13 results on '"Thobois S"'
Search Results
2. Bilateral subthalamic nucleus stimulation in advanced Parkinson’s disease: Five year follow-up
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Gervais-Bernard, H., Xie-Brustolin, J., Mertens, P., Polo, G., Klinger, H., Adamec, D., Broussolle, E., and Thobois, S.
- Published
- 2009
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3. Subthalamic nucleus stimulation in Parkinson’s disease: Anatomical and electrophysiological localization of active contacts
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Godinho, F., Thobois, S., Magnin, M., Guenot, M., Polo, G., Benatru, I., Xie, J., Salvetti, A., Garcia-Larrea, L., Broussolle, E., and Mertens, P.
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- 2006
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4. Chronic subthalamic nucleus stimulation and striatal D2 dopamine receptors in Parkinson’s disease: A[11C]-raclopride PETstudy
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Thobois, S., Fraix, V., Savasta, M., Costes, N., Pollak, P., Mertens, P., Koudsie, A., Le Bars, D., Benabid, A. L., and Broussolle, E.
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- 2003
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5. Neurostimulation for Parkinson's Disease with Early Motor Complications
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Schuepbach, W.M., Rau, J., Knudsen, K., Volkmann, J., Krack, P., Timmermann, L., Halbig, T.D., Hesekamp, H., Navarro, S.M., Meier, N., Falk, D., Mehdorn, M., Paschen, S., Maarouf, M., Barbe, M.T., Fink, G.R., Kupsch, A., Gruber, D., Schneider, G.H., Seigneuret, E., Kistner, A., Chaynes, P., Ory-Magne, F., Brefel Courbon, C., Vesper, J., Schnitzler, A., Wojtecki, L., Houeto, J.L., Bataille, B., Maltete, D., Damier, P., Raoul, S., Sixel-Doering, F., Hellwig, D., Gharabaghi, A., Kruger, R., Pinsker, M.O., Amtage, F., Regis, J.M., Witjas, T., Thobois, S., Mertens, P., Kloss, M., Hartmann, A., Oertel, W.H., Post, B., Speelman, H., Agid, Y., Schade-Brittinger, C., Deuschl, G., Neurology, Krack, Paul, and Diener, Hans Christoph (Beitragende*r)
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Adult ,Male ,medicine.medical_specialty ,Parkinson's disease ,DCN MP - Plasticity and memory ,medicine.medical_treatment ,Medizin ,Electric Stimulation Therapy ,610 Medicine & health ,Implantable Neurostimulators/adverse effects ,law.invention ,Antiparkinson Agents ,Randomized controlled trial ,Quality of life ,Subthalamic Nucleus ,law ,Surveys and Questionnaires ,Internal medicine ,Activities of Daily Living ,Dopamine Agonists/adverse effects/therapeutic use ,Clinical endpoint ,Humans ,Medicine ,Adverse effect ,Neurostimulation ,Electric Stimulation Therapy/adverse effects ,Dyskinesias ,Quality of Life ,Intention-to-treat analysis ,business.industry ,Parkinson Disease ,General Medicine ,Middle Aged ,medicine.disease ,Combined Modality Therapy ,Intention to Treat Analysis ,Implantable Neurostimulators ,Parkinson Disease/drug therapy/physiopathology/*therapy ,Treatment Outcome ,Dyskinesia ,Dopamine Agonists ,Antiparkinson Agents/adverse effects/therapeutic use ,Physical therapy ,Female ,medicine.symptom ,business ,Dyskinesias/etiology - Abstract
Item does not contain fulltext BACKGROUND: Subthalamic stimulation reduces motor disability and improves quality of life in patients with advanced Parkinson's disease who have severe levodopa-induced motor complications. We hypothesized that neurostimulation would be beneficial at an earlier stage of Parkinson's disease. METHODS: In this 2-year trial, we randomly assigned 251 patients with Parkinson's disease and early motor complications (mean age, 52 years; mean duration of disease, 7.5 years) to undergo neurostimulation plus medical therapy or medical therapy alone. The primary end point was quality of life, as assessed with the use of the Parkinson's Disease Questionnaire (PDQ-39) summary index (with scores ranging from 0 to 100 and higher scores indicating worse function). Major secondary outcomes included parkinsonian motor disability, activities of daily living, levodopa-induced motor complications (as assessed with the use of the Unified Parkinson's Disease Rating Scale, parts III, II, and IV, respectively), and time with good mobility and no dyskinesia. RESULTS: For the primary outcome of quality of life, the mean score for the neurostimulation group improved by 7.8 points, and that for the medical-therapy group worsened by 0.2 points (between-group difference in mean change from baseline to 2 years, 8.0 points; P=0.002). Neurostimulation was superior to medical therapy with respect to motor disability (P
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- 2013
6. Molecular analyses of the LRRK2 gene in European and North African autosomal dominant Parkinson's disease
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Lesage, S, Condroyer, C, Lannuzel, A, Lohmann, E, Troiano, A, Tison, F, Damier, P, Thobois, S, Ouvrard-Hernandez, A-M, Rivaud-Péchoux, S, Brefel-Courbon, C, Destée, A, Tranchant, C, Romana, M, Leclere, L, Dürr, A, Brice, A, French Parkinson's Disease Genetics Study Group, Neurologie et thérapeutique expérimentale, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR70-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Neurologie, CHU Pointe-à-Pitre/Abymes [Guadeloupe], Service de neurologie, Hôpital Haut-Lévêque [CHU Bordeaux], CHU Bordeaux [Bordeaux]-CHU Bordeaux [Bordeaux], Clinique neurologique, Hôpital Laennec, Service de neurologie C [Hôpital Pierre Wertheimer - HCL], Hôpital neurologique et neurochirurgical Pierre Wertheimer [CHU - HCL], Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Département de neurologie, Université Joseph Fourier - Grenoble 1 (UJF)-CHU Grenoble, Centre d'investigation clinique de Toulouse (CIC 1436), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Pôle Santé publique et médecine publique [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Service de neurochirurgie générale et stéréotaxique fonctionnelle, Hôpital Roger Salengro [Lille]-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Service de Neurologie [Strasbourg], CHU Strasbourg-Hopital Civil, Pharmacogénétique et abords thérapeutiques des maladies héréditaires, Université des Antilles et de la Guyane (UAG)-Université Paris Diderot - Paris 7 (UPD7)-IFR2-Institut National de la Santé et de la Recherche Médicale (INSERM), Université des Antilles et de la Guyane (UAG), French Parkinson's Disease Genetics Study Group, ANR-05-NEUR-0019,LRRK2 in PD,Pathologie moléculaire et modèles murins du gène LRRK2, impliqué dans la maladie de Parkinson(2005), Pollak, Pierre, Fédération des Maladies du Système Nerveux, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Pôle Santé publique et médecine publique [CHU Toulouse], Service de Génétique Cytogénétique et Embryologie [CHU Pitié-Salpêtrière], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Savasta, Marc, Neurosciences, neurologie et psychiatrie - Pathologie moléculaire et modèles murins du gène LRRK2, impliqué dans la maladie de Parkinson - - LRRK2 in PD2005 - ANR-05-NEUR-0019 - NEURO - VALID, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR70-Université Pierre et Marie Curie - Paris 6 (UPMC), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)
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Male ,Proband ,MESH: Chi-Square Distribution ,Parkinson's disease ,DNA Mutational Analysis ,[SDV.GEN] Life Sciences [q-bio]/Genetics ,medicine.disease_cause ,Exon ,MESH: Aged, 80 and over ,0302 clinical medicine ,Gene Frequency ,European Continental Ancestry Group/genetics ,MESH: DNA Mutational Analysis ,Genetics (clinical) ,Aged, 80 and over ,MESH: Aged ,Genetics ,LRRK2 Gene ,0303 health sciences ,Mutation ,MESH: Middle Aged ,MESH: European Continental Ancestry Group ,Middle Aged ,LRRK2 ,Pedigree ,3. Good health ,Female ,Adult ,MESH: Mutation ,Adolescent ,MESH: Pedigree ,Protein-Serine-Threonine Kinases/genetics ,DNA Mutational Analysis/methods ,Black People ,Protein Serine-Threonine Kinases ,Parkinsonian Disorders/diagnosis/genetics ,Biology ,Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 ,White People ,MESH: Protein-Serine-Threonine Kinases ,03 medical and health sciences ,Parkinsonian Disorders ,MESH: Analysis of Variance ,MESH: Gene Frequency ,medicine ,Humans ,Gene ,Allele frequency ,Aged ,030304 developmental biology ,MESH: Adolescent ,Analysis of Variance ,[SDV.GEN]Life Sciences [q-bio]/Genetics ,Chi-Square Distribution ,MESH: Humans ,MESH: Parkinsonian Disorders ,African Continental Ancestry Group/genetics ,MESH: Adult ,medicine.disease ,MESH: Male ,ddc:616.8 ,nervous system diseases ,MESH: African Continental Ancestry Group ,MESH: Female ,030217 neurology & neurosurgery - Abstract
International audience; BACKGROUND: Mutations in the leucine-rich-repeat kinase 2 (LRRK2) gene have been identified in families with autosomal dominant Parkinson's disease (ADPD), the most common of which is the p.G2019S substitution that has been found at varying frequencies worldwide. Because of the size of the LRRK2 gene, few studies have analysed the entire gene in large series of ADPD families. METHODS: We performed extensive mutation analyses of all 51 coding exons of the LRRK2 gene in index cases from 226 Parkinson's disease families compatible with autosomal dominant inheritance, mostly from France (n = 182) and North Africa (n = 14). RESULTS: We found 79 sequence variants, 29 of which were novel. Eight potentially or proven pathogenic mutations were found in 22 probands (9.7%). There were four novel amino acid substitutions that are potentially pathogenic (p.S52F, p.N363S, p.I810V, p.R1325Q) and two novel variants, p.H1216R and p.T1410M, that are probably not causative. The common p.G2019S mutation was identified in 13 probands (5.8%) including six from North Africa (43%). The known heterozygous p.R1441H and p.I1371V mutations were found in two probands each, and the p.E334K variant was identified in one single patient. Most potentially or proven pathogenic mutations were located in the functional domains of the Lrrk2 protein. CONCLUSION: This study leads us to conclude that LRRK2 mutations are a common cause of autosomal dominant Parkinson's disease in Europe and North Africa.
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- 2009
7. Motor urgency is mediated by the contralateral cerebellum in Parkinson's disease.
- Author
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Ballanger, B., Baraduc, P., Broussolle, E., Le Bars, D., Desmurget, M., and Thobois, S.
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MOTOR ability ,CEREBELLUM ,PARKINSON'S disease ,PSYCHOLOGICAL stress ,MENTAL health ,CEREBRAL cortex - Abstract
Background: In patients with Parkinson's disease (PD), motor performance may be dramatically improved in urgent and stressful situations. Objective: The aim of this PET H
2 15 0 study was to determine the changes in brain activation pattern related to this unconscious increase in motor speed observed in the context of urgency in patients with PD. Methods: Eight right-handed patients with PD, who had been off medication for at least 12 hours, without tremor, were enrolled. A reaching task with the right hand was performed under three conditions: self-initiated (SI), externally cued (EC) and externally cued-urgent (ECu). Results: (1) Self-initiated movements (SI-EC) revealed activations in the prefrontal cortex bilaterally, the right lateral premotor cortex, anterior cingulate cortex and cerebellum, and the left primary motor cortex and thalamus; (2) Externally driven responses (EC-SI) did not involve any statistically detectable activation; (3) Urgent situations (ECu-EC) engaged the left cerebellum. Compared with a control group previously studied, the cerebellar activation was greater in patients with PD. Conclusions: This study demonstrates that the increase in movement speed in urgent situations in patients with PD is associated with the recruitment of the left (contralateral) cerebellum. This structure is a key node of the accessory motor circuitry typically recruited by patients with PD to compensate for basal ganglia dysfunction and by healthy subjects to increase movement velocity in urgent motor contexts. [ABSTRACT FROM AUTHOR]- Published
- 2008
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8. Manic behaviour induced by deep-brain stimulation in Parkinson's disease: evidence of substantia nigra implication?
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Ulla, M., Thobois, S., Lemaire, J.-J., Schmitt, A., Derost, P., Broussolle, E., Llorca, P.-M., and Durif, F.
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BRAIN stimulation , *PARKINSON'S disease , *SUBSTANTIA nigra , *SUBTHALAMUS , *MANIA , *POSITRON emission tomography - Abstract
We report the case of a patient who had benefited from bilateral subthalamic nucleus deep brain stimulation for Parkinson's disease and who presented acute and reproducible manic behaviour when stimulated mainly in the substantia nigra. A positron emission tomography scan showed an activation of the right dorsolateral prefrontal and inferior temporal cortex, the left anterior cingulate cortex and a deactivation of the left insula. This suggests that changes in cortical activation related to mania are subcortically driven, involving notably the substantia nigra. [ABSTRACT FROM AUTHOR]
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- 2006
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9. PET and SPECT functional imaging studies in Parkinsonian syndromes: from the lesion to its consequences
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Thobois, S., Jahanshahi, M., Pinto, S., Frackowiak, R., and Limousin-Dowsey, P.
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PARKINSON'S disease , *SYMPTOMS , *PATIENTS , *THERAPEUTICS - Abstract
Functional imaging techniques provide major insights into understanding the pathophysiology, progression, complications, and differential diagnosis of Parkinson''s disease (PD). The dopaminergic system has been particularly studied allowing now early, presymptomatic diagnoses, which is of interest for future neuroprotective strategies. The existence of a compensatory hyperactivity of dopa-decarboxylase at disease onset has been recently demonstrated in the nigrostriatal and also extrastriatal dopaminergic pathways. Modification of dopamine receptors expression is observed during PD, but the respective contribution of dopaminergic drugs and the disease process towards these changes is still debated. Abnormalities of cerebral activation are seen and are clearly task-dependent, but the coexistence of hypoactivation in some areas and hyperactivation in others is also now well established. Such hyperactivation may be compensatory but could also reflect an inability to select appropriate motor circuits and inhibit inappropriate ones by PD patients. Interestingly, dopaminergic medications or surgical therapy reverse such abnormalities of brain activation. [Copyright &y& Elsevier]
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- 2004
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10. Subthalamic nucleus stimulation in Parkinson's disease : Clinical evaluation of 18 patients.
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Thobois, S., Mertens, P., Guenot, M., Hermier, M., Mollion, H., Bouvard, M., Chazot, G., Broussolle, E., and Sindou, M.
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PARKINSON'S disease ,NEURAL stimulation ,BRAIN stimulation ,SUBTHALAMUS ,BRAIN surgery ,MOVEMENT disorders - Abstract
The aim of the present study was to assess the efficacy and safety of chronic subthalamic nucleus deep-brain stimulation (STN-DBS) in patients with Parkinson's disease (PD). 18 consecutive severely affected PD patients were included (mean age, SD: 56.9±6 years; mean disease duration: 13.5±4.4 years). All the patients were evaluated clinically before and 6 months after the surgical procedure using the Unified Parkinson's Disease Rating Scale (UPDRS). Additionally, a 12 months follow-up was available in 14 patients. The target coordinates were determined by ventriculography under stereotactic conditions, followed by electrophysiology and intraoperative stimulation. After surgery, continuous monopolar stimulation was applied bilaterally in 17 patients at 2.9±0.4 V through 1 (n = 31) or 2 contacts (n = 3). One patient had bilateral bipolar stimulation. The mean frequency of stimulation was 140±16 Hz and pulse width 68±13 μs. Off medication, the UPDRS part III score (max = 108) was reduced by 55 % during on stimulation (score before surgery: 44.9±13.4 vs at 6 months: 20.2±10; p < 0.001). In the on medication state, no difference was noted between the preoperative and the postoperative off stimulation conditions (scores were respectively: 17.9±9.2 and 23±12.6). The severity of motor fluctuations and dyskinesias assessed by UPDRS IV was reduced by 76 % at 6 months (scores were respectively: 10.3±3 and 2.5±3; p < 0.001). Off medication, the UPDRS II or ADL score was reduced by 52.8 % during on stimulation (26.9±6.5 preop versus 12.7±7 at 6 months). The daily dose of antiparkinsonian treatment was diminished by 65.5 % (levodopa equivalent dose – mg/D – was 1045 ± 435 before surgery and 360 ± 377 at 6 months; p < 0.01). These results remained stable at 12 months for the 14 patients studied. Side effects comprised lower limb phlebitis (n = 2), pulmonary embolism (n = 1), depression (n = 6), dysarthria and freezing (n = 1), sialorrhea and drooling (n = 1), postural imbalance (n = 1), transient paresthesias and dyskinesias. This study confirms the great value of subthalamic nucleus stimulation in the treatment of intractable PD. Some adverse events such as depression may be taken into account in the inclusion criteria and also in the post-operative outcome. [ABSTRACT FROM AUTHOR]
- Published
- 2002
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11. P.322 Progression of dopaminergic and serotonergic dysfunction related to neuropsychiatric signs in Parkinson's disease.
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Prange, S., Metereau, E., Klinger, H., Schmitt, E., Lhommée, E., Bichon, A., Le Bars, D., Maillet, A., Pelissier, P., Meoni, S., Broussolle, E., Castrioto, A., Krack, P., and Thobois, S.
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PARKINSON'S disease , *RAPHE nuclei , *SEROTONIN transporters - Abstract
B Background: b De novo parkinsonian patients with apathy, depression and anxiety exhibit profound serotonergic dysfunction and microstructural disarray in the limbic system in comparison to non-apathetic parkinsonian patients. B Results: b Eleven patients with apathy and 11 patients without apathy at diagnosis completed the follow-up evaluation at median (IQR) 4.3 (0.6) years after diagnosis. Apathy, depression, anxiety and fatigue improved in apathetic parkinsonian patients over time, whereas these symptoms worsened in non apathetic parkinsonian patients (p<0.001). [Extracted from the article]
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- 2020
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12. Possible Parkinson's disease revealed by a pure head resting tremor
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Gan, J., Xie-Brustolin, J., Gervais-Bernard, H., Vallet, A.E., Broussolle, E., and Thobois, S.
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PARKINSON'S disease diagnosis , *TREMOR , *HEAD diseases , *DOPA , *FOLLOW-up studies (Medicine) , *PHOTON emission , *POSITRON emission tomography , *THERAPEUTICS - Abstract
Abstract: Head tremor is very unusual in Parkinson''s disease (PD). Five PD patients presenting a head tremor during the disease evolution have recently been reported. Here we describe a 74 year-old woman with a pure head resting tremor. The tremor was responsive to levodopa and had a 4.7 Hz frequency. A [123I]FP-CIT SPECT imaging confirmed a reduction of tracer uptake in the right striatum consistent with PD, that should be confirmed by long-term follow-up. [Copyright &y& Elsevier]
- Published
- 2009
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13. Microstructural changes in white and grey matter related to apathy, depression and anxiety in de novo Parkinson's disease patients.
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Prange, S., Metereau, E., Maillet, A., Lhommée, E., Klinger, H., Pellissier, P., Ibarrola, D., Heckemann, R.A., Broussolle, E., Castrioto, A., Tremblay, L., Sgambato, V., Krack, P., and Thobois, S.
- Subjects
- *
APATHY , *PARKINSON'S disease - Published
- 2019
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