66 results on '"R. A. C. Hughes"'
Search Results
2. Vigorimeter grip strength in CIDP: a responsive tool that rapidly measures the effect of IVIG the ICE study
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R. A. C. Hughes, Chunqin Deng, Kim Hanna, Norman Latov, Marinos C. Dalakas, P.A. van Doorn, Ingemar S. J. Merkies, Peter D. Donofrio, Els K. Vanhoutte, Vera Bril, H.-P. Hartung, MUMC+: DA KG Polikliniek (9), Klinische Neurowetenschappen, RS: MHeNs School for Mental Health and Neuroscience, and Neurology
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medicine.medical_specialty ,Placebo ,Placebo group ,inflammatory neuropathy ,Disability Evaluation ,Grip strength ,Double-Blind Method ,Daily practice ,Humans ,Immunologic Factors ,Medicine ,In patient ,chronic inflammatory demyelinating polyradiculoneuropathy ,Hand Strength ,business.industry ,Immunoglobulins, Intravenous ,Polyradiculoneuropathy ,medicine.disease ,immune globulin ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Neurology ,disability ,grip strength ,Physical therapy ,Neurology (clinical) ,business ,Inflammatory neuropathy - Abstract
Background and purpose In a recent trial in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), the ICE study, grip strength measurement captured significantly more improvement in patients receiving immune globulin (IGIV-C) intravenously than in those receiving placebo. Methods We conducted a systematic analysis to determine the sensitivity of grip strength as an indicator of meaningful clinical changes in CIDP. Results A randomized double-blind trial was undertaken in 117 CIDP patients who received IGIV-C or placebo every 3 weeks for up to 24 weeks. Grip strength and inflammatory neuropathy cause and treatment (INCAT) disability scores were assessed at each visit, and the responsiveness of each scale was compared. A minimum clinically important difference cut-off value for grip strength (>8 kPa) and INCAT score (>1 point) was applied to assess the proportion of responders to IGIV-C versus placebo. This analysis showed that grip strength demonstrated significant improvement earlier (as early as day 16) than the INCAT disability scale in patients receiving IGIV-C compared with placebo. A significantly higher proportion of improvers were seen in the IGIV-C group (37.5%–50.9%) than in the placebo group (21.1%–25.9%) for grip strength at day 16, week 3, week 6 and the end of the first period. Also, grip strength showed within the first 6 weeks in the placebo group significantly more patients with a clinically meaningful deterioration (>8 kPa), compared with the INCAT (>1-point deterioration) findings. Conclusions Grip strength can be considered a sensitive tool for assessing clinically relevant changes in patients with CIDP. Its use in daily practice is suggested.
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- 2013
3. Abstracts of the 2001 Meeting of the Peripheral Nerve Society
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Hugh J. Willison, Eduardo Nobile-Orazio, R. A. C. Hughes, S Bensa, Giacomo P. Comi, A. V. Swan, P. Van den Bergh, Isabel Illa, Martin Bojar, and P.A. van Doorn
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medicine.medical_specialty ,business.industry ,General Neuroscience ,Polyradiculoneuropathy ,medicine.disease ,Gastroenterology ,Oral prednisolone ,law.invention ,Randomized controlled trial ,law ,Internal medicine ,Medicine ,Neurology (clinical) ,business - Published
- 2001
4. Management of Chronic Peripheral Neuropathy
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R. A. C. Hughes
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General Medicine ,Education - Published
- 2000
5. Effect of a Matrix Metalloproteinase Inhibitor (BB-1101) on Nerve Regeneration
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K.M. Miller, Kenneth Smith, Andrew J. H. Gearing, Maria Demestre, N A Gregson, and R. A. C. Hughes
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Male ,Time Factors ,Nerve Crush ,Matrix metalloproteinase inhibitor ,Pharmacology ,Dexamethasone ,General Biochemistry, Genetics and Molecular Biology ,History and Philosophy of Science ,Benzyl Compounds ,Reflex ,Succinates ,Animals ,Medicine ,Protease Inhibitors ,Pentoxifylline ,Electromyography ,business.industry ,General Neuroscience ,Regeneration (biology) ,Metalloendopeptidases ,Sciatic Nerve ,Nerve Regeneration ,Rats ,Drug Combinations ,Rats, Inbred Lew ,Nerve crush ,Immunology ,business - Published
- 1999
6. Matrix metalloproteinase expression during experimental autoimmune neuritis
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John M. Clements, Graham M. A. Wells, M. C. Brown, Meirion Davies, P Hughes, K.M. Miller, E. J. Redford, Kenneth Smith, Andrew J. H. Gearing, and R. A. C. Hughes
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Pathology ,medicine.medical_specialty ,Transcription, Genetic ,medicine.medical_treatment ,Inflammation ,Matrix metalloproteinase ,Polymerase Chain Reaction ,Autoimmune Diseases ,Schwann cell proliferation ,Neuritis ,Reference Values ,medicine ,Animals ,Tissue Distribution ,Matrilysin ,Cellular localization ,biology ,Tumor Necrosis Factor-alpha ,business.industry ,Metalloendopeptidases ,Immunohistochemistry ,Sciatic Nerve ,Rats ,Myelin basic protein ,Cytokine ,Rats, Inbred Lew ,biology.protein ,Tumor necrosis factor alpha ,Neurology (clinical) ,medicine.symptom ,business - Abstract
Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barré syndrome. We have shown recently that BB-1101, a broad-spectrum matrix metalloproteinase (MMP) inhibitor, prevents development of EAN when given from the day of immunization and, more important clinically, reduces disease severity when given from symptom onset. This suggests the involvement of MMP activity in the pathogenesis of EAN. However, the exact function and expression patterns of MMPs in acute inflammation of the PNS have not been investigated. MMP-like enzymes are also involved in the processing of tumour necrosis factor-alpha (TNF-alpha), which has been implicated previously in the pathology associated with EAN. In the present study we investigated the profile of MMP and TNF-alpha expression and their localization in sciatic nerve tissue during EAN, using a semiquantitative competitive reverse transcriptase-coupled polymerase chain reaction and immunohistochemistry. In the normal rat PNS, four of the 10 MMPs studied were constitutively expressed and four MMPs were differentially regulated during EAN. Expression of TNF-alpha was elevated at peak disease severity and localized to Schwann cells, macrophages and endoneurial blood vessels. Expression levels of 92 kDa gelatinase and stromelysin-1 were significantly increased early in the development of EAN and continued to rise, peaking at day 15 coincident with maximum disease severity. Schwann cells and endothelial cells were the main cellular source of these enzymes. Prominent infiltration of inflammatory cells into the sciatic nerve was concordant with a significant increase in the expression levels of matrilysin and macrophage metalloelastase. Both matrilysin and macrophage metalloelastase were detected in invading macrophages, T lymphocytes and resident Schwann cells. The selective upregulation of specific MMPs during EAN and their varied cellular localization suggests that MMPs play a multifactorial role in the aetiology of EAN. Activity of MMPs could participate in the disruption of the blood-nerve barrier, breakdown of the myelin sheath, the release of TNF-alpha, and facilitate leukocyte invasion into the PNS. These observations highlight MMPs as potential targets for therapeutic intervention in acute peripheral neuropathies, such as Guillain-Barré syndrome.
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- 1998
7. A combined inhibitor of matrix metalloproteinase activity and tumour necrosis factor-alpha processing attenuates experimental autoimmune neuritis
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K. Miller, Andrew J. H. Gearing, P Hughes, Meirion Davies, Kenneth Smith, R. A. C. Hughes, N A Gregson, and E. J. Redford
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Male ,medicine.medical_treatment ,Neuritis ,Inflammation ,Matrix metalloproteinase ,Dexamethasone ,Pathogenesis ,Benzyl Compounds ,medicine ,Animals ,Protease Inhibitors ,Tissue Distribution ,Pentoxifylline ,Tumor Necrosis Factor-alpha ,business.industry ,Multiple sclerosis ,Metalloendopeptidases ,Succinates ,Polyradiculoneuropathy ,medicine.disease ,Immunohistochemistry ,Neuritis, Autoimmune, Experimental ,Sciatic Nerve ,Extracellular Matrix ,Rats ,Drug Combinations ,Cytokine ,Gelatinases ,Rats, Inbred Lew ,Immunology ,Female ,Tumor necrosis factor alpha ,Neurology (clinical) ,medicine.symptom ,business - Abstract
Matrix metalloproteinases (MMPs) and the cytokine tumour necrosis factor (TNF)-alpha are implicated in the pathology of inflammatory demyelinating diseases of the CNS, and may also be involved in peripheral demyelinating diseases such as acute inflammatory demyelinating polyradiculoneuropathy. We have tested an inhibitor of MMP activity and TNF-alpha processing, BB-1101, in experimental autoimmune neuritis (EAN), an animal model of Guillain-Barré syndrome. Treatment with BB-1101 from the time of immunization prevented the development of EAN, and when given from the onset of symptoms, it significantly reduced disease severity. These results indicate that MMPs and/or TNF-alpha are involved in the pathogenesis of EAN, and that drugs of this type may have potential as novel therapeutic agents in the therapy of peripheral nervous system demyelinating diseases.
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- 1997
8. Human immunoglobulin ameliorates rat experimental autoimmune neuritis
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E. J. Redford, R. A. C. Hughes, Kenneth Smith, N A Gregson, Meirion Davies, and C. M. Gabriel
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Male ,Cauda Equina ,Neuritis ,Immunoglobulin E ,Antibodies ,Myelin ,medicine ,Animals ,Humans ,Remyelination ,Myelin Sheath ,Autoimmune disease ,biology ,Guillain-Barre syndrome ,business.industry ,Immunization, Passive ,medicine.disease ,Neuritis, Autoimmune, Experimental ,Rats ,Microscopy, Electron ,medicine.anatomical_structure ,Mechanism of action ,Rats, Inbred Lew ,Antibody Formation ,Immunology ,biology.protein ,Cattle ,Neurology (clinical) ,medicine.symptom ,Antibody ,Spinal Nerve Roots ,business - Abstract
Human immunoglobulin is an effective treatment for Guillain-Barré syndrome, although the mechanism of action is not understood. We have investigated the effect of human immunoglobulin in an animal model of Guillain-Barré syndrome, namely experimental autoimmune neuritis (EAN), induced in Lewis rats by immunization with bovine spinal root myelin. Human immunoglobulin administered intraperitoneally at the time of onset of disease accelerated the rate of recovery from EAN. This improvement was associated with a reduction in the titre of anti-rat myelin antibodies and may be due to earlier remyelination of demyelinated nerve fibres. This model may facilitate further investigation of the mechanism of therapeutic action of immunoglobulin in inflammatory neuropathy.
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- 1997
9. Increased virulence of Cunninghamella bertholletiae in experimental pulmonary mucormycosis: Correlation with circulating molecular biomarkers, sporangiospore germination and hyphal metabolism
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Petraitis, V. Petraitiene, R. Antachopoulos, C. Hughes, J.E. Cotton, M.P. Kasai, M. Harrington, S. Gamaletsou, M.N. Bacher, J.D. Kontoyiannis, D.P. Roilides, E. Walsh, T.J.
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Members of the order Mucorales are emerging invasive molds that cause infections in immunocompromised patients. However, little is known about the relation between different species of Mucorales and their virulence in invasive pulmonary mucormycosis. Based upon our earlier epidemiological studies, we hypothesized that Cunninghamella bertholletiae would demonstrate increased virulence. Therefore, we studied the relative virulence of C. bertholletiae (CB), Rhizopus oryzae (RO), R. microsporus (RM), and Mucor circinelloides (MC) in experimental invasive pulmonary mucormycosis in persistently neutropenic rabbits in relation to the fungi in vitro sporangiospore germination rate and hyphal metabolic activity. Rabbits infected with CB demonstrated (1) higher lung weights in comparison to RM (P ≤ 0.05), RO and MC (P ≤ 0.001), (2) pulmonary infarcts in comparison to RO and MC (P ≤ 0.001), (3) tissue fungal burden (CFU/g) vs. MC (P ≤ 0.001), and (4) the lowest survival of 0% (0/18), in comparison to 16% (3/18, P ≤ 0.01) of RM, 81% (21/26) of RO, and 83% (15/18) of MC-infected rabbits (P ≤ 0.001). Serum PCR concentration-time- curve showed the greatest amplitude for CB. Virulence correlated directly with sporangiospore germination rate at 4 h among species, i.e., CB (67 - 85%) > RM (14 - 56%) > RO (4 - 30%) > MC (0%), and hyphal metabolic activity, i.e., CB (1.22 - 1.51) > MC (0.54 - 0.64) = RM (0.38 - 0.41) = RO (0.37 - 0.59). C. bertholletiae was significantly more virulent in experimental invasive pulmonary mucormycosis than R. microsporus, R. oryzae, and M. circinelloides. In vivo virulence correlated with species-dependent differences of in vitro germination rate and hyphal metabolic activity. © 2013 ISHAM.
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- 2013
10. Sensory neuropathy and anti-Hu antibodies in a patient with seminoma
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Norman A. Gregson, R. A. C. Hughes, and C. M. Gabriel
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medicine.medical_specialty ,biology ,business.industry ,medicine.medical_treatment ,Testicular Neoplasm ,Seminoma ,medicine.disease ,Gastroenterology ,Radiation therapy ,Titer ,Peripheral neuropathy ,Cerebrospinal fluid ,Neurology ,Internal medicine ,Immunology ,medicine ,biology.protein ,Prednisolone ,Neurology (clinical) ,Antibody ,business ,medicine.drug - Abstract
A man with subacute sensory ncuronopathy (SSN) had a stage 1 seminoma. His serum and cerebrospinal fluid (CSF) contained anti-Hu antibodies (type 1 anti-neuronal nuclear antibodies, ANNA-1). Following orchidectomy, radiotherapy, prednisolone, plasma exchange and intravenous immunoglobulin the antineuronal antibody titre fell and the neuropathy improved.
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- 1996
11. Letters to the editor
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A. Robert Spitzer, Shalom Stahl, David Yarnitsky, Ernest W. Johnson, John R. Wilson, R. A. C. Hughes, Stefania Morino, Giovanni Antonini, Kiyotoshi Kaneko, Yoji Ohnishi, Tetsushi Atsumi, Isao Hozumi, Tadashi Miyatake, Tetsuo Furukawa, James P. Knochel, Ikuo Mineo, Seiichiro Tarui, Francis O. Walker, Andrew J. Gitter, Walter C. Stolov, and Nicholas J. Capozzoli
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Cellular and Molecular Neuroscience ,medicine.medical_specialty ,Text mining ,Physiology ,business.industry ,Physiology (medical) ,General surgery ,medicine ,Neurology (clinical) ,business - Published
- 1996
12. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain
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H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. Navon, Giovanni Antonini, K. Al Moutaery, E. Chamas, R. Schönhuber, M. Giannini, B. Debilly, I. Labatut, H. Henon, J. A. Egido, M. Baudrimont, J. N. Lorenzo, J. E. C. Bromberg, R. Antonacci, J. J. Vilchez, T. Moulin, B. Rautenstrauss, Giovanni Meola, J. Noth, S Mammi, P. Laforet, F. Lopez, C. Gehring, S. Bort, G. Rancurel, D. Decamps, S. Kostadinova, Y. Shapira, B. Neundoerfer, D. Chavrot, M. Solimena, J. P. Salier, W. Deberdt, R. Hoff-Jörgensen, A. Messina, S. Meairs, G. Rosoklija, E. Nelis, I. Bertran, C. Ertekin, J. Lohmeyer, Mitermayer Galvao dos Reis, L. Calo, E. Maccagnano, A. P. Hays, J. Verlooy, M. G. Forno, T. Blanco, L. Bail, Gabriella Silvestri, J. Montero, F. Bertrand, R. T. Ghnassia, C. Besses, T. Sereghy, F. Shalit, G. Bogliun, S. Braghi, St. Baykouchev, C. Franke, A. Lasa, L. C. Archard, J. Kriebel, S. Shaunak, M. Nocito, Alexander Tsiskaridze, E. Manfredini, T. Seigal, David G. Gadian, M. Barlas, J. D. Degos, C. Seeber, J. Caemert, J. L. Mas, R. B. Pepinsky, M. G. D'Angelo, N. Baumann, S. Yorifuji, H. P. Endtz, M. A. Cassatella, R. A. C. Hughes, V. Golzi, A. Bittencourt, A. Ferreira, M. Sanson, C. Alper, M. Vermeulen, M. A. A. van Walderveen, E. Alexiou, C. H. Lucas, M. Fiorelli, Y. N. Debbink, R. Gil, S. Congia, T. Banerjee, J. M. Bouchard, A. N. Pinto, A. Ceballos-Baumann, G. Grollier, P. I. M. Schmitz, M. D. Catata, N. Lahat, N. S. Rao, P. Papathanasopoulos, J. Valls-Solé, D. Claus, G. Schroter, A. Castro, C. Videbaek, R. Martinez Dreke, A. D. Platts, M. Hermesl, A. C. PeÇanha-Martins, M. Cardoso Silva, P. Masnou, M. J. A. Tanner, Ch. Confavreux, B. Mishu, H. Rasmussen, L. Valenciano, Carlo Pozzilli, S. W. Li, V. Salzman, Y. Vashtang, Massimo Franceschi, M. Severo, G. Deuschl, S. Setien, G. Mariani, A. Protti, J. Castillo, M. J. B. Taphoorn, M. Frontali, I. Milonas, D. Decoq, J. A. Navarro, S. Castellvi-Pel, C. Ertikin, M. Urtasun, Y. Lajat, B. E. Kendall, E. Verdu, B. Gueguen, E. Boisen, R. Couderc, A Danek, JM Stevens, F. Nicoli, L. 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Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. Santoro, J. Roda, A. Bordoni, D. J. Taylor, S. Ertas, H. H. Emmen, J. Vichez, V. BesanÇon, R. E. Passingham, M. L. Malosio, A. Vérier, M. Bamberg, A. W. Hansen, E. Mostacero, G. Gaudriault, Marie Vidailhet, B. Birebent, K. Strijckmans, F. Giannini, T. Kammer, I. Araujo, J. Nowicki, E. Nikolov, A. Hutzelmann, R. Gherardi, J. Verroust, L. Austoni, A. Scheller, A. Vazquez, S. Matheron, H. Holthausen, J. M. Gerard, M. Bataillard, S. Dethy, V. H. Patterson, V. Ivanez, N. P. Hirsch, F. Ozer, M. Sutter, C. Jacomet, M. Mora, Bruno Colombo, A. Sarropoulos, T. H. Papapetropoulos, M. Schwarz, D. S. Dinner, N. Acarin, B. Iandolo, J. O. Riis, P. R. J. Barnes, F. Taroni, J. Kazenwadel, L. Torre, A. Lugaresi, I. L. Henriques, S. Pauli, S. Alfonso, Pedro Quesada, A. S. T. Planting, J. M. Castilla, Thomas Gasser, M. Van der Linden, A. Alfaro, E. Nobile-Orazio, G. Popova, W. Vaalburg, F. G. A. van der Mech, L. Williams, F. Medina, J. P. Vernant, J. Yaouanq, B. Storch-Hagenlocher, A. Potemkowski, R. Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. Bauermann, Nereo Bresolin, J. Vallée, B. C. Jacobs, A. Campos, Werner Poewe, J. A. Villanueva, A. W. Kornhuber, A. Malafosse, E. Diez-Tejedor, G. Jungreia, M. J. A. Puchner, A. Komiyama, O. Saribas, V. Volpini, L. Geremia, S. Bressi, A. Nibbio, Timothy E. Bates, T. z. Tzonev, E. Ideman, G. A. Damlacik, G. Martino, G. Crepaldi, T. Martino, Kjell Någren, E. Idiman, D. Samuel, J. M. Perez Trullen, Y. van der Graaf, J. O. Thorell, M. J. M. Dupuis, E. Sieber, R. D'Alessandro, C. Cazzaniga, J. Faiss, A. Tanguy, A. Schick, I. Hoksergen, A. Cardozo, R. Shakarishvili, G. K. Wennlng, J. L. Marti-Vilalta, J. Weissenbach, I. L. Simone, Amalia C. Bruni, Darius J. Adams, C. Weiller, A. Pietrangeli, F. Croria, C. Vigo-Pelfrey, Patricia Limousin, A. Ducros, G. Conti, O. Lindvall, E. Richter, M. Zuffi, A. Nappo, T. Riise, J. Wijdenes, M. J. Fernandez, J. Rosell, P. Vermersh, S. Servidei, M. S. C. Verdugo, F. Gouttiere, W. Solbach, M. Malbezin, I. S. Watanabe, A. Tumac, W. I. McDonald, D. A. Butterfield, P. P. Costa, F. deRino, F. Bamonti, J. M. Cesar, C. H. Lahoz, I. Mosely, M. Starck, M. H. Lemaitre, K. M. Stephan, S. Tex, R. Bokonjic, I. Mollee, L. Pastena, M. Gutierrez, F. Boiler, M. C. Martinez-Para, M. Velicogna, O. Obuz, A. Grinspan, M. Guarino, L. M. Cartier, E. Ruiz, D. Gambi, S. Messina, M. Villa, Michael G. Hanna, J. Valk, Leone Pascual, M. Clanet, Z. Argov, B. Ryniewicz, E. Magni, B. Berlanga, K. S. Wong, C. Gellera, C. Prevost, F. Gonzalez-Huix, R. Petraroli, J. E. G. Benedikz, I. Kojder, C. Bommelaer, L. Perusse, M. R. Bangioanni, Guy M. McKhann, A. Molina, C. Fresquet, E. Sindern, Florence Pasquier, M. J. Rosas, M. Altieri, O. Simoncini, M. Koutroumanidis, C. A. F. Tulleken, M. Dary-Auriol, S. Oueslati, H. Kruyer, I. Nishisho, C. R. Horning, A. Vital, G. V. Czettritz, J. Ph. Neau, B. Mihout, A. Ameri, M. Francis, S. Quasthoff, D. Taussig, S. Blunt, P. Valentin, C. Y. Gao, O. Heinzlef, H. d'Allens, C. Coudero, M. Erfas, G. Borghero, P. J. Modrego Pardo, M. C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg
- Subjects
Neurology ,business.industry ,Media studies ,Library science ,Medicine ,Neurology (clinical) ,business - Published
- 1994
13. Immunological Mechanisms of Demyelination
- Author
-
R A C Hughes
- Subjects
General Medicine - Published
- 1992
14. Chronic Inflammatory Demyelinating Polyradiculoneuropathy
- Author
-
R. A. C. Hughes, P. Bouche, D. R. Cornblath, E. Evers, R. D. M. Hadden, A. Hahn, I. Illa, C. L. Koski, J. M. Lger, E. Nobile-Orazio, J. Pollard, C. Sommer, P. Van den Bergh, P. A. van Doorn, and I. N. van Schaik
- Published
- 2008
15. Multifocal Motor Neuropathy
- Author
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I. N. van Schaik, P. Bouche, I. Illa, J. M. Lger, P. Van den Bergh, D. R. Cornblath, E. Evers, R. D. M. Hadden, R. A. C. Hughes, C. L. Koski, E. Nobile-Orazio, J. Pollard, C. Sommer, and P. A. van Doorn
- Published
- 2008
16. Corticosteroids for Guillain-Barré syndrome
- Author
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R A C, Hughes, A V, Swan, R, van Koningsveld, and P A, van Doorn
- Subjects
Adult ,Adrenocorticotropic Hormone ,Anti-Inflammatory Agents ,Humans ,Child ,Guillain-Barre Syndrome ,Glucocorticoids ,Randomized Controlled Trials as Topic - Abstract
The cause of Guillain-Barré syndrome is inflammation of the peripheral nerves, which corticosteroids would be expected to benefit.To examine the ability of corticosteroids to hasten recovery and reduce the long-term morbidity from Guillain-Barré syndrome.We searched the Cochrane Neuromuscular Disease Group Register (May 2005), MEDLINE (January 2000 to May 2005) and EMBASE (January 1980 to May 2005) and contacted trial authors and other experts.We included quasi-randomised or randomised controlled trials of people of all ages and all degrees of severity of Guillain-Barré syndrome who were treated with any form of corticosteroid or adrenocorticotrophic hormone. Our primary outcome measure was change in disability grade on a commonly used, validated seven-point scale at four weeks after randomisation. Secondary outcome measures were: time from randomisation until recovery of unaided walking, time from randomisation until discontinuation of ventilation (for those ventilated), mortality, proportion of participants dead or disabled (unable to walk without aid) after 12 months, improvement in disability grade after six and 12 months, relapse, and adverse events related to corticosteroid treatment.Two authors extracted the data.Six trials with 587 participants provided data for our primary outcome measure . The overall evidence showed no significant difference between the corticosteroid and non-corticosteroid treated patients in disability grade. In four trials of oral corticosteroids with 120 participants in total, there was significantly less improvement after four weeks with corticosteroids than without corticosteroids (weighted mean difference of 0.82 of a disability grade less improvement, 95% confidence intervals 0.17 to 1.47). In two trials with a combined total of 467 participants, there was a trend towards more benefit from intravenous corticosteroids which was not quite significant, weighted mean difference 0.17 (95% confidence intervals -0.06 to 0.39) of a disability grade more improvement after four weeks than with placebo. There were no important significant differences between the corticosteroid-treated participants and the control group in any of the secondary outcome measures. Diabetes was significantly more common and hypertension much less common in the corticosteroid-treated participants.Limited evidence shows that oral corticosteroids significantly slow recovery from Guillain-Barré syndrome. Substantial evidence shows that intravenous methylprednisolone alone does not produce significant benefit or harm. In combination with intravenous immunoglobulin, intravenous methylprednisolone may hasten recovery but does not significantly affect the long-term outcome. More research is needed and more effective treatments for Guillain-Barré syndrome should be sought.
- Published
- 2006
17. Treatment of chronic inflammatory demyelinating polyradiculoneuropathy with methotrexate
- Author
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R. A. C. Hughes, D. Fialho, Y C Chan, David Allen, and Mary M. Reilly
- Subjects
Adult ,Male ,medicine.medical_specialty ,Antimetabolites, Antineoplastic ,Neuromuscular disease ,Short Report ,Disability Evaluation ,Internal medicine ,medicine ,Humans ,Treatment resistant ,Aged ,Retrospective Studies ,business.industry ,Multiple sclerosis ,Retrospective cohort study ,Polyradiculoneuropathy ,Middle Aged ,medicine.disease ,Surgery ,Psychiatry and Mental health ,Peripheral neuropathy ,Methotrexate ,Treatment Outcome ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Female ,Neurology (clinical) ,business ,Polyneuropathy ,medicine.drug - Abstract
We discovered many reports of other immunosuppressive drugs being used in adults with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) but none of methotrexate. As weekly low dose oral methotrexate is safe, effective, and well tolerated in other diseases, we treated 10 patients with otherwise treatment resistant CIDP. Seven showed improvement in strength by at least two points on the MRC sum score and three worsened. Only two showed an improvement in disability and both were also receiving corticosteroids. We discuss the difficulty of detecting an improvement in treatment resistant CIDP and propose methotrexate as a suitable agent for testing in a randomised trial.
- Published
- 2006
18. More immunotherapy for multiple sclerosis
- Author
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R. A. C. Hughes and B. Sharrack
- Subjects
Oncology ,medicine.medical_specialty ,medicine.diagnostic_test ,Interferon beta ,business.industry ,medicine.medical_treatment ,Multiple sclerosis ,Disease progression ,MEDLINE ,Magnetic resonance imaging ,Immunotherapy ,medicine.disease ,Psychiatry and Mental health ,Text mining ,Internal medicine ,Immunology ,medicine ,Surgery ,Neurology (clinical) ,Glatiramer acetate ,business ,medicine.drug - Published
- 1996
19. Plasma exchange for chronic inflammatory demyelinating polyradiculoneuropathy
- Author
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M M, Mehndiratta, R A C, Hughes, and P, Agarwal
- Subjects
Plasma Exchange ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Humans ,Randomized Controlled Trials as Topic - Abstract
Chronic inflammatory demyelinating polyradiculoneuropathy is an uncommon progressive or relapsing paralysing disease caused by inflammation of the peripheral nerves. If the hypothesis that it is due to autoimmunity is correct, removal of autoantibodies in the blood by plasma exchange should be beneficial.To evaluate the efficacy of plasma exchange in chronic inflammatory demyelinating polyradiculoneuropathy.We searched the Neuromuscular Disease Group Register (December 2003), and MEDLINE (January 1966 to January 2003), EMBASE (January 1980 to January 2003), CINAHL (January 1982 to December 2002) and LILACS (January 1982 to January 2003). We also scrutinised the bibliographies of the trials, and contacted the trial authors and other disease experts.Randomised or quasi-randomised controlled trials in participants of any age comparing plasma exchange with sham treatment or no treatment. A trial showing no significant difference in the benefit from plasma exchange with intravenous immunoglobulin has been included in a separate Cochrane review.Two authors selected the trials, extracted the data and assessed methodological quality independently. Where possible data were combined according to the methods of the Cochrane Neuromuscular Disease Review Group.one crossover trial including 18 participants showed 2 (95% confidence interval (CI) 0.8 to 3.0) points more improvement after four weeks in an 11-point disability scale with plasma exchange (10 exchanges over four weeks) than with sham exchange. Rapid deterioration after plasma exchange occurred in eight of 12 who had improved.when the results of this trial and another with 29 participants treated in a parallel group design trial were combined, there were 31 points (95% CI 16 to 45) more improvement in an impairment scale after plasma exchange (six exchanges over three weeks) than after sham exchange. There were significant improvements in both trials in an electrophysiological measure, the proximally evoked compound muscle action potential, after three or four weeks. Non-randomised evidence indicates that plasma exchange induces adverse events in 3% to 17% of procedures. These are sometimes serious.Evidence from two small trials showed that plasma exchange provides significant short-term benefit in about two-thirds of patients with chronic inflammatory demyelinating polyradiculoneuropathy but rapid deterioration may occur afterwards. Adverse events related to difficulty with venous access, use of citrate and haemodynamic changes are not uncommon. More research is needed to identify agents which will prolong the beneficial action of plasma exchange.
- Published
- 2004
20. [Systematic reviews of treatment for chronic inflammatory demyelinating neuropathy]
- Author
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R A C, Hughes
- Subjects
Plasma Exchange ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Humans ,Immunoglobulins, Intravenous ,Immunosuppressive Agents - Abstract
Chronic inflammatory demyelinating polyradiculoneuropathies include chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy (MMN) and paraprotein-associated demyelinating neuropathy. This review summarises the evidence from randomised controlled trials (RCTs) for the treatment of these conditions. It leads to the conclusions that: 1) steroids are beneficial in CIDP but not MMN and their efficacy in paraproteinaemic demyelinating neuropathy (PDN) is uncertain; 2) intravenous immunoglobulin (IVIg) produces short-term benefit in CIDP, MMN and IgM PDN. Its effect in IgG or IgA PDN has not been tested in RCTs; 3) plasma exchange (PE) also produces short-term benefit in CIDP and IgG or IgA PDN but probably not in MMN; 4) there is almost no information from RCTs concerning the possible benefits of immunosuppressive agents; and 5) volunteers are needed to write Cochrane systematic reviews of IVIg for MMN and of interventions for PDN associated with IgG and IgA.
- Published
- 2003
21. Intravenous immunoglobulin in neurological disease: a specialist review
- Author
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C M, Wiles, P, Brown, H, Chapel, R, Guerrini, R A C, Hughes, T D, Martin, P, McCrone, J, Newsom-Davis, J, Palace, J H, Rees, M R, Rose, N, Scolding, and A D B, Webster
- Subjects
Vasculitis ,Evidence-Based Medicine ,Multiple Sclerosis ,Myositis ,Humans ,Immunoglobulins, Intravenous ,Peripheral Nervous System Diseases ,Health Care Costs ,Stiff-Person Syndrome ,Review ,Drug Costs ,Randomized Controlled Trials as Topic - Abstract
Treatment of neurological disorders with intravenous immunoglobulin (IVIg) is an increasing feature of our practice for an expanding range of indications. For some there is evidence of benefit from randomised controlled trials, whereas for others evidence is anecdotal. The relative rarity of some of the disorders means that good randomised control trials will be difficult to deliver. Meanwhile, the treatment is costly and pressure to "do something" in often distressing disorders considerable. This review follows a 1 day meeting of the authors in November 2000 and examines current evidence for the use of IVIg in neurological conditions and comments on mechanisms of action, delivery, safety and tolerability, and health economic issues. Evidence of efficacy has been classified into levels for healthcare interventions (tables 1 and 2).
- Published
- 2002
22. Induction of experimental autoimmune neuritis with peripheral myelin protein-22
- Author
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F. S. Walsh, C. M. Gabriel, R. A. C. Hughes, Kenneth Smith, and S. E. Moore
- Subjects
Male ,medicine.medical_specialty ,Nerve root ,Cauda Equina ,Neuritis ,Action Potentials ,Antigen-Antibody Reactions ,Myelin ,Internal medicine ,Peripheral myelin protein 22 ,medicine ,Animals ,Humans ,Tibial nerve ,Myelin Sheath ,business.industry ,medicine.disease ,Fusion protein ,Neuritis, Autoimmune, Experimental ,Sciatic Nerve ,Rats ,Endocrinology ,Peripheral neuropathy ,medicine.anatomical_structure ,Rats, Inbred Lew ,Immunology ,Neurology (clinical) ,Sciatic nerve ,business ,Myelin Proteins ,Demyelinating Diseases - Abstract
Two myelin proteins, P2 basic protein and P0 glycoprotein, can induce experimental autoimmune neuritis (EAN), a model of human inflammatory neuropathy. We investigated whether peripheral nerve myelin protein-22 (PMP22), the gene for which is duplicated in hereditary motor sensory neuropathy type la, can also induce EAN. PMP22 cDNA produced by the reverse transcriptase-polymerase chain reaction from rat sciatic nerve was expressed in Escherichia coli as a fusion protein with glutathione-S-transferase (GST). Ten Lewis rats were immunized with purified PMP22 fusion protein (50-100 microg) and eight controls with the same amount of GST. Two additional animals were immunized with each of two peptides (250 microg) of the human PMP22 extracellular sequences. Animals were examined daily until 20 days following immunization, when they underwent neurophysiological examination. A serum sample was then taken, prior to perfusion with glutaraldehyde and removal of the sciatic nerves and cauda equina. PMP22-immunized animals developed antibodies to the fusion protein and five out of 10 developed limp tails. No changes were observed in controls immunized with GST or in animals immunized with peptide. The mean compound motor action potentials elicited in the foot muscles by stimulation of the sciatic nerve at the sciatic notch and of the tibial nerve at the ankle were significantly reduced in the PMP22-immunized group (P < 0.05). Spinal roots from the group of animals immunized with PMP22 showed sparse infiltration of mononuclear cells, oedema and demyelination. PMP22 now deserves consideration as an autoantigen in human acute inflammatory demyelinating polyradiculoneuropathy.
- Published
- 1998
23. Inflammatory and immune mediated sensory neuropathies
- Author
-
R. A. C. Hughes
- Subjects
Pathology ,medicine.medical_specialty ,business.industry ,Inflammation ,Polyradiculoneuropathy ,medicine.disease ,Pathogenesis ,Trigeminal ganglion ,Myelin ,medicine.anatomical_structure ,Immune system ,Dorsal root ganglion ,Antigen ,medicine ,medicine.symptom ,business - Abstract
Human sensory neuropathies having an inflammatory component or presumed immune pathogenesis are reviewed. Sensory forms of acute (Miller Fisher syndrome) and chronic idiopathic demyelinating polyradiculoneuropathy are probably due to autoimmune responses against antigens relatively restricted to the myelin of sensory nerves. Subacute sensory neuronopathy associated with small cell carcinoma of the lung is caused by dorsal root ganglionitis: an antibody against a neuronal nuclear antigen is characteristically present in this syndrome and may be important in pathogenesis. Similar mechanisms might explain the dorsal root ganglionitis associated with Sjogren’s syndrome and the inflammation of the trigeminal ganglion which is thought to underlie benign trigeminal neuropathy. Nonspecific inflammatory disorders, including amyloid deposition, granulomas associated with leprosy or sarcoidosis, and vasculitis, also produce sensory neuropathy. The leakiness of the blood-nerve barrier and the presence of satellite cells expressing MHC class II antigen in the dorsal root ganglion may contribute to the susceptibility of sensory nerves to autoimmune damage.
- Published
- 1995
24. Immunotherapy for multiple sclerosis
- Author
-
R. A. C. Hughes
- Subjects
Male ,Multiple Sclerosis ,Cyclophosphamide ,medicine.medical_treatment ,Azathioprine ,Central nervous system disease ,Recurrence ,medicine ,Humans ,Interferon beta ,business.industry ,Multiple sclerosis ,Immunotherapy ,Interferon-beta ,medicine.disease ,Psychiatry and Mental health ,Immunology ,Cyclosporine ,Surgery ,Female ,Neurology (clinical) ,business ,medicine.drug ,Research Article ,Forecasting - Published
- 1994
25. JNNP in the Decade of the Brain
- Author
-
R A C Hughes
- Subjects
Psychiatry and Mental health ,Editorial Announcement ,Text mining ,business.industry ,Medicine ,Surgery ,Neurology (clinical) ,Bioinformatics ,business ,Decade of the Brain ,Data science - Published
- 1993
26. Plasma Exchange in Peripheral Neuropathy
- Author
-
R. A. C. Hughes
- Subjects
medicine.medical_specialty ,Peripheral neuropathy ,business.industry ,medicine ,Demyelinating polyneuropathy ,medicine.disease ,business ,Dermatology - Abstract
It is remarkable that we should have discovered a useful treatment for neurological disorders which we do not fully understand. There is evidence from controlled trials that plasma exchange (PE) helps each of the conditions in bold type in Table 1 and 2, and anecdotal evidence that it helps the others.
- Published
- 1991
27. Intravenous IgG in Guillain-Barre syndrome
- Author
-
R A C Hughes
- Subjects
education.field_of_study ,medicine.medical_specialty ,Pediatrics ,Guillain-Barre syndrome ,business.industry ,Incidence (epidemiology) ,Population ,Central nervous system ,General Engineering ,Polyradiculoneuropathy ,General Medicine ,Disease ,medicine.disease ,Surgery ,medicine.anatomical_structure ,Peripheral nervous system ,General Earth and Planetary Sciences ,Medicine ,business ,education ,Pathological ,General Environmental Science - Abstract
Same short term benefit as plasma exchange but easier to administer The commonest misdiagnosis of Guillain-Barre syndrome by the doctor of first contact is hysteria. This is understandable when most doctors have not seen a case since medical school. However, the syndrome is neither rare nor trivial. With an incidence of one or two cases per 100 000 population per year, new cases are about half as common as new cases of multiple sclerosis—a disease confined to the central nervous system as closely as Guillain-Barre syndrome is restricted to the peripheral nervous system. A quarter of adult patients require artificial ventilation, 10% die as a result of complications of the disease, and 10% are left with such severe disability that they cannot walk unaided a year later.1 The pathological process underlying Guillain-Barre syndrome is heterogeneous. Most patients have an acute multifocal lymphocytic infiltration in their peripheral nerves and spinal roots causing primary demyelination, which will recover quickly. Severely affected patients usually have additional axonal degeneration, which causes delayed and often incomplete recovery. About 10% of patients have an acute motor, or motor and sensory, axonal neuropathy in which macrophages invade the axons, especially in the spinal roots.2 3 Both types of Guillain-Barre syndrome are thought to be due to an autoimmune response triggered …
- Published
- 1996
28. Immunological Study Of Hereditary Motor And Sensory Neuropathy Type 1 A (HMSN1 A)
- Author
-
N A Gregson, Nicholas W. Wood, C. M. Gabriel, and R. A. C. Hughes
- Subjects
Pathology ,medicine.medical_specialty ,Necrosis ,biology ,business.industry ,General Neuroscience ,Cauda equina ,Sural nerve ,medicine.disease ,Serology ,Myelin ,medicine.anatomical_structure ,biology.protein ,Medicine ,Immunohistochemistry ,Neurology (clinical) ,Antibody ,medicine.symptom ,business ,Hereditary motor and sensory neuropathy - Abstract
Objectives: Fifty three patients were studied to investigate whether autoimmune or inflammatory mechanisms could explain the phenotypic heterogeneity of patients with hereditary motor and sensory neuropathy type 1a (HMSN1a). Methods: Serum samples were examined for antibodies to peripheral nerve myelin protein 22 (PMP22), ganglioside GM1 and cauda equina homogenate, and interleukin-6 (IL-6) and soluble tumour necrosis factor receptor 1 (sTNF R1) concentrations. Serological results were compared with those from patients with other neuropathies (ONPs, n = 30) and with normal subjects (n = 51). Results: In the group as a whole, no relation emerged between clinical severity and any immune parameters. Immunohistochemical examination of four sural nerve biopsies did not show significant inflammatory infiltration. In a subset of 12 patients who experienced stepwise progression of disease, there was a trend towards a higher proportion having anti-PMP22 antibodies (33% v 15% of those with gradual disease progression, 3% ONPs, and no normal controls) and complement fixing antibodies to human cauda equina (25% v 5% with gradual progression, 8.6% ONPs, 3.9% normal controls, p = 0.07). Conclusions: Patients with HMSN1a and a stepwise disease progression may have an inflammatory, autoimmune component superimposed on the genetic condition.
- Published
- 2002
29. Investigating a Role for Peripheral Myelin Protein 22 as An Autoantigen in Guillain-Barré Syndrome
- Author
-
R. A. C. Hughes, Adrian Hayday, Norman A. Gregson, and Jane Pritchard
- Subjects
Guillain-Barre syndrome ,business.industry ,Peripheral myelin protein 22 ,Immunology ,medicine ,General Medicine ,medicine.disease ,business - Published
- 2002
30. Efficacy of leukaemia inhibitory factor in experimental autoimmune neuritis
- Author
-
M. Laurà, Kenneth Smith, Norman A. Gregson, and R. A. C. Hughes
- Subjects
endocrine system ,Pathology ,medicine.medical_specialty ,Histology ,biology ,urogenital system ,business.industry ,medicine.medical_treatment ,Neuritis ,Cauda equina ,Pathology and Forensic Medicine ,Myelin ,medicine.anatomical_structure ,Cytokine ,Neurology ,Physiology (medical) ,biology.protein ,Medicine ,Neurology (clinical) ,Remyelination ,business ,Pathological ,reproductive and urinary physiology ,Neurotrophin - Abstract
Objective: To test the efficacy of leukaemia inhibitory factor (LIF) in experimental autoimmune neuritis (EAN), an animal model of Guillain–Barre Syndrome. Background: Growth factors might be promising treatment in human inflammatory neuropathy. LIF is a cytokine, which exerts neurotrophic and myotrophic properties. Materials and methods: EAN was induced in 24 Lewis rats by the injection of peripheral bovine myelin. At the onset of the disease they were injected in pairs on a random basis either with placebo or murine LIF 10 µg/kg. The injections continued until day 25 when they were killed. The clinical course of the disease and histological pattern of the cauda equina were examined. Results: The severity of the disease was slightly less in the LIF treated group and these animals also had a more rapid recovery. The main pathological features in the cauda equina of both groups were demyelination and remyelination with varying degrees of axonal degeneration, but there were no significant differences in the pathological changes between the groups. Conclusion: The administration of LIF showed a slight, but not significant, improvement in the clinical course of EAN, but no significant evidence on nerve histology. Further investigation of the therapeutic role of LIF would be worthwhile in view of its favourable effects in nerve regeneration.
- Published
- 2002
31. Treatment of Oesophageal Cancer
- Author
-
J S Tobias and R A C Hughes
- Subjects
03 medical and health sciences ,0302 clinical medicine ,030212 general & internal medicine ,General Medicine ,030227 psychiatry - Published
- 2002
32. Rare Cause of Cardiomyopathy
- Author
-
L. C. Fuller, R. A. C. Hughes, E. B. Wu, and John C. Chambers
- Subjects
medicine.medical_specialty ,Systemic disease ,Heart disease ,business.industry ,Cardiovascular examination ,Cardiomyopathy ,medicine.disease ,Connective tissue disease ,Surgery ,medicine.anatomical_structure ,Ventricle ,Physiology (medical) ,Internal medicine ,cardiovascular system ,medicine ,Cardiology ,Scleredema ,cardiovascular diseases ,Cardiology and Cardiovascular Medicine ,business ,Cardiac symptoms - Abstract
A 62-year-old man with scleredema of Buschke was referred to the cardiology clinic because of an abnormal ECG. He had no cardiac symptoms, and the cardiovascular examination was unremarkable. The echocardiogram showed a dilated, nonhypertrophied left ventricle with no regional wall …
- Published
- 2001
33. Role Of Campylobacter Jejuni In Experimental Allergic Neuritis: A Morphological And Biochemical Study
- Author
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G Vita, M. Laurà, R. A. C. Hughes, and Norman A. Gregson
- Subjects
Pathology ,medicine.medical_specialty ,biology ,business.industry ,General Neuroscience ,Immunogenicity ,medicine.medical_treatment ,Neuritis ,biology.organism_classification ,Campylobacter jejuni ,Myelin ,medicine.anatomical_structure ,Antigen ,Immunology ,medicine ,biology.protein ,Neurology (clinical) ,Sciatic nerve ,Antibody ,business ,Adjuvant - Abstract
Objective: The aim of the study was to evaluate if Campylobacter jejuni (C.j.) when used as an adjuvant would be able to produce a different form of Experimental Allergic Neuritis (EAN). We present here some preliminary results. Background: EAN is considered the in vivo model of Guillain-Barre Syndrome (GBS), which is often preceded by c.j. infection. EAN can be induced in Lewis rats by immunization with bovine peripheral nerve myelin in complete Freund's adjuvant (CFA), an emulsion formed by oil-in-water and dead mycobacteria. An adjuvant is usually necessary for the induction of EAN because it enhances the immunogenicity of the antigen. Clinically EAN is characterized by an acute monophasic course and progressive tail and limb weakness. The pathological finding is represented by marked demyelination affecting the roots and the sciatic nerve. Methods: 4 Lewis rats were immunized with an emulsion containing 2 mg of bovine peripheral myelin and C.j. strain Penner 0:41 in incomplete Freund's adjuvant (IFA). They were compared to 4 controls immunized with the same amount of peripheral myelin in CFA. The clinical course of the disease and the histological pattern of the roots and the sciatic nerve were examined. Anti-peripheral myelin, anti-C.jejuni and anti-GM1 antibodies' reactivity was detected by an ELISA assay. A biochemical study was performed to test the role of cell- and humoral-mediated responses. Results: The Lewis rats immunized with the C.j. as an adjuvant showed a delayed onset and a milder course of disease. Pathology in the roots was characterized by predominant demyelination, whereas the sciatic nerve presented very little signs of damage. Conclusion: This serotype of C.j. appears to be a less effective adjuvant in inducing EAN rather than Mycobacteria. Further studies are necessary to elucidate the pathogenetic mechanisms involved in GBS.
- Published
- 2001
34. The Association between Campylobacter Jejuni and Guillain—Barre Syndrome
- Author
-
JR Rees, R. A. C. Hughes, and Norman A. Gregson
- Subjects
biology ,Guillain-Barre syndrome ,business.industry ,Immunology ,medicine ,General Medicine ,biology.organism_classification ,medicine.disease ,business ,Campylobacter jejuni - Published
- 1995
35. Reduced Frequency of Memory CD8+T Lymphocytes in Cerebrospinal Fluid and Blood of Patients with Multiple Sclerosis
- Author
-
R. A. C. Hughes
- Subjects
Sweden ,Reduced frequency ,Ethics Committees ,Pathology ,medicine.medical_specialty ,Multiple Sclerosis ,business.industry ,Multiple sclerosis ,Immunology ,medicine.disease ,Spinal Puncture ,United Kingdom ,Cerebrospinal fluid ,Text mining ,medicine ,Humans ,Immunology and Allergy ,Ethics, Medical ,business ,CD8 - Published
- 1995
36. A controlled investigation of the cause of chronic idiopathic axonal polyneuropathy.
- Author
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R. A. C. Hughes, T. Umapathi, I. A. Gray, N. A. Gregson, M. Noori, A. S. Pannala, A. Proteggente, and A. V. Swan
- Published
- 2004
- Full Text
- View/download PDF
37. History of the journal and change of style
- Author
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R A C Hughes
- Subjects
Editorial Announcement ,Psychiatry and Mental health ,business.industry ,Medicine ,Surgery ,Neurology (clinical) ,business ,Bioinformatics ,Linguistics ,Style (sociolinguistics) - Published
- 1990
38. Controlled trial of plasma exchange in acute inflammatory polyradiculoneuropathy
- Author
-
R. J. Greenwood, R. A. C. Hughes, A. N. Bowden, N. S. Gordon, P. Millac, J. Newsom Davis, S. Asian, D. W. Chadwick, D. L. McLellan, and R. B. Stott
- Subjects
medicine.medical_specialty ,Treated group ,business.industry ,Polyradiculoneuropathy ,Hematology ,General Medicine ,medicine.disease ,Body weight ,Surgery ,law.invention ,Randomized controlled trial ,law ,Anesthesia ,medicine ,Functional ability ,business - Abstract
A randomized controlled trial of exchange versus no exchange was conducted to find out whether plasma exchange would be useful in acute inflammatory polyradiculoneuropathy. It was calculated that 15 patients would be required in each group to demonstrate a worthwhile improvement in functional ability one month after completion of treatment. Treatment comprised five exchanges in 10 days (55 ml plasma/kg body weight/exchange). Both groups received normal supportive care and were followed up periodically for a year. Overall the treated group showed a slight but not significant benefit (p>0.05); at two weeks' follow-up of patients admitted to the trial within 14 days of onset of neuropathic symptoms, p=0.07. These results do not provide grounds for recommending plasma exchange for the treatment of severe AIP.
- Published
- 1985
39. TRIGEMINAL SENSORY NEUROPATHY A STUDY OF 22 CASES
- Author
-
B. R. F. Lecky, R. A. C. Hughes, and N. M. F. Murray
- Subjects
Adult ,Male ,medicine.medical_specialty ,Biopsy ,Sensation ,Sensory system ,Nervous System ,Lesion ,Trigeminal ganglion ,Mixed connective tissue disease ,medicine ,Humans ,Trigeminal Nerve ,Corneal reflex ,Evoked potential ,Aged ,Autoantibodies ,Mixed Connective Tissue Disease ,Trigeminal nerve ,Scleroderma, Systemic ,Blinking ,business.industry ,Middle Aged ,medicine.disease ,Cranial Nerve Diseases ,Surgery ,Electrophysiology ,Anesthesia ,Female ,Neurology (clinical) ,Trigeminal Nerve Diseases ,medicine.symptom ,business ,Orbit - Abstract
The clinical and electrophysiological findings in 22 patients with chronic trigeminal sensory neuropathy are described. The main clinical feature was slowly evolving unilateral or bilateral facial numbness sometimes associated with pain and paraesthesiae and commonly with disturbed taste. Nine patients had either systemic sclerosis or mixed connective tissue disease. Of the 13 other patients, 9 had either organ or nonorgan specific serum autoantibodies. Blink reflex latencies were recorded in 17 patients, the commonest abnormality being an 'afferent' defect with modest prolongation of latency. Trigeminal sensory evoked responses were recorded in 14 cases, 6 showing mild prolongation of latencies. It is suggested that the lesion in this type of trigeminal neuropathy is in the trigeminal ganglion or in the proximal part of the main trigeminal divisions. This conclusion is supported by limited pathological data.
- Published
- 1987
40. Autonomic nerves in experimental allergic neuritis in the rat
- Author
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Henry C. Powell, M. K. Morey, Clayton A. Wiley, and R. A. C. Hughes
- Subjects
Male ,Pathology ,medicine.medical_specialty ,Sympathetic Nervous System ,Neuritis ,Enzyme-Linked Immunosorbent Assay ,Galactosylceramides ,Autonomic Nervous System ,Antibodies ,Pathology and Forensic Medicine ,Cellular and Molecular Neuroscience ,Myelin ,Edema ,Paralysis ,Animals ,Medicine ,biology ,business.industry ,Vagus Nerve ,Neuritis, Autoimmune, Experimental ,Rats ,Autonomic nervous system ,medicine.anatomical_structure ,Rats, Inbred Lew ,Immunology ,biology.protein ,Galactocerebroside ,Neurology (clinical) ,Endoneurium ,Antibody ,medicine.symptom ,business ,Neck - Abstract
After experimental allergic neuritis (EAN) was induced in 16 male Lewis rats with bovine peripheral myelin and adjuvants, peripheral nerves were examined morphologically at intervals of 12-21 days post inoculation (dpi). Signs of motor involvement were present in ten rats and were first elicited 12 dpi. They ranged from tail droop to complete lower limb paralysis. Autonomic nervous system (ANS) involvement was studied by contrasting morphological findings in the cervical sympathetic nerves (CSN), which are poorly myelinated and vagal nerves (VN) which contain numerous myelinated fibers in the endoneurium. Edema, perivenular infiltrates, and demyelination appeared in the VN of seven of nine neurologically affected rats, while the CSN showed edema and infiltrates in only one rat. ELISA assays were negative for anti-galactocerebroside antibody, and electron microscopy failed to show abnormalities of Schwann cells.
- Published
- 1985
41. Mixed or immune complex cryoglobulinaemia and neuropathy
- Author
-
I. C. K. Mackenzie, J. E. C. Hern, R. A. C. Hughes, and J. J. Cream
- Subjects
Pathology ,medicine.medical_specialty ,Sural nerve ,Cryoglobulins ,Antigen-Antibody Reactions ,Pathogenesis ,Sural Nerve ,immune system diseases ,hemic and lymphatic diseases ,medicine ,Humans ,cardiovascular diseases ,Purpura ,Aged ,Autoantibodies ,Mixed cryoglobulinaemia ,integumentary system ,business.industry ,Autoantibody ,Peripheral Nervous System Diseases ,Articles ,Middle Aged ,medicine.disease ,Immune complex ,Cold Temperature ,Psychiatry and Mental health ,Peripheral neuropathy ,Agglutinins ,Immunology ,Female ,Surgery ,Anemia, Hemolytic, Autoimmune ,Neurology (clinical) ,medicine.symptom ,business - Abstract
Three patients with peripheral neuropathy and mixed or immune complex cryoglobulinaemia are reported. The significance of mixed cryoglobulinaemia and the pathogenesis of the peripheral neuropathy are discussed.
- Published
- 1974
42. Experimental Allergic Neuritis
- Author
-
Henry C. Powell and R. A. C. Hughes
- Subjects
medicine.medical_specialty ,Wallerian degeneration ,animal diseases ,Neuritis ,chemical and pharmacologic phenomena ,Biology ,Glucocerebroside ,Pathology and Forensic Medicine ,Cellular and Molecular Neuroscience ,Myelin ,Internal medicine ,medicine ,Autoimmune disease ,General Medicine ,biochemical phenomena, metabolism, and nutrition ,medicine.disease ,Cerebroside ,Cellular infiltration ,Endocrinology ,medicine.anatomical_structure ,nervous system ,Neurology ,Immunology ,bacteria ,Galactocerebroside ,Neurology (clinical) - Abstract
Experimental allergic neuritis was induced in male inbred Lewis rats immunized with myelin, P2 alone, P2 mixed with galactocerebroside and P2 mixed with glucocerebroside. Neurological deficit started significantly earlier in myelin-immunized rats than in P2-immunized rats. Although myelin-immunized rats appeared most severely affected, differences between of groups in maximum neurological deficit were not significant. The course of the disease of P2-galactocerebroside-immunized animals did not differ from that of P2-glucocerebroside-immunized group. Histologically, cellular infiltration and demyelination were more conspicuous 12 days after immunization in the group immunized with myelin than in the other rats. After 21 days, primary demyelination was prominent in all groups: its frequency and severity were similar in the myelin-immunized and P2-immunized animals. The P2-galactocerebroside-immunized group had significantly more frequent demyelination than of P2-immunized rats, but did not differ in this or any other respect from of P2-glucocerebroside-immunized group. Wallerian degeneration was prominent in all groups at this stage. We conclude that P2 alone does induce demyelination and that galactocerebroside added to the immunizing emulsion enhances of response but no more than the non-myelin lipid glucocerebroside
- Published
- 1984
43. Relationship of adjuvants and swine influenza vaccine to experimental neuropathy in rabbits
- Author
-
Andrew P. Mizisin, Henry C. Powell, M. K. Morey, R. A. C. Hughes, and C. A. Wiley
- Subjects
viruses ,medicine.medical_treatment ,Freund's Adjuvant ,Pathology and Forensic Medicine ,Antigen-Antibody Reactions ,Cellular and Molecular Neuroscience ,Immune system ,Gangliosides ,Demyelinating disease ,Animals ,Medicine ,biology ,business.industry ,Antibody titer ,Peripheral Nervous System Diseases ,biochemical phenomena, metabolism, and nutrition ,medicine.disease ,Myelin basic protein ,Cholesterol ,Influenza A virus ,Influenza Vaccines ,Freund's adjuvant ,Immunology ,Phosphatidylcholines ,biology.protein ,Female ,lipids (amino acids, peptides, and proteins) ,Galactocerebroside ,Rabbits ,Neurology (clinical) ,Antibody ,business ,Adjuvant - Abstract
Experimental neuropathy, characterized by endoneurial edema and demyelination, was induced by inoculating rabbits with a combination of Freund's complete adjuvant (FCA), gangliosides, lecithin and cholesterol. A less severe demyelinating neuropathy could be induced by treatment with FCA alone but no significant change could be elicited by injection of swine influenza vaccine (SFV) alone. When FCA was combined with gangliosides, lecithins, cholesterol and SFV, neuropathy occurred, but the changes were less severe than if these agents were used without SFV. Sera were tested for myelin basic protein (MBP) and galactocerebroside (GC) antibodies in each experimental group. Neither SFV alone nor SFV combined with Freund's complete adjuvant, gangliosides, cholesterol and lecithin evoked significant antibody titers to MBP or GC. However, rabbits inoculated with FCA, gangliosides, lecithin and cholesterol had rising titers of antibody to both MBP and GC over the 3-month experimental period. One rabbit inoculated with FCA alone had significant antibody to MBP. The findings suggest that Freund's complete adjuvant alone can induce demyelination in the peripheral nerves of rabbits and that SFV may modulate the immune response acting either as an adjuvant or suppressant in the experimental demyelinating disease.
- Published
- 1987
44. Section of Public and Industrial Medicine
- Author
-
M. R. Finlayson, R. T. C. Hughes, H. M. James, P. S. Woodruff, H. M. L. Murray, and D. Gordon
- Subjects
Section (archaeology) ,Political science ,Forensic engineering ,General Medicine - Published
- 1955
45. Section of Public Health, Industrial Medicine and Hospital Administration
- Author
-
A. R. Southwood, P. Nolan, D. Gordon, J. Edis, K. Brennan, and R. T. C. Hughes
- Subjects
medicine.medical_specialty ,Political science ,Public health ,Section (typography) ,medicine ,General Medicine ,Medical emergency ,medicine.disease ,Health administration - Published
- 1958
46. A case of fatal peri-partum cardiomyopathy
- Author
-
G. C. Sutton, P. Kapur, R. A. C. Hughes, and M. Honey
- Subjects
Adult ,Aetiological factor ,Cardiac Catheterization ,medicine.medical_specialty ,Heart Diseases ,Peri ,Cardiomyopathy ,Blood Pressure ,Case Reports ,Electrocardiography ,Pregnancy ,Internal medicine ,medicine ,Humans ,Intensive care medicine ,reproductive and urinary physiology ,business.industry ,Myocardium ,Heart ,Puerperal Disorders ,medicine.disease ,female genital diseases and pregnancy complications ,Oxygen ,Radiography ,Cardiology ,Female ,Cardiology and Cardiovascular Medicine ,business - Abstract
A case of fatal cardiomyopathy presenting in the puerperium is described. Despite extensive investigation and post-mortem examination no aetiological factor was found. The diagnosis of specific peri-partum cardiomyopathy is discussed.
- Published
- 1970
47. Relapsing Polychondritis
- Author
-
R A C Hughes, N Curry, and M H Lessof
- Subjects
03 medical and health sciences ,0302 clinical medicine ,030211 gastroenterology & hepatology ,030212 general & internal medicine - Published
- 1971
48. A prospective study of acute idiopathic neuropathy. III. Immunological studies
- Author
-
N A Gregson, J B Winer, S. Leibowitz, V Yewdall, W A Taylor, R. A. C. Hughes, P Shepherd, and I A Gray
- Subjects
Adult ,Male ,Pathology ,medicine.medical_specialty ,Adolescent ,T-Lymphocytes ,Polyradiculoneuropathy ,Galactosylceramides ,Antigen-Antibody Complex ,T-Lymphocytes, Regulatory ,Immunoglobulin G ,Autoimmune Diseases ,Leukocyte Count ,Immune system ,Idiopathic Neuropathy ,Antigen ,medicine ,Animals ,Humans ,Child ,Aged ,Autoantibodies ,biology ,business.industry ,Autoantibody ,Optic Nerve ,Complement System Proteins ,T-Lymphocytes, Helper-Inducer ,Middle Aged ,Sciatic Nerve ,Rats ,Psychiatry and Mental health ,Immunoglobulin M ,Child, Preschool ,Immunology ,biology.protein ,Surgery ,Galactocerebroside ,Female ,Neurology (clinical) ,Antibody ,business ,Research Article - Abstract
The immune responses of 100 patients who presented with an acute idiopathic neuropathy were compared with those of age and sex matched controls. Blood lymphocytes and their subsets were counted with a fluorescent activated cell sorter. CD8+ (putative suppressor) lymphocytes were significantly reduced in the first week of the disease but total lymphocytes, total T and CD4+ (putative helper) cells were not altered. This reduction depended on the nature of the preceding infection. Serum complement C3 and C4 concentrations remained normal and immune complexes were rarely detected with a C1q binding assay. Complement-fixing antibodies to human peripheral nerve antigens were discovered in the serum of 7% of patients but only 1% of controls. Complement-fixing antibodies to galactocerebroside were not discovered in any sera. Enzyme-linked immunoassays detected increased antibody responses to galactocerebroside but none at all to human P2 myelin protein in the patient sera. Forty microliter of serum from five patients injected into the sciatic nerves of rats did not induce significantly more demyelination than the serum from control patients. It is concluded that auto-immune responses can only be detected by these techniques in a small minority of patients with acute idiopathic neuropathy.
- Published
- 1988
49. Use of Azathioprine in Multiple Sclerosis
- Author
-
R. A. C. Hughes
- Subjects
Immunosuppressive treatment ,medicine.medical_specialty ,business.industry ,Multiple sclerosis ,fungi ,Lupus nephritis ,food and beverages ,Chronic inflammatory demyelinating polyneuropathy ,Azathioprine ,medicine.disease ,Dermatology ,humanities ,medicine ,business ,health care economics and organizations ,medicine.drug - Abstract
Many arguments can be marshalled to support the use of immunosuppressive treatment in multiple sclerosis (MS)
- Published
- 1988
50. Relapsing Polychondritis and Pulseless Disease
- Author
-
M. H. Lessof, R. A. C. Hughes, and W. M. Seymour
- Subjects
Pathology ,medicine.medical_specialty ,business.industry ,General Engineering ,General Medicine ,Disease ,medicine.disease ,Dermatology ,Correspondence ,medicine ,General Earth and Planetary Sciences ,business ,Relapsing polychondritis ,General Environmental Science - Published
- 1974
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