic, due to HC BPPV, and a positional downbeat nystagmus related to various central disorders are the 3 most common types of positional nystagmus. Geotropic horizontal positional nystagmus and, most certainly, horizontal positional nystagmus changing from geotropic to ageotropic or the reverse point to HC BPPV. In contrast, an ageotropic horizontal positional nystagmus that is not changing (from ageotropic to geotropic) may indicate a central lesion.The Annals of otology, rhinology, and laryngology 09/2006; 115(8):587-94. · 1.05 Impact Factor -
Article: Expression of the onconeural CV2/CRMP5 antigen in thymus and thymoma.
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ABSTRACT: Anti-CV2 antibodies (AB) react with the developmentally regulated neural proteins CRMPs and particularly with CRMP5. They occur with small cell lung cancer (SCLC) and thymoma. SCLCs universally express CRMP5. We investigated the expression of CRMPs in thymoma and thymus. In thymoma, none of the CRMPs were detected by immunohistochemistry in tumorous epithelial cells with specific antibodies including CRMP5 but an antibody reacting with a peptide common to the CRMPs labeled a 66-kDa protein in Western blot of rat brain, thymus, and thymoma extracts. Thus, the normal CRMP5 is probably not expressed by tumorous epithelial cells. These results indicate that the mechanisms leading to CRMP5 autoimmunization are different in SCLC and thymoma.Journal of Neuroimmunology 06/2006; 174(1-2):168-73. · 2.96 Impact Factor -
Article: [Advantages and limitations of electroneuromyography for analysis of upper limb pain].
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ABSTRACT: To study the utility of electroneuromyography in analysis of upper limb pain as a function of the existence of a diagnostic hypothesis. We retrospectively compared the consecutive electroneuromyographic examinations performed between 1 January and 30 September 2004. All recordings were performed by the same examiner in the neurophysiology clinic in the department of neurology of Saint-Etienne university hospital UHC at the request of hospital specialists or surgeon and private general practitioners. In each examination, at a minimum and regardless of the specific situation, motor conduction speed, F waves, and sensory conduction speed were recorded for the median nerve and the ulnar nerve on the right and left. For the arm in question, needle electromyography explored the muscles depending on the C5-T1 roots. In all, 76 patients had ENMG examinations, 38 for whom the physician had a diagnostic hypothesis and 38 patients without. In the case of a diagnosis based on clinical suspicions, examination was normal in 73.7% of cases compared with 23.7% when there was a clinically based hypothesis (p<0.01). These findings did not vary significantly according to the specialization of the referring physician. Electromyography and nerve conduction studies are useful to confirm a diagnosis based on patient reports and clinical data, it is not useful when no diagnosis has been suggested.La Presse Médicale 05/2006; 35(4 Pt 1):584-6. · 0.67 Impact Factor
Top co-authors
Top Journals
Institutions
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2006–2013
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Centre Hospitalier Universitaire de Saint-Étienne
- Department of Neurology
Saint-Étienne, Rhone-Alpes, France
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2008
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CHU de Lyon - Institut d'hématologie et d'oncologie pédiatrique
Lyon, Rhone-Alpes, France
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2007
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Université Claude Bernard Lyon 1
Villeurbanne, Rhone-Alpes, France
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2002–2006
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Université Jean Monnet
Saint-Étienne, Rhone-Alpes, France
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