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102. G.P.71

Author

Allenbach, Y., primary, Leroux, G., additional, Rigolet, A., additional, Hervier, B., additional, Maisonobe, T., additional, Authier, F.J., additional, Aouizerate, J., additional, Limal, N., additional, Meyer, A., additional, Hufnagl, P., additional, Zerbe, N., additional, Preusse, C., additional, Mariampillai, K., additional, Herson, S., additional, Benveniste, O., additional, and Stenzel, W., additional

Published
2014
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103. T.P.32

Author

Souvannanorath, S., primary, Maisonobe, T., additional, Valayannopoulos, V., additional, Nadjar, Y., additional, Mochel, F., additional, Boutron-Corriat, A., additional, Brivet, M., additional, and Laforêt, P., additional

Published
2014
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105. [Chronic inflammatory demyelinating polyneuropathy (CIDP) revealing an associated disease diagnostic and therapeutic pitfalls]

Author

Maisonobe, T., Jaccard, Arnaud, Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), and Carrion, Claire

Subjects
Male, [SDV.IMM] Life Sciences [q-bio]/Immunology, MESH: Anti-Infective Agents, Hypertrichosis, Neural Conduction, MESH: POEMS Syndrome, Anti-Infective Agents, MESH: Skin, MESH: Neural Conduction, MESH: Median Nerve, Humans, Osteitis, Skin, Motor Neurons, MESH: Humans, MESH: Hypertrichosis, MESH: Middle Aged, Electrodiagnosis, MESH: Electrodiagnosis, Middle Aged, MESH: Male, Median Nerve, MESH: Polyradiculoneuropathy, Chronic Inflammatory Demyelinating, Radiography, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating, POEMS Syndrome, MESH: Osteitis, Prednisone, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Prednisone, MESH: Motor Neurons
Abstract

International audience; The objective of this case report is to illustrate the problem's diagnosis of a CIDP revealing a associated disease. The patient had initially a sensory CIDP wich respond to prednisone. After 2 years, he worsened with motor deficit, pain and atypical skin's lesions. The diagnosis of POEMS syndrome was made only in the fourth research of monoclonal gammopathy. A specific treatment was realised but too late and a important motor deficit with axonal loss unfortunately persisted.

Published
2007

107. Phenotypic spectrum of Charcot−Marie−Tooth disease due to LITAF/ SIMPLE mutations: a study of 18 patients.

Author

Guimarães ‐ Costa, R., Iancu Ferfoglia, R., Leonard ‐ Louis, S., Ziegler, F., Magy, L., Fournier, E., Dubourg, O., Bouche, P., Maisonobe, T., Lacour, A., Moerman, A., Latour, P., and Stojkovic, T.

Subjects
GENETIC mutation, GENES, CHARCOT-Marie-Tooth disease, NEUROPATHY, NERVOUS system abnormalities
Abstract

Background and purpose Charcot−Marie−Tooth ( CMT) 1C due to mutations in LITAF/ SIMPLE is a rare subtype amongst the autosomal dominant demyelinating forms of CMT. Our objective was to report the clinical and electrophysiological characteristics of 18 CMT1C patients and compare them to 20 patients with PMP22 mutations: 10 CMT1A patients and 10 patients with hereditary neuropathy with liability to pressure palsies ( HNPP). Methods Charcot−Marie−Tooth 1C patients were followed-up in referral centres for neuromuscular diseases or were identified by familial survey. All CMT1A and HNPP patients were recruited at the referral centre for neuromuscular diseases of Pitié-Salpêtrière Hospital. Results Two phenotypes were identified amongst 18 CMT1C patients: the classical CMT form (' CMT-like', 11 cases) and a predominantly sensory form ('sensory form', seven cases). The mean CMT neuropathy score was 4.45 in CMT1C patients. Motor nerve conduction velocities in the upper limbs were significantly more reduced in CMT1A than in CMT1C patients. On the other hand, the motor nerve conduction velocity of the median nerve was significantly lower in CMT1C compared to the HNPP group. Distal motor latency was significantly more prolonged in CMT1A patients compared to the CMT1C and HNPP groups, the latter two groups having similar distal motor latency values. Molecular analysis revealed five new LITAF/ SIMPLE mutations (Ala111Thr, Gly112Ala, Trp116Arg, Pro135Leu, Arg160Cys). Conclusions Our study delineates CMT1C as mostly a mild form of neuropathy, and gives clinical and electrophysiological clues differentiating CMT1C from CMT1A and HNPP. Delineating phenotypes in CMT subtypes is important to orient molecular diagnosis and to help to interpret complex molecular findings. [ABSTRACT FROM AUTHOR]

Published
2017
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108. The pleiotropic movement disorders phenotype of adult ataxia-telangiectasia

Author

Meneret, A., primary, Ahmar-Beaugendre, Y., additional, Rieunier, G., additional, Mahlaoui, N., additional, Gaymard, B., additional, Apartis, E., additional, Tranchant, C., additional, Rivaud-Pechoux, S., additional, Degos, B., additional, Benyahia, B., additional, Suarez, F., additional, Maisonobe, T., additional, Koenig, M., additional, Durr, A., additional, Stern, M.-H., additional, Dubois d'Enghien, C., additional, Fischer, A., additional, Vidailhet, M., additional, Stoppa-Lyonnet, D., additional, Grabli, D., additional, and Anheim, M., additional

Published
2014
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119. P.14.11 Auto-immune necrotizing myopathies with anti-HMGCR antibodies are related to statin-exposure only for a minority of cases

Author

Allenbach, Y., primary, Rigolet, A., additional, Drouot, L., additional, Charuel, J.L., additional, Jouen, F., additional, Maisonobe, T., additional, Dubourg, O., additional, Behin, A., additional, Eymard, B., additional, Laforet, P., additional, Stojkovic, T., additional, Konepaut, I., additional, Cacoub, P., additional, Kieffer, P., additional, Fain, O., additional, Cosserat, J., additional, Morati, L., additional, Salort, E., additional, Menard, D., additional, Antoine, J.C., additional, Tournadre, A., additional, Menier, V. Bader, additional, Ferrer, X., additional, Laroche, C., additional, Musset, L., additional, Herson, S., additional, Boyer, O., additional, and Benveniste, O., additional

Published
2013
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120. [Neurological manifestations in cryoglobulinemia]

Author

Maisonobe T, Jm, Léger, Musset L, and Patrice Cacoub

Subjects
Cryoglobulinemia, Central Nervous System Diseases, Humans, Peripheral Nervous System Diseases, Nervous System Diseases, Hepatitis C, Cryoglobulins
Abstract

Cryoglobulins are immunoglobulins that persist in the serum, precipitate at cold temperature and resolubilize when rewarmed. Type I is often associated with hematological disorders. Type II and III are mixed cryoglobulins, composed of different immunoglobulins with a monoclonal component in type II and only polyclonal immunoglobulins in type III. Mixed cryoglobulins are associated with connective tissues or infectious diseases. Hepatitis C virus is involved in most of previously called "essential" mixed cryoglobulinemia. Dermatological, rhumatological, and nephrological manifestations are the most frequent, and neurological complications are found in 20 percent of cases. However, in mixed cryoglobulinemia with low cryoglobulins level, neurological signs may reveal the disease. Ischemic central nervous system complications are rare, but sensory, axonal, peripheral neuropathies or sensory and motor multiple mononeuropathies are more frequent. Prognostic and treatment depend on association with hepatitis C, and presence of vasculitis lesions in the nerve biopsy.

Published
2002

121. Systemic vasculitis in patients with hepatitis C

Author

Patrice Cacoub, Maisonobe T, Thibault V, Gatel A, Servan J, Musset L, and Jc, Piette

Subjects
Adult, Male, Plasma Exchange, Angiography, Interferon-alpha, Peroneal Nerve, Hepacivirus, Hepatitis C, Chronic, Middle Aged, Kidney, Polyarteritis Nodosa, Electrophysiology, Cryoglobulinemia, Humans, Prednisone, Female, Mesentery, Muscle, Skeletal, Peroneal Neuropathies, Cryoglobulins, Aged, Retrospective Studies
Abstract

To analyze the main characteristics of patients infected with hepatitis C virus (HCV) presenting with different types of vasculitis syndrome.We retrospectively compared 2 groups of patients with HCV presenting with systemic vasculitis: 10 with biopsy proven polyarteritis nodosa-type systemic vasculitis (PAN, Group 1) and 7 with mixed cryoglobulinemia syndrome (MC, Group 2).Patients of Group 1 presented with different features than Group 2: life threatening systemic vasculitis (10 vs 0; p0.01), severe multifocal sensorimotor mononeuropathies versus distal moderate sensory polyneuropathies, malignant hypertension (5 vs 0; p = 0.04), cerebral angiitis (2 vs 0), ischemic abdominal pain (2 vs 0), kidney and liver microaneurisms (2 vs 0), increased erythrocyte sedimentation rate and C-reactive protein (7 vs 0; p0.01), renal insufficiency (5 vs 0; p = 0.04), HCV genotype 1b (3 vs 6; p = 0.06), and lower activity of chronic hepatitis (p = 0.02). Neuromuscular biopsies showed lesions of vasculitis in all patients, but the type of vasculitis was different in Group 1 compared to Group 2: medium size artery involvement (7 vs 0; p0.01), necrotizing vasculitis (10 vs 0; p0.01), and mononuclear cell infiltrate in perivascular areas (0 vs 7; p0.01). Using prednisone, plasma exchanges, and interferon-alpha, complete recovery was obtained in all PAN-type patients except one. In Group 2 patients, interferon-alpha did not have any effect on the peripheral neuropathy.HCV infection may be associated with different types of systemic vasculitis, i.e., polyarteritis nodosa or mixed cryoglobulinemia. Because of differences in clinical and pathological features and therapeutic strategy, PAN-type vasculitis should be distinguished from MC-type vasculitis in HCV patients.

Published
2001

122. [What's new in primary lateral sclerosis?]

Author

Le Forestier N, Maisonobe T, Spelle L, Lesort A, Salachas F, Chassande B, Bouche P, yves samson, and Meininger V

Subjects
Adult, Diagnosis, Differential, Male, Electromyography, Biopsy, Amyotrophic Lateral Sclerosis, Bulbar Palsy, Progressive, Humans, Female, Peripheral Nerves, Middle Aged, Muscle, Skeletal
Abstract

Primary lateral sclerosis as a nosological entity distinct from amyotrophic lateral sclerosis has been the subject of controversy since it was first described in the nineteenth century. Primary lateral sclerosis has been defined as a rare, non-hereditary disease characterized by highly progressive spinobulbar spasticity, related to the exclusive loss of precentral pyramidal neurons, with secondary pyramidal tract degeneration and preservation of anterior horn motor neurons. We carried out a study in nine patients with a diagnosis of primary lateral sclerosis. Our clinical, electrophysiological and pathological investigations provide evidence that the disease has a heterogeneous clinical presentation and that degeneration is not restricted to the central motor system but also affects the lower motor neuron. In view of this similarity with amyotrophic lateral sclerosis, primary lateral sclerosis may represent a slowly progressive syndrome closely related to motor neuron disease and amyotrophic lateral sclerosis.

Published
2000

123. [Macrophagic myofasciitis. Study and Research Group on Acquired and Dysimmunity-related muscular diseases (GERMMAD)]

Author

Chérin P, Laforêt P, Rk, Ghérardi, Francois Jerome AUTHIER, Maisonobe T, Coquet M, Jm, Mussini, Jf, Pellissier, Eymard B, and Herson S

Subjects
Adult, Male, Muscle Weakness, Biopsy, Macrophages, Pain, Clinical Enzyme Tests, Middle Aged, Magnetic Resonance Imaging, Diagnosis, Differential, Muscular Diseases, Humans, Female, Fasciitis, Muscle, Skeletal, Creatine Kinase, Aged
Abstract

MACROPHAGIC MYOFASCIITIS: A most unusual inflammatory myopathy, first described by Germmad had been reported with increasing frequency since 1993 in the leading French myopathology centers. We present our experience with this new disease: macrophagic myofasciitis.By November 1999, 70 cases of macrophagic myofasciitis had been recorded since our first description. The first 22 patients (sex ratio M/F = 1:3) referred with the presumptive diagnosis of polymyositis (n = 11), polymyalgia rheumatica (n = 5), mitochondrial cytopathy (n = 4), and congenital myopathy or muscle dystrophy (n = 1 each). Symptoms included myalgia (91%), anthralgia (68%), marked asthenia (55%), muscle weakness (45%), and fever (32%).Abnormal laboratory findings included elevated CK levels (50%), markedly increased erythrocyte sedimentation rate (37%), and myopathic EMG (35%). Muscle biopsy showed a unique myopathological pattern characterized by: i) centripetal infiltration of epimysium, perimysium and perifascicular endomysium by sheets of large cells of the monocyte/macrophage lineage (CD68+, CD1a-, S100-, with a PAS-positive content; ii) absence of necrosis, of both epithelioid and giant cells, and of mitotic figures; iii) presence of occasional CD8+ T-cells; iv) inconspicuous muscle fiber damage. The picture was easily distinguishable from sarcoid myopathy and fasciitis-panniculitis syndromes. The infectious diseases know to be associated with reactive histiocytes, including Whippleís disease, Mycobacterium avium intracellulare infection and malakoplakia, could not be documented. Patients improved under corticosteroid therapy and/or immunomodulatory therapeuticA new inflammatory muscle disorder, characterized by a distinctive pathological pattern of macrophagic myofasciitis is emerging in France.

Published
2000

124. [Distal Miyoshi muscular dystrophy in a Moroccan patient]

Author

Mouton P, Maisonobe T, Behin A, Cohen L, and Pierrot-Deseilligny C

Subjects
Adult, Diagnosis, Differential, Male, Morocco, Humans, Muscular Dystrophies
Abstract

Muscular dystrophy usually involves a deficiency in the proximal muscles. We report a case of distal muscular dystrophy in a Moroccan patient.A 21-year-old Moroccan complained of progressive onset weakness of the lower limbs and frequent falls. The neurological examination demonstrated amyotrophy involving both legs and almost complete regression of the posterior muscle compartment. Clinical findings were confirmed by muscle scans. The electromyogram showed a progressive myogenic process. Creatine kinase was elevated. The severe dystrophic aspect was evidenced at muscle biopsy and led to the diagnosis of distal Miyoshi muscular dystrophy.Miyoshi muscular dystrophy, a distal myopathy transmitted by autosomal recessive inheritance, is usually observed in young adults who present characteristic amyotrophy of the posterior leg muscles. The proximal muscles of the lower and upper limbs may become involved during the disease course. Approximately one-third of the patients require wheel chair assistance after 10 years. Creatine kinase levels are constantly elevated. The differential diagnosis with other muscular dystrophies predominating in the distal muscles, particularly Steinert's myotonic dystrophy and inclusion body myositis, is discussed.

Published
1999

130. Première série française de myopathies nécrosantes auto-immunes associées à l’autoanticorps anti-HMGCoA réductase : la prise de statine n’est pas retrouvée pour la majorité des patients

Author

Allenbach, Y., primary, Rigolet, A., additional, Drouot, L., additional, Charuel, J.-L., additional, Jouen, F., additional, Maisonobe, T., additional, Stojkovic, T., additional, Cacoub, P., additional, Kieffer, P., additional, Herson, S., additional, Boyer, O., additional, and Benveniste, O., additional

Published
2012
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131. G.P.120 FHL1-related Reducing Body Myopathy and Emery–Dreifuss muscular dystrophy: A comparative histoenzymological, immunohistochemical and ultrastructural study

Author

Malfatti, E., primary, Olivé, M., additional, Taratuto, A.L., additional, Richard, P., additional, Bitoun, M., additional, Brochier, G., additional, Laforêt, P., additional, Stojkovic, T., additional, Alexianu, M., additional, Maisonobe, T., additional, Saccoliti, M., additional, Prudhon, B., additional, Lacène, E., additional, Eymard, B., additional, Fardeau, M., additional, Bonne, G., additional, and Romero, N.B., additional

Published
2012
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134. Sweet syndrome revealing microscopic polyangiitis

Author

Saussine, A., primary, Gueguen, A., additional, de Menthon, M., additional, Maisonobe, T., additional, Battistella, M., additional, Serrato, T., additional, Bagot, M., additional, Lebbe, C., additional, Mahr, A., additional, and Viguier, M., additional

Published
2012
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138. Eosinophilic fasciitis (Shulman disease): new insights into the therapeutic management from a series of 34 patients

Author

Lebeaux, D., primary, Frances, C., additional, Barete, S., additional, Wechsler, B., additional, Dubourg, O., additional, Renoux, J., additional, Maisonobe, T., additional, Benveniste, O., additional, Gatfosse, M., additional, Bourgeois, P., additional, Amoura, Z., additional, Cacoub, P., additional, Piette, J.-C., additional, and Sene, D., additional

Published
2011
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139. Long-term observational study of sporadic inclusion body myositis

Author

Benveniste, O., primary, Guiguet, M., additional, Freebody, J., additional, Dubourg, O., additional, Squier, W., additional, Maisonobe, T., additional, Stojkovic, T., additional, Leite, M. I., additional, Allenbach, Y., additional, Herson, S., additional, Brady, S., additional, Eymard, B., additional, and Hilton-Jones, D., additional

Published
2011
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141. Une myopathie lupique très atypique

Author

Rigolet, A., primary, Mangin, O., additional, Maisonobe, T., additional, Closs-Prophette, F., additional, Ankri, A., additional, Charuel, JL., additional, Benveniste, O., additional, and Herson, S., additional

Published
2011
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142. Myopathies associées au VIH

Author

Allenbach, Y., primary, Dubourg, O., additional, Maisonobe, T., additional, Herson, S., additional, Duyckaerts, C., additional, and Benveniste, O., additional

Published
2011
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147. P1.35 Amphiphysin 2 (BIN1) and triad defects in several forms of centronuclear myopathies

Author

Toussaint, A., primary, Maurer, M., additional, Cowling, B.S., additional, Hnia, K., additional, Mohr, M., additional, Oldfors, A., additional, Schwab, Y., additional, Yis, U., additional, Maisonobe, T., additional, Stojkovic, T., additional, Laugel, V., additional, Echaniz-Laguna, A., additional, Blot, S., additional, Mandel, J.L., additional, Tiret, L., additional, Nishino, I., additional, and Laporte, J., additional

Published
2010
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150. Rôle de l’interleukine-25 et de son récepteur au cours du syndrome de Churg-Strauss : un lien entre les éosinophiles et l’immunité adaptative

Author

Terrier, B., primary, Bieche, I., additional, Maisonobe, T., additional, Rosenzwajg, M., additional, Musset, L., additional, Amoura, Z., additional, Sene, D., additional, Costedoat-Chalumeau, N., additional, Le Thi-Huong, D., additional, Klatzmann, D., additional, Cacoub, P., additional, and Saadoun, D., additional

Published
2010
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