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3. Cost-utility of oral methylprednisolone in the treatment of multiple sclerosis relapses: Results from the COPOUSEP trial

Author

Michel, M., primary, Le Page, E., additional, Laplaud, D.A., additional, Wardi, R., additional, Lebrun, C., additional, Zagnoli, F., additional, Wiertlewski, S., additional, Coustans, M., additional, Edan, G., additional, Chevreul, K., additional, Veillard, D., additional, Lallement, F., additional, Cohen, M., additional, Blanchard, C., additional, Sartori, E., additional, Demarco, O., additional, Rouhart, F., additional, Papeix, C., additional, Taurin, G., additional, Anani, T., additional, Kassiotis, P., additional, Hamon, C., additional, Lester, M.A., additional, and Merienne, M., additional

Published
2022
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11. Splitting kinetics of Si0.8Ge0.2 layers implanted with H or sequentially with He and H.

Author

Nguyen, Phuong, Bourdelle, K. K., Aulnette, C., Lallement, F., Daix, N., Daval, N., Cayrefourcq, I., Letertre, F., Mazuré, C., Bogumilowicz, Y., Tauzin, A., Deguet, C., Cherkashin, N., and Claverie, A.

Subjects
ION implantation, ION bombardment, PARTICLES (Nuclear physics), TRANSMISSION electron microscopy, BACKSCATTERING, SCATTERING (Physics), CHANNELING (Physics)
Abstract

We have performed systematic measurements of the splitting kinetics induced by H-only and He+H sequential ion implantation into relaxed Si0.8Ge0.2 layers and compared them with the data obtained in Si. For H-only implants, Si splits faster than Si0.8Ge0.2. Sequential ion implantation leads to faster splitting kinetics than H-only in both materials and is faster in Si0.8Ge0.2 than in Si. We have performed secondary ion mass spectrometry, Rutherford backscattering spectroscopy in channeling mode, and transmission electron microscopy analyses to elucidate the physical mechanisms involved in these splitting phenomena. The data are discussed in the framework of a simple phenomenological model in which vacancies play an important role. [ABSTRACT FROM AUTHOR]

Published
2008
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12. Splitting kinetics of [Si.sub.0.8][Ge.sub.0.2] layers implanted with H or sequentially with He and H

Author

Nguyen, Phuong, Bourdelle, K.K., Aulnette, C., Lallement, F., Daix, N., Daval, N., Cayrefourcq, F., Mazure, C., Bogumilowicz, Y., Tauzin, A., Deguet, C., Cherkashin, N., and Claverie, A.

Subjects
Germanium -- Mechanical properties, Germanium -- Electric properties, Helium -- Thermal properties, Hydrogen -- Thermal properties, Silicon-on-isolator -- Mechanical properties, Silicon-on-isolator -- Electric properties, X-rays -- Diffraction, X-rays -- Usage, Physics
Abstract

The splitting kinetics of [Si.sub.0.8][Ge.sub.0.2] substrates implanted with H-only or sequentially implanted with He and then with H is studied. The extended physical characterization of the implanted and annealed substrates has provided insights into the mechanism of splitting in [Si.sub.0.8][Ge.sub.0.2].

Published
2008

13. Placebo effect characteristics observed in a single, international, longitudinal study in Huntington's disease

Author

Cubo, E, González, M, del Puerto, I, de Yébenes, Jg, Arconada, Of, Gabriel Galán, Jm, Ehdi, Sg, Zangerl, A, Seppi, K, Wenning, G, Poewe, W, Foeldy, D, Auff, E, Schober, T, Wenzel, K, Ott, E, Walli, J, Leblhuber, F, Dürr, A, Bloch, F, Messouak, O, Tallaksen, C, Dubois, B, Guillamo, Js, Bachoud Lévi, Ac, Engles, A, Krystkowiak, P, Destée, A, Memin, A, Thibaut Tanchou, S, Pasquier, F, Azulay, Jp, Demonet, Jf, Galitzky, M, Rascol, O, Mollion, H, Broussolle, E, Madigand, M, Lallement, F, Goizet, C, Tison, F, Arguillère, S, Viallet, F, Bakchine, S, Khoris, J, Pages, M, Camu, W, Resch, F, Hannequin, D, Durif, F, Saudeau, D, Autret, A, Andrich, J, Saft, C, Kraus, Ph, Przuntek, H, Ecker, D, Kramer, B, Landwehrmeyer, Gb, Ludolph, Ac, Priller, J, Meierkord, H, Kuznik, D, Dose, M, Squitieri, F, Albanese, A, Abbruzzese, Giovanni, Filla, A, van de Warrenburg, B, de Jong, D, Kremer, H, van Vugt, J, Grimbergen, Y, Roos, R, Gawel, M, Janik, P, Kowalczys, H, Pilczuk, B, Kwiecinski, H, Świat, M, Ochudło, S, Modestowicz, R, Niezgoda, A, Łukasik, M, Lukasik, M, García Ruiz, P, Descals, Am, Rojo, A, Fontán, A, Hernández, J, Cantarero, S, Fanjul, S, Alegre, J, Roldán, Sg, Mateo, D, Burguera, Ja, Solis, P, Calopa, M, Jaumà, S, Bas, J, Tolosa, E, Muñoz, Je, Gámez, J, Cervera, C, Zarranz, Jj, Lezcano, E, Gómez, Jc, Chacón, J, Dinca, L, Gamero, Ma, Redondo, L, Castro, A, Sesar, A, López del Val, J, López, E, Ríos, C, Castillio, V, Burgunder, Jm, Nirkko, A, Kälin, A, Vingerhoets, F, and Wider, C.

Published
2012

14. How to Capitalize on the Retest Effect in Future Trials on Huntington's Disease.

Author

European Huntington's Disease Initiative Study Group, the Multicentre Intracerebral Grafting in Huntington's Disease Group, Bachoud-Lévi, AC., Boissé, MF., Lemoine, L., Verny, C., Aubin, G., Demonet, JF., Calvas, F., Krystkowiak, P., Simonin, C., Delliaux, M., Damier, P., Renou, P., Supiot, F., Slama, H., Guillamo, J., Dürr, A., Bloch, F., Messouak, O., Tallaksen, C., Dubois, B., Engles, A., Destee, A., Memin, A., Thibaut-Tanchou, S., Pasquier, F., Galitzky, M., Rascol, O., Mollion, H., Broussolle, E., Madigand, M., Lallement, F., Goizet, C., Tison, F., Arguillère, S., Bakchine, S., Khoris, J., Camu, W., Resch, F., Hannequin, D., Durif, F., Saudeau, D., Autret, A., Schramm, C., Katsahian, S., Youssov, K., Démonet, J.F., Cleret de Langavant, L., Bachoud-Lévi, A.C., European Huntington's Disease Initiative Study Group, the Multicentre Intracerebral Grafting in Huntington's Disease Group, Bachoud-Lévi, AC., Boissé, MF., Lemoine, L., Verny, C., Aubin, G., Demonet, JF., Calvas, F., Krystkowiak, P., Simonin, C., Delliaux, M., Damier, P., Renou, P., Supiot, F., Slama, H., Guillamo, J., Dürr, A., Bloch, F., Messouak, O., Tallaksen, C., Dubois, B., Engles, A., Destee, A., Memin, A., Thibaut-Tanchou, S., Pasquier, F., Galitzky, M., Rascol, O., Mollion, H., Broussolle, E., Madigand, M., Lallement, F., Goizet, C., Tison, F., Arguillère, S., Bakchine, S., Khoris, J., Camu, W., Resch, F., Hannequin, D., Durif, F., Saudeau, D., Autret, A., Schramm, C., Katsahian, S., Youssov, K., Démonet, J.F., Cleret de Langavant, L., and Bachoud-Lévi, A.C.

Abstract

The retest effect-improvement of performance on second exposure to a task-may impede the detection of cognitive decline in clinical trials for neurodegenerative diseases. We assessed the impact of the retest effect in Huntington's disease trials, and investigated its possible neutralization. We enrolled 54 patients in the Multicentric Intracerebral Grafting in Huntington's Disease (MIG-HD) trial and 39 in the placebo arm of the Riluzole trial in Huntington's Disease (RIL-HD). All were assessed with the Unified Huntington's Disease Rating Scale (UHDRS) plus additional cognitive tasks at baseline (A1), shortly after baseline (A2) and one year later (A3). We used paired t-tests to analyze the retest effect between A1 and A2. For each task of the MIG-HD study, we used a stepwise algorithm to design models predictive of patient performance at A3, which we applied to the RIL-HD trial for external validation. We observed a retest effect in most cognitive tasks. A decline in performance at one year was detected in 3 of the 15 cognitive tasks with A1 as the baseline, and 9 of the 15 cognitive tasks with A2 as the baseline. We also included the retest effect in performance modeling and showed that it facilitated performance prediction one year later for 14 of the 15 cognitive tasks. The retest effect may mask cognitive decline in patients with neurodegenerative diseases. The dual baseline can improve clinical trial design, and better prediction should homogenize patient groups, resulting in smaller numbers of participants being required.

Published
2015

15. Weight loss in Huntington disease increases with higher CAG repeat number

Author

Aziz, Na, van der Burg, Jm, Landwehrmeyer, Gb, Brundin, P, Stijnen, T, Ehdi, Sg, Roos, Ra, Zangerl, A, Seppi, K, Wenning, G, Poewe, W, Foeldy, D, Auff, E, Schober, T, Wenzel, K, Ott, E, Walli, J, Leblhuber, F, Dürr, A, Bloch, F, Messouak, O, Tallaksen, C, Dubois, B, Guillamo, Js, Bachoud Lévi, Ac, Engles, A, Krystkowiak, P, Destée, A, Memin, A, Thibaut Tanchou, S, Pasquier, F, Azulay, Jp, Demonet, Jf, Galitzky, M, Rascol, O, Mollion, H, Broussolle, E, Madigand, M, Lallement, F, Goizet, C, Tison, F, Arguillère, S, Viallet, F, Bakchine, S, Khoris, J, Pages, M, Camu, W, Resch, F, Hannequin, D, Durif, F, Saudeau, D, Autret, A, Andrich, J, Saft, C, Kraus, Ph, Przuntek, H, Ecker, D, Kramer, B, Ludolph, Ac, Priller, J, Meierkord, H, Kuznik, D, Dose, M, Squitieri, F, Albanese, A, Abbruzzese, Giovanni, Filla, A, van de Warrenburg, B, de Jong, D, Kremer, H, van Vugt, J, Grimbergen, Y, Roos, R, Gawel, M, Janik, P, Kowalczys, H, Pilczuk, B, Kwiecinski, H, Swiat, M, Ochudło, S, Modestowicz, R, Niezgoda, A, Łukasik, M, Garcia de Yébenes, J, García Ruiz, P, Martínez Descals, A, Rojo, A, Fontán, A, Hernández, J, Cantarero, S, Fanjul, S, Alegre, J, Giménez Roldán, S, Mateo, D, Burguera, Ja, Solis, P, Calopa, M, Jaumà, S, Bas, J, Tolosa, E, Muñoz, Je, Gámez, J, Cervera, C, Zarranz, Jj, Lezcano, E, Gómez, Jc, Chacón, J, Dinca, L, Gamero, Ma, Redondo, L, Castro, A, Sesar, A, López del Val, J, López, E, Ríos, C, Castillio, V, Burgunder, Jm, Nirkko, A, Kälin, A, Vingerhoets, F, Wider, C., N. A., Aziz, J. M., M, G. B., Landwehrmeyer, P., Brundin, T., Stijnen, E. H. D., R. A. C., and Filla, Alessandro

Subjects
Male, Pathology, therapeutic use, Nuclear Protein, Neurology, Disease, Body Mass Index, Placebos, Mice, Degenerative disease, Trinucleotide Repeats, Weight loss, genetics, Huntingtin Protein, Riluzole, Nuclear Proteins, Middle Aged, Huntington Disease, Neuroprotective Agents, Inbred C57BL, Mice, genetics/metabolism, Placebos, Riluzole, Female, medicine.symptom, Psychology, Adult, congenital, hereditary, and neonatal diseases and abnormalities, medicine.medical_specialty, Mice, Transgenic, Nerve Tissue Proteins, Animal, Energy Intake, Female, Humans, Huntington Disease, Central nervous system disease, therapeutic use, Trinucleotide Repeats, Weight Lo, Internal medicine, Weight Loss, mental disorders, medicine, Animals, Humans, Hereditary Neurodegenerative Disorder, Transgenic, Middle Aged, Nerve Tissue Protein, Aged, drug therapy/genetics/physiopathology, Male, Mice, Mice, Body Weight, medicine.disease, Adult, Aged, Animals, Body Mass Index, Body Weight, Disease Model, Mice, Inbred C57BL, Disease Models, Animal, Endocrinology, genetics/metabolism, Neuroprotective Agent, Neurology (clinical), Energy Intake, Body mass index
Abstract

Huntington disease (HD) is a hereditary neurodegenerative disorder caused by an expanded number of CAG repeats in the huntingtin gene. A hallmark of HD is unintended weight loss, the cause of which is unknown. In order to elucidate the underlying mechanisms of weight loss in HD, we studied its relation to other disease characteristics including motor, cognitive, and behavioral disturbances and CAG repeat number.In 517 patients with early stage HD, we applied mixed-effects model analyses to correlate weight changes over 3 years to CAG repeat number and various components of the Unified Huntington's Disease Rating Scale (UHDRS). We also assessed the relation between CAG repeat number and body weight and caloric intake in the R6/2 mouse model of HD.In patients with HD, mean body mass index decreased with -0.15 units per year (p < 0.001). However, no single UHDRS component, including motor, cognitive, and behavioral scores, was independently associated with the rate of weight loss. Patients with HD with a higher CAG repeat number had a faster rate of weight loss. Similarly, R6/2 mice with a larger CAG repeat length had a lower body weight, whereas caloric intake increased with larger CAG repeat length.Weight loss in Huntington disease (HD) is directly linked to CAG repeat length and is likely to result from a hypermetabolic state. Other signs and symptoms of HD are unlikely to contribute to weight loss in early disease stages. Elucidation of the responsible mechanisms could lead to effective energy-based therapeutics.

Published
2008

25. Switching from natalizumab to fingolimod: risk of disease reactivation during the washout period is due to the previous activity of the disease. Follow-up of the ENIGM survey

Author

Cohen, M., Maillart, E., Papeix, C., Vukusic, S., Brassat, D., Seze, J., Tourbah, A., Wiertlewski, S., Laplaud, D., Camu, W., Courtois, S., Derouiche, F., Chambaud, L., Boulay, C., Brochet, B., Debouverie, M., Casez, O., Heinzlef, O., Ouallet, J., Stankoff, B., Castelnovo, G., Le Page, E., Defer, G., Derache, N., Anne, O., Berger, E., Camdessanche, J., Kopf, A., Fleury, M., Malikova, I., Pelletier, J., Al Khedr, A., Zaenker, C., Edan, G., Moreau, T., Fromont, A., Rico, A., Blanc, F., nicolas collongues, Barth, P., Louiset, P., Pittion, S., Clavelou, P., Thaite, F., Vermersch, P., Sephir, H., Creange, A., Gout, O., Guennoc, A., Coustans, M., Thaurin, G., Lallement, F., Rouhart, F., Thouvenot, E., Labauge, P., Seeldrayers, P., Lebrun, C., and Club Francophone Sclerose Plaques

30. How to Capitalize on the Retest Effect in Future Trials on Huntington's Disease

Author

Schramm, Catherine, Katsahian, Sandrine, Youssov, Katia, Démonet, Jean-François, Krystkowiak, Pierre, Supiot, Frédéric, Verny, Christophe, de Langavant, Laurent, Bachoud-Lévi, Anne-Catherine, Group, European, Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Unité de Biostatistiques, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Service d’informatique et statistiques, CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Leenaards de la Mémoire, Université de Lausanne = University of Lausanne (UNIL)-CHUV, Laboratoire de Neurosciences Fonctionnelles et Pathologies - UR UPJV 4559 (LNFP), Université de Picardie Jules Verne (UPJV), Service de neurologie [Amiens], CHU Amiens-Picardie, Hôpital Erasme [Bruxelles] (ULB), Faculté de Médecine [Bruxelles] (ULB), Université libre de Bruxelles (ULB)-Université libre de Bruxelles (ULB), Centre de Référence des Maladies Neurogénétiques, Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Service de neurologie [Mondor], Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de référence maladie de Huntington, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Trousseau [APHP], Université de Lausanne (UNIL)-CHUV, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-CHU Trousseau [APHP], Univ Angers, Okina, Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut Mondor de Recherche Biomédicale ( IMRB ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-CHU Pitié-Salpêtrière [APHP]-CHU Trousseau [APHP], Université de Lausanne ( UNIL ) -CHUV, Laboratoire de Neurosciences Fonctionnelles et Pathologies, Hôpital Roger Salengro-PRES Université Lille Nord de France-EA 4559/1046-Université de Lille, Droit et Santé, Hôpital Erasme, Université Libre de Bruxelles ( ULB ), Université Libre de Bruxelles [Bruxelles] ( ULB ), CHU Angers, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-CHU Pitié-Salpêtrière [APHP]-CHU Trousseau [APHP], Hôpital Erasme, Université Libre de Bruxelles (ULB), Université Libre de Bruxelles [Bruxelles] (ULB), European Huntington's Disease Initiative Study Group, the Multicentre Intracerebral Grafting in Huntington's Disease Group, Bachoud-Lévi, AC., Boissé, MF., Lemoine, L., Verny, C., Aubin, G., Demonet, JF., Calvas, F., Krystkowiak, P., Simonin, C., Delliaux, M., Damier, P., Renou, P., Supiot, F., Slama, H., Guillamo, J., Dürr, A., Bloch, F., Messouak, O., Tallaksen, C., Dubois, B., Engles, A., Destee, A., Memin, A., Thibaut-Tanchou, S., Pasquier, F., Galitzky, M., Rascol, O., Mollion, H., Broussolle, E., Madigand, M., Lallement, F., Goizet, C., Tison, F., Arguillère, S., Bakchine, S., Khoris, J., Camu, W., Resch, F., Hannequin, D., Durif, F., Saudeau, D., and Autret, A.

Subjects
Adult, Male, Elementary cognitive task, medicine.medical_specialty, Psychologie appliquée, lcsh:Medicine, behavioral disciplines and activities, Cohort Studies, Cognition, Huntington's disease, Rating scale, Models, Medicine, Dementia, Humans, Cognitive decline, lcsh:Science, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Multidisciplinary, Models, Statistical, business.industry, Clinical study design, lcsh:R, Reproducibility of Results, Sciences bio-médicales et agricoles, Huntington disease, Middle Aged, Statistical, medicine.disease, 3. Good health, Clinical trial, [ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Physical therapy, Disease Progression, lcsh:Q, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Female, business, Biologie, Algorithms, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Research Article
Abstract

The retest effect - improvement of performance on second exposure to a task - may impede the detection of cognitive decline in clinical trials for neurodegenerative diseases. We assessed the impact of the retest effect in Huntington's disease trials, and investigated its possible neutralization.We enrolled 54 patients in the Multicentric Intracerebral Grafting in Huntington's Disease (MIG-HD) trial and 39 in the placebo arm of the Riluzole trial in Huntington's Disease (RIL-HD). All were assessed with the Unified Huntington's Disease Rating Scale (UHDRS) plus additional cognitive tasks at baseline (A1), shortly after baseline (A2) and one year later (A3). We used paired t-tests to analyze the retest effect between A1 and A2. For each task of the MIG-HD study, we used a stepwise algorithm to design models predictive of patient performance at A3, which we applied to the RIL-HD trial for external validation. We observed a retest effect in most cognitive tasks. A decline in performance at one year was detected in 3 of the 15 cognitive tasks with A1 as the baseline, and 9 of the 15 cognitive tasks with A2 as the baseline.We also included the retest effect in performance modeling and showed that it facilitated performance prediction one year later for 14 of the 15 cognitive tasks. The retest effect may mask cognitive decline in patients with neurodegenerative diseases. The dual baseline can improve clinical trial design, and better prediction should homogenize patient groups, resulting in smaller numbers of participants being required., 0, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2015
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31. Disease reactivation after fingolimod cessation in Multiple Sclerosis patients with pregnancy desire: A retrospective study.

Author

Callens A, Leblanc S, Le Page E, Edan G, Jourdain A, Coustans M, Wiertlewski S, Laplaud D, Videt D, Lallement F, Leray E, and Michel L

Subjects
Female, Fingolimod Hydrochloride adverse effects, Humans, Immunosuppressive Agents adverse effects, Pregnancy, Recurrence, Retrospective Studies, Multiple Sclerosis chemically induced, Multiple Sclerosis complications, Multiple Sclerosis drug therapy, Multiple Sclerosis, Relapsing-Remitting chemically induced
Abstract

Reactivation of Multiple Sclerosis (MS) activity has been described after fingolimod cessation. Because of its contra indication during pregnancy, switch towards lower efficacy treatments are frequent in MS patients with childbearing desire but expose them to a risk of disease reactivation. In this retrospective study including 44 women with MS, a significant increase of the median annualized relapse rate was found in the year following fingolimod discontinuation compared to the period before (p < 0.0001), and 57% of women experienced at least one relapse. When considering to start fingolimod, particular attention should be paid to women with a short-term pregnancy desire., Competing Interests: Declaration of Competing Interest The authors declare that there is no conflict of interest., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Published
2022
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32. Pallidal stimulation in advanced Parkinson's patients with contraindications for subthalamic stimulation.

Author

Rouaud T, Dondaine T, Drapier S, Haegelen C, Lallement F, Péron J, Raoul S, Sauleau P, and Vérin M

Subjects
Aged, Female, Humans, Male, Middle Aged, Neuropsychological Tests, Severity of Illness Index, Treatment Outcome, Deep Brain Stimulation, Globus Pallidus surgery, Parkinson Disease therapy, Subthalamic Nucleus surgery
Abstract

The aim of this study was to evaluate the efficacy and safety of bilateral pallidal (GPi) deep brain stimulation (DBS) 6 months after surgery in advanced parkinsonian patients whose dopa-resistant axial motor signs or cognitive decline constituted contraindications for subthalamic nucleus (STN) DBS. Seventeen patients with a mean age of 59.3 ± 7.1 years (range, 45-70), mean disease duration of 12.5 ± 4.3 years (range, 7-20), and contraindications for STN DBS, underwent bilateral GPi DBS. They were evaluated before surgery and 6 months afterward, in accordance with Core Assessment Program for Intracerebral Transplantation recommendations. There were mean improvements of 41.1% in the UPDRS III motor score in the off-dopa condition and 20.3% in the activities of daily living score. Motor fluctuations were reduced by 22.9% and dyskinesias by 68.6%. Axial motor signs improved in the off-dopa condition by 34.2%. Neuropsychological performances remained unchanged at the 6-month assessment. Bilateral GPi DBS is both safe and effective in advanced parkinsonian patients with untreatable motor fluctuations, for whom STN DBS is contraindicated due to dopa-resistant axial motor signs or cognitive decline. As such, it should be regarded as a viable option for these patients., (© 2010 Movement Disorder Society.)

Published
2010
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33. Fear recognition is impaired by subthalamic nucleus stimulation in Parkinson's disease.

Author

Biseul I, Sauleau P, Haegelen C, Trebon P, Drapier D, Raoul S, Drapier S, Lallement F, Rivier I, Lajat Y, and Verin M

Subjects
Aged, Discrimination, Psychological physiology, Female, Humans, Male, Middle Aged, Parkinson Disease physiopathology, Parkinson Disease therapy, Reference Values, Statistics, Nonparametric, Subthalamic Nucleus physiopathology, Subthalamic Nucleus surgery, Electric Stimulation Therapy psychology, Facial Expression, Fear, Parkinson Disease psychology, Recognition, Psychology physiology, Subthalamic Nucleus physiology
Abstract

Behavioural disturbances such as disorders of mood, apathy or indifference are often observed in Parkinson's disease (PD) patients with chronic high frequency deep brain stimulation of subthalamic nucleus (STN DBS). Neuropsychological modifications causing these adverse events induced by STN DBS remain unknown, even if limbic disturbances are hypothesised. The limbic system supports neural circuits processing emotional information. The aim of this work is to evaluate changes of emotional recognition in PD patients induced by STN DBS. Thirty PD patients were assessed using a computerised paradigm of recognition of emotional facial expressions [Ekman, P., & Friesen, W. V. (1976). Pictures of facial affect. Palo Alto, CA: Consulting Psychologists Press], 15 before STN DBS and 15 after. The two patients groups were compared to a group of 15 healthy control subjects. One series of 55 pictures of emotional facial expressions was presented to each patient. Patients had to classify the pictures according to seven basic emotions (happiness, sadness, fear, surprise, disgust, anger and no emotion). The intact ability to percept faces was firstly assured using the Benton Recognition Test. Recognition of fear expressions was significantly and selectively reduced in the post-operative group in comparison to both pre-operative and control groups. Our results demonstrate for the first time a selective reduction of recognition of facial expressions of fear by STN DBS. This impairment could be the first neuropsychological marker of a more general limbic dysfunction, thought to be responsible for the behavioural disorders reported after STN DBS.

Published
2005
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