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3. Prognosis of impulse control disorders in Parkinson’s disease: a prospective controlled study

Author

Wirth, Thomas, Goetsch, Thibaut, Corvol, Jean-Christophe, Roze, Emmanuel, Mariani, Louise-Laure, Vidailhet, Marie, Grabli, David, Mallet, Luc, Pelissolo, Antoine, Rascol, Olivier, Brefel-Courbon, Christine, Ory-Magne, Fabienne, Arbus, Christophe, Bekadar, Samir, Krystkowiak, Pierre, Marques, Ana, Llorca, Michel, Krack, Paul, Castrioto, Anna, Fraix, Valérie, Maltete, David, Defebvre, Luc, Kreisler, Alexandre, Houeto, Jean-Luc, Tranchant, Christine, Meyer, Nicolas, and Anheim, Mathieu

Published
2024
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4. Clinical and genetic keys to cerebellar ataxia due to FGF14 GAA expansions

Author

Méreaux, Jean-Loup, Davoine, Claire-Sophie, Pellerin, David, Coarelli, Giulia, Coutelier, Marie, Ewenczyk, Claire, Monin, Marie-Lorraine, Anheim, Mathieu, Le Ber, Isabelle, Thobois, Stéphane, Gobert, Florent, Guillot-Noël, Léna, Forlani, Sylvie, Jornea, Ludmila, Heinzmann, Anna, Sangare, Aude, Gaymard, Bertrand, Guyant-Maréchal, Lucie, Charles, Perrine, Marelli, Cecilia, Honnorat, Jérôme, Degos, Bertrand, Tison, François, Sangla, Sophie, Simonetta-Moreau, Marion, Salachas, François, Tchikviladzé, Maya, Castelnovo, Giovanni, Mochel, Fanny, Klebe, Stephan, Castrioto, Anna, Fenu, Silvia, Méneret, Aurélie, Bourdain, Frédéric, Wandzel, Marion, Roth, Virginie, Bonnet, Céline, Riant, Florence, Stevanin, Giovanni, Noël, Sandrine, Fauret-Amsellem, Anne-Laure, Bahlo, Melanie, Lockhart, Paul J., Brais, Bernard, Renaud, Mathilde, Brice, Alexis, and Durr, Alexandra

Published
2024
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6. Hoehn and Yahr Stage and Striatal Dat-SPECT Uptake Are Predictors of Parkinson’s Disease Motor Progression

Author

Jackson, Holly, Anzures-Cabrera, Judith, Taylor, Kirsten I, Pagano, Gennaro, Investigators, PASADENA, Group, Prasinezumab Study, Altendorf, Claudia, Anandan, Chareyna, Andrews, Giulia, Ansquer, Solène, Arrouasse, Raphaele, Aslam, Sana, Azulay, Jean-Philippe, Baker, Jeanette, Martinez, Ernest Balaguer, Barbu, Shadi, Bardram, Kara, Bega, Danny, Marco, Helena Bejr-Kasem, Benatru, Isabelle, Benchetrit, Eve, Bernhard, Felix, Besharat, Amir, Bette, Sagari, Bichon, Amelie, Billnitzer, Andrew, Blondeau, Sophie, Boraud, Thomas, Borngräber, Freiderike, Boyd, James, Brockmann, Kathrin, Brodsky, Matthew, Brown, Ethan, Bruecke, Christof, Calvas, Fabienne, Canelo, Monica, Carbone, Federico, Carroll, Claire, Fernandez, Laura Casado, Cassé-Perrot, Catherine, Castrioto, Anna, Catala, Helene, Chan, Justine, Cheriet, Samia, Ciabarra, Anthony, Classen, Joseph, Coleman, Juliana, Coleman, Robert, Compta, Yaroslau, Corbillé, Anne-Gaëlle, Corvol, Jean-Christophe, Cosgaya, Mariana, Dahodwala, Nabila, Damier, Philippe, David, Elodie, Davis, Thomas, Dean, Marissa, Debilly, Berengere, DeGiorgio, Janell, Deik, Andres, Delaby, Laure, Delfini, Marie-Helene, Derkinderen, Pascal, Derost, Philipp, de Toledo, Maria, Deuel, Lisa, Diaz-Hernandez, Ann Marie, Dietiker, Cameron, Dimenshteyn, Karina, Dotor, Julio, Durif, Franck, Ebentheuer, Jens, Eggert, Karla Maria, Madueño, Sara Eichau, Eickhoff, Claudia, Ellenbogen, Aaron, Ellmerer, Philipp, Vazquez, Ines Esparragosa, Eusebio, Alexandre, Ewert, Siobhan, Fang, John, Feigenbaum, Danielle, Fluchere, Frederique, Foubert-Samier, Alexandra, Fournier, Marie, Fradet, Anne, Fraix, Valerie, Frank, Samuel, Fries, Franca, Galitzky, Monique, Pérez, Marisol Gallardó, Moreno, Jose Manuel García, Gasca, Carmen, Gasser, Thomas, Gibbons, Joyce, Giordana, Caroline, Martinez, Alicia Gonzalez, Goodman, Ira, Gorospe, Arantza, and Goubeaud, Marie

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Psychology, Biomedical Imaging, Parkinson's Disease, Brain Disorders, Clinical Research, Aging, Neurosciences, Neurodegenerative, Clinical Trials and Supportive Activities, Neurological, PASADENA Investigators, Prasinezumab Study Group, Dat-SPECT imaging, MDS-UPDRS, PASADENA, PPMI, Parkinson’s disease, disease stage, progression predictors, ridge regression, Cognitive Sciences, Biological psychology
Abstract

Currently, no treatments available for Parkinson's disease (PD) can slow PD progression. At the early stage of the disease, only a subset of individuals with PD progress quickly, while the majority have a slowly progressive form of the disease. In developing treatments that aim to slow PD progression, clinical trials aim to include individuals who are likely to progress faster, such that a treatment effect, if one exists, can be identified easier and earlier. The aim of the present study was to identify baseline predictors of clinical progression in early PD. We analyzed 12-month data acquired from the PASADENA trial Part 1 (NCT03100149, n = 76 participants who were allocated to the placebo arm and did not start symptomatic therapy) and the Parkinson's Progression Markers Initiative (PPMI) study (n = 139 demographically and clinically matched participants). By using ridge regression models including clinical characteristics, imaging, and non-imaging biomarkers, we found that Hoehn and Yahr stage and dopamine transporter single-photon emission computed tomography specific binding ratios (Dat-SPECT SBR) in putamen ipsilateral to the side of motor symptom onset predicted PD progression at the early stage of the disease. Further studies are needed to confirm the validity of these predictors to identify with high accuracy individuals with early PD with a faster progression phenotype.

Published
2021

7. A Phase II Study to Evaluate the Safety and Efficacy of Prasinezumab in Early Parkinson's Disease (PASADENA): Rationale, Design, and Baseline Data

Author

Pagano, Gennaro, Boess, Frank G, Taylor, Kirsten I, Ricci, Benedicte, Mollenhauer, Brit, Poewe, Werner, Boulay, Anne, Anzures-Cabrera, Judith, Vogt, Annamarie, Marchesi, Maddalena, Post, Anke, Nikolcheva, Tania, Kinney, Gene G, Zago, Wagner M, Ness, Daniel K, Svoboda, Hanno, Britschgi, Markus, Ostrowitzki, Susanne, Simuni, Tanya, Marek, Kenneth, Koller, Martin, Sevigny, Jeff, Doody, Rachelle, Fontoura, Paulo, Umbricht, Daniel, Bonni, Azad, Investigators, PASADENA, Group, Prasinezumab Study, Altendorf, Claudia, Anandan, Chareyna, Andrews, Giulia, Ansquer, Solène, Arrouasse, Raphaele, Aslam, Sana, Azulay, Jean-Philippe, Baker, Jeanette, Martinez, Ernest Balaguer, Barbu, Shadi, Bardram, Kara, Bega, Danny, Marco, Helena Bejr-Kasem, Benatru, Isabelle, Benchetrit, Eve, Bernhard, Felix, Besharat, Amir, Bette, Sagari, Bichon, Amelie, Billnitzer, Andrew, Blondeau, Sophie, Boraud, Thomas, Borngräber, Freiderike, Boyd, James, Brockmann, Kathrin, Brodsky, Matthew, Brown, Ethan, Bruecke, Christof, Calvas, Fabienne, Canelo, Monica, Carbone, Federico, Carroll, Claire, Fernandez, Laura Casado, Cassé-Perrot, Catherine, Castrioto, Anna, Catala, Helene, Chan, Justine, Cheriet, Samia, Ciabarra, Anthony, Classen, Joseph, Coleman, Juliana, Coleman, Robert, Compta, Yaroslau, Corbillé, Anne-Gaëlle, Corvol, Jean-Christophe, Cosgaya, Mariana, Dahodwala, Nabila, Damier, Philippe, David, Elodie, Davis, Thomas, Dean, Marissa, Debilly, Berengere, DeGiorgio, Janell, Deik, Andres, Delaby, Laure, Delfini, Marie-Helene, Derkinderen, Pascal, Derost, Philipp, de Toledo, Maria, Deuel, Lisa, Diaz-Hernandez, Ann Marie, Dietiker, Cameron, Dimenshteyn, Karina, Dotor, Julio, Durif, Franck, Ebentheuer, Jens, Eggert, Karla Maria, Madueño, Sara Eichau, Eickhoff, Claudia, Ellenbogen, Aaron, Ellmerer, Philipp, and Vazquez, Ines Esparragosa

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Neurodegenerative, Parkinson's Disease, Clinical Research, Neurosciences, Aging, Clinical Trials and Supportive Activities, Brain Disorders, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Neurological, PASADENA Investigators, Prasinezumab Study Group, MDS-UPDRS = Movement Disorder Society—Unified Parkinson's Disease Rating Scale, Parkinson's disease, Phase II clinical trial, alpha-synuclein, disease modification treatments, disease progression, monoclonal antibodies, prasinezumab, Psychology, Clinical sciences, Biological psychology
Abstract

Background: Currently available treatments for Parkinson's disease (PD) do not slow clinical progression nor target alpha-synuclein, a key protein associated with the disease. Objective: The study objective was to evaluate the efficacy and safety of prasinezumab, a humanized monoclonal antibody that binds aggregated alpha-synuclein, in individuals with early PD. Methods: The PASADENA study is a multicenter, randomized, double-blind, placebo-controlled treatment study. Individuals with early PD, recruited across the US and Europe, received monthly intravenous doses of prasinezumab (1,500 or 4,500 mg) or placebo for a 52-week period (Part 1), followed by a 52-week extension (Part 2) in which all participants received active treatment. Key inclusion criteria were: aged 40-80 years; Hoehn & Yahr (H&Y) Stage I or II; time from diagnosis ≤2 years; having bradykinesia plus one other cardinal sign of PD (e.g., resting tremor, rigidity); DAT-SPECT imaging consistent with PD; and either treatment naïve or on a stable monoamine oxidase B (MAO-B) inhibitor dose. Study design assumptions for sample size and study duration were built using a patient cohort from the Parkinson's Progression Marker Initiative (PPMI). In this report, baseline characteristics are compared between the treatment-naïve and MAO-B inhibitor-treated PASADENA cohorts and between the PASADENA and PPMI populations. Results: Of the 443 patients screened, 316 were enrolled into the PASADENA study between June 2017 and November 2018, with an average age of 59.9 years and 67.4% being male. Mean time from diagnosis at baseline was 10.11 months, with 75.3% in H&Y Stage II. Baseline motor and non-motor symptoms (assessed using Movement Disorder Society-Unified Parkinson's Disease Rating Scale [MDS-UPDRS]) were similar in severity between the MAO-B inhibitor-treated and treatment-naïve PASADENA cohorts (MDS-UPDRS sum of Parts I + II + III [standard deviation (SD)]; 30.21 [11.96], 32.10 [13.20], respectively). The overall PASADENA population (63.6% treatment naïve and 36.4% on MAO-B inhibitor) showed a similar severity in MDS-UPDRS scores (e.g., MDS-UPDRS sum of Parts I + II + III [SD]; 31.41 [12.78], 32.63 [13.04], respectively) to the PPMI cohort (all treatment naïve). Conclusions: The PASADENA study population is suitable to investigate the potential of prasinezumab to slow disease progression in individuals with early PD. Trial Registration: NCT03100149.

Published
2021

8. Imbalanced motivated behaviors according to motor sign asymmetry in drug-naïve Parkinson’s disease

Author

Béreau, Matthieu, Castrioto, Anna, Servant, Mathieu, Lhommée, Eugénie, Desmarets, Maxime, Bichon, Amélie, Pélissier, Pierre, Schmitt, Emmanuelle, Klinger, Hélène, Longato, Nadine, Phillipps, Clélie, Wirth, Thomas, Fraix, Valérie, Benatru, Isabelle, Durif, Franck, Azulay, Jean-Philippe, Moro, Elena, Broussolle, Emmanuel, Thobois, Stéphane, Tranchant, Christine, Krack, Paul, and Anheim, Mathieu

Published
2023
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9. Intermediate repeat expansions of TBP and STUB1: Genetic modifier or pure digenic inheritance in spinocerebellar ataxias?

Author

Barbier, Mathieu, Davoine, Claire-Sophie, Petit, Emilien, Porché, Maximilien, Guillot-Noel, Léna, Sayah, Sabrina, Fauret, Anne-Laure, Neau, Jean-Philippe, Guyant-Maréchal, Lucie, Deffond, Didier, Tranchant, Christine, Goizet, Cyril, Coarelli, Giulia, Castrioto, Anna, Klebe, Stephan, Ewenczyk, Claire, Heinzmann, Anna, Charles, Perrine, Tchikviladzé, Maya, Van Broeckhoven, Christine, Brice, Alexis, and Durr, Alexandra

Published
2023
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11. High rate of hypomorphic variants as the cause of inherited ataxia and related diseases: study of a cohort of 366 families

Author

Benkirane, Mehdi, Marelli, Cecilia, Guissart, Claire, Roubertie, Agathe, Ollagnon, Elizabeth, Choumert, Ariane, Fluchère, Frédérique, Magne, Fabienne Ory, Halleb, Yosra, Renaud, Mathilde, Larrieu, Lise, Baux, David, Patat, Olivier, Bousquet, Idriss, Ravel, Jean-Marie, Cuntz-Shadfar, Danielle, Sarret, Catherine, Ayrignac, Xavier, Rolland, Anne, Morales, Raoul, Pointaux, Morgane, Lieutard-Haag, Cathy, Laurens, Brice, Tillikete, Caroline, Bernard, Emilien, Mallaret, Martial, Carra-Dallière, Clarisse, Tranchant, Christine, Meyer, Pierre, Damaj, Lena, Pasquier, Laurent, Acquaviva, Cecile, Chaussenot, Annabelle, Isidor, Bertrand, Nguyen, Karine, Camu, William, Eusebio, Alexandre, Carrière, Nicolas, Riquet, Audrey, Thouvenot, Eric, Gonzales, Victoria, Carme, Emilie, Attarian, Shahram, Odent, Sylvie, Castrioto, Anna, Ewenczyk, Claire, Charles, Perrine, Kremer, Laurent, Sissaoui, Samira, Bahi-buisson, Nadia, Kaphan, Elsa, Degardin, Adrian, Doray, Bérénice, Julia, Sophie, Remerand, Ganaëlle, Fraix, Valerie, Haidar, Lydia Abou, Lazaro, Leila, Laugel, Vincent, Villega, Frederic, Charlin, Cyril, Frismand, Solène, Moreira, Marinha Costa, Witjas, Tatiana, Francannet, Christine, Walther-Louvier, Ulrike, Fradin, Mélanie, Chabrol, Brigitte, Fluss, Joel, Bieth, Eric, Castelnovo, Giovanni, Vergnet, Sylvain, Meunier, Isabelle, Verloes, Alain, Brischoux-Boucher, Elise, Coubes, Christine, Geneviève, David, Lebouc, Nicolas, Azulay, Jean Phillipe, Anheim, Mathieu, Goizet, Cyril, Rivier, François, Labauge, Pierre, Calvas, Patrick, and Koenig, Michel

Published
2021
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13. De novo and inherited monoallelic variants in TUBA4A cause ataxia and spasticity.

Author

Benkirane, Mehdi, Bonhomme, Marion, Morsy, Heba, Safgren, Stephanie L, Marelli, Cecilia, Chaussenot, Annabelle, Smedley, Damian, Cipriani, Valentina, Sainte-Agathe, Jean-Madeleine de, Ding, Can, Larrieu, Lise, Vestito, Letizia, Margot, Henri, Lesca, Gaetan, Ramond, Francis, Castrioto, Anna, Baux, David, Verheijen, Jan, Sansa, Emna, and Giunti, Paola

Subjects
CEREBELLAR ataxia, FRIEDREICH'S ataxia, AMYOTROPHIC lateral sclerosis, FRONTOTEMPORAL dementia, MISSENSE mutation
Abstract

Alpha-tubulin 4A encoding gene (TUBA4A) has been associated with familial amyotrophic lateral sclerosis and frontotemporal dementia, based on identification of likely pathogenic variants in patients from distinct amyotrophic lateral sclerosis and frontotemporal dementia cohorts. By screening a multicentric French cohort of 448 unrelated probands presenting with cerebellar ataxia, we identified ultra-rare TUBA4A missense variants, all being absent from public databases and predicted pathogenic by multiple in silico tools. In addition, gene burden analyses in the 100 000 Genomes project (100KGP) showed enrichment of TUBA4A rare variants in the inherited ataxia group compared to controls [odds ratio: 57.0847 (10.2−576.7); P = 4.02 ×10−7]. Taken together, we report 12 patients presenting with spasticity and/or cerebellar ataxia and harbouring a predicted pathogenic TUBA4A missense mutation, including five confirmed de novo cases and a mutation previously reported in a large family presenting with spastic ataxia. Cultured fibroblasts from three patients harbouring distinct TUBA4A missense showed significant alterations in microtubule organization and dynamics, providing insight of TUBA4A variants pathogenicity. Our data confirm the identification of a hereditary spastic ataxia disease gene with variable age of onset, expanding the clinical spectrum of TUBA4A associated phenotypes. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Early cognitive decline after bilateral subthalamic deep brain stimulation in Parkinson's disease patients with GBA mutations

Author

Benchetrit, Eve, Delaby, Laure, Berthet, Deborah, Danjou, Fabrice, Vidaihlet, Marie, Krack, Paul, Pelissier, Pierre, Morand, Dominique, Delaigue, Christine, Barun, Nadia, Anheim, Mathieu, Pleuvret, Marie, Destée, Alain, Defebvre, Luc, Moreau, Caroline, Simonin, Clémence, Ryckewaert, Gilles, Kreisler, Alexandre, Mutez, Eugénie, Carrière, Nicolas, Hopes, Lucie, Tard, Céline, Grolez, Guillaume, Dujardin, Kathy, Pecheux, Nathalie, Delliaux, Marie, Rolland, Anne-Sophie, Broussolle, Emmanuel, Laurencin, Chloè, Tison, François, Burbaud, Pierre, Mangone, Graziella, Bekadar, Samir, Cormier-Dequaire, Florence, Tahiri, Khadija, Welaratne, Arlette, Czernecki, Virginie, Pineau, Fanny, Karachi, Carine, Castrioto, Anna, Durif, Frank, Tranchant, Christine, Devos, David, Thobois, Stéphane, Meissner, Wassilios G, Navarro, Maria Soledad, Cornu, Philippe, Lesage, Suzanne, Brice, Alexis, Welter, Marie Laure, and Corvol, Jean-Christophe

Published
2020
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15. Disentangling Bradykinesia and Rigidity in Parkinson Disease: Evidence from Short‐ and Long‐Term Subthalamic Nucleus Deep Brain Stimulation

Author

Zampogna, Alessandro, primary, Suppa, Antonio, additional, Bove, Francesco, additional, Cavallieri, Francesco, additional, Castrioto, Anna, additional, Meoni, Sara, additional, Pelissier, Pierre, additional, Schmitt, Emmanuelle, additional, Chabardes, Stephan, additional, Fraix, Valerie, additional, and Moro, Elena, additional

Published
2024
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23. Spatiotemporal Gait Differences before and after Botulinum Toxin in People with Focal Dystonia: A Pilot Study.

Author

Cuinat, Justine, Debû, Bettina, Meoni, Sara, Pelissier, Pierre, Castrioto, Anna, Fraix, Valérie, and Moro, Elena

Subjects
FOCAL dystonia, BOTULINUM toxin, BOTULINUM A toxins, GAIT in humans, NONPARAMETRIC statistics
Abstract

Background: The impact of focal dystonia on gait has attracted little attention and remains elusive. Considering the importance of both visual and head control in gait, blepharospasm and cervical dystonia should affect gait. Improvement of cervical/eyelid control following botulinum toxin (BTX) injections would translate into gait changes. Objectives: To assess gait differences in people with focal dystonia before and after BTX treatment. Methods: Ten patients with blepharospasm, 10 patients with cervical dystonia, and 20 healthy age‐ and gender‐matched controls were included. Gait was assessed before and 1‐month after BTX injections using Biodex Gait Trainer™ 3. Gait velocity, cadence, step length, step asymmetry, and variability of step length were compared between patients and controls, and between the two time‐points using non‐parametric statistics. Results: At baseline, compared to controls, cervical dystonia patients showed reduced gait velocity, step length, and cadence. After BTX injections, while gait velocity and step length were significantly increased and step length variability reduced, gait parameters still differed between patients and controls. In blepharospasm patients, baseline gait velocity and step length were significantly smaller than in controls. After BTX injections, these gait parameters were significantly increased and variability decreased, so that patients no longer differed from controls. Conclusion: Gait differences exist between patients with focal dystonia not directly affecting the lower limbs and healthy controls. These gait abnormalities were improved differently by BTX treatment according to the type of dystonia. These disparities suggest different pathophysiological mechanisms and support the need for changes in rehabilitation routines in cervical dystonia. [ABSTRACT FROM AUTHOR]

Published
2024
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24. Imbalanced motivated behaviors according to motor sign asymmetry in drug-naïve Parkinson’s Disease

Author

Béreau, Matthieu, primary, Castrioto, Anna, additional, Servant, Mathieu, additional, Lhommée, Eugénie, additional, Desmarets, Maxime, additional, Bichon, Amélie, additional, Pelissier, Pierre, additional, Schmitt, Emmanuelle, additional, Klinger, Hélène, additional, Longato, Nadine, additional, Phillipps, Clélie, additional, Wirth, Thomas, additional, Fraix, Valérie, additional, Benatru, Isabelle, additional, Durif, Franck, additional, Azulay, Jean-Philippe, additional, Moro, Elena, additional, Broussolle, Emmanuel, additional, Thobois, Stéphane, additional, Tranchant, Christine, additional, Krack, Paul, additional, and Anheim, Mathieu, additional

Published
2023
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25. Fast and reliable detection of repeat expansions in spinocerebellar ataxia using exomes

Author

Méreaux, Jean-Loup, primary, Davoine, Claire-Sophie, additional, Coutelier, Marie, additional, Guillot-Noël, Léna, additional, Castrioto, Anna, additional, Charles, Perrine, additional, Coarelli, Giulia, additional, Ewenczyk, Claire, additional, Klebe, Stephan, additional, Heinzmann, Anna, additional, Méneret, Aurélie, additional, Fauret-Amsellem, Anne-Laure, additional, de Sainte Agathe, Jean-Madeleine, additional, Brice, Alexis, additional, and Durr, Alexandra, additional

Published
2023
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34. Fluctuations in Parkinson's disease and personalized medicine: bridging the gap with the neuropsychiatric fluctuation scale.

Author

Schmitt, Emmanuelle, Debu, Bettina, Castrioto, Anna, Kistner, Andrea, Fraix, Valerie, Bouvard, Martine, and Moro, Elena

Subjects
APATHY, PARKINSON'S disease, INDIVIDUALIZED medicine, CRONBACH'S alpha, PSYCHOMETRICS, PRINCIPAL components analysis
Abstract

Background: Neuropsychiatric fluctuations (NpsyF) are frequent and disabling in people with Parkinson's disease (PD). In OFF-medication, NpsyF entail minus neuropsychiatric symptoms (NPS) like anxiety, apathy, sadness, and fatigue. In ON-medication, NpsyF consist in plus NPS, such as high mood, hypomania, and hyperactivity. Accurate identification of these NpsyF is essential to optimize the overall PD management. Due to lack of punctual scales, the neuropsychiatric fluctuation scale (NFS) has been recently designed to assess NpsyF in real time. The NFS comprises 20 items with two subscores for plus and minus NPS, and a total score. Objective: To evaluate the psychometric properties of the NFS in PD. Methods: PD patients with motor fluctuations and healthy controls (HC) were assessed. In PD patients, the NFS was administrated in both the ON-and OFF- medication conditions, together with the movement disorders society-unified Parkinson disease rating scale parts I--IV. Depression (Beck depression scale II), apathy (Starkstein apathy scale) and non-motor fluctuations items of the Ardouin scale of behaviour in PD (ASBPD OFF and ON items) were also assessed. NFS internal structure was evaluated with principal component analysis consistency (PCA) in both medication conditions in PD patients and before emotional induction in HC. NFS internal consistency was assessed using Cronbach's alpha coefficient. NFS convergent and divergent validity was measured through correlations with BDI- II, Starktein, and ASBPD OFF and ON non motor items. Specificity was assessed comparing NFS global score between the HC and PD populations. Sensitivity was evaluated with t-student test comparing the ON-and the OFF-medication conditions for NFS global score and for minus and plus subscores. Results: In total, 101 consecutive PD patients and 181 HC were included. In PD patients and HC, PCA highlighted one component that explained 32--35 and 42% of the variance, respectively. Internal consistency was good for both the NFS- plus (alpha =0.88) and NFS-minus items (alpha =0.8). The NFS showed a good specifity for PD (p < 0.0001) and a good sensitivity to the medication condition (p < 0.0001). Conclusion: The satisfactory properties of the NFS support its use to assess acute neuropsychiatric fluctuations in PD patients, adding to available tools. [ABSTRACT FROM AUTHOR]

Published
2023
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37. Long‐term independence and quality of life after subthalamic stimulation in Parkinson disease

Author

Castrioto, Anna, primary, Debû, Bettina, additional, Cousin, Emilie, additional, Pelissier, Pierre, additional, Lhommée, Eugénie, additional, Bichon, Amélie, additional, Schmitt, Emmanuelle, additional, Kistner, Andrea, additional, Meoni, Sara, additional, Seigneuret, Eric, additional, Chabardes, Stephan, additional, Krack, Paul, additional, Moro, Elena, additional, and Fraix, Valérie, additional

Published
2022
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38. Does Motor Symptoms Asymmetry Predict Motor Outcome of Subthalamic Deep Brain Stimulation in Parkinson's Disease Patients?

Author

Bove, Francesco, primary, Cavallieri, Francesco, additional, Castrioto, Anna, additional, Meoni, Sara, additional, Schmitt, Emmanuelle, additional, Bichon, Amélie, additional, Lhommée, Eugénie, additional, Pélissier, Pierre, additional, Kistner, Andrea, additional, Chevrier, Eric, additional, Seigneuret, Eric, additional, Chabardès, Stephan, additional, Valzania, Franco, additional, Fraix, Valerie, additional, and Moro, Elena, additional

Published
2022
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39. Fatigue in de novo Parkinson’s Disease: Expanding the Neuropsychiatric Triad?

Author

Béreau, Matthieu, primary, Castrioto, Anna, additional, Lhommée, Eugénie, additional, Maillet, Audrey, additional, Gérazime, Aurélie, additional, Bichon, Amélie, additional, Pélissier, Pierre, additional, Schmitt, Emmanuelle, additional, Klinger, Hélène, additional, Longato, Nadine, additional, Fraix, Valérie, additional, Benatru, Isabelle, additional, Durif, Franck, additional, Azulay, Jean-Philippe, additional, Moro, Elena, additional, Broussolle, Emmanuel, additional, Tranchant, Christine, additional, Anheim, Mathieu, additional, Thobois, Stéphane, additional, and Krack, Paul, additional

Published
2022
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41. Limbic Serotonergic Plasticity Contributes to the Compensation of Apathy in Early Parkinson's Disease

Author

Prange, St��phane, Metereau, Elise, Maillet, Audrey, Klinger, H��l��ne, Schmitt, Emmanuelle, Lhomm��e, Eug��nie, Bichon, Am��lie, Lancelot, Sophie, Meoni, Sara, Broussolle, Emmanuel, Castrioto, Anna, Tremblay, L��on, Krack, Paul, and Thobois, St��phane

Subjects
610 Medicine & health
Abstract

BACKGROUND De novo Parkinson's disease (PD) patients with apathy exhibit prominent limbic serotonergic dysfunction and microstructural disarray. Whether this distinctive lesion profile at diagnosis entails different prognosis remains unknown. OBJECTIVES To investigate the progression of dopaminergic and serotonergic dysfunction and their relation to motor and nonmotor impairment in PD patients with or without apathy at diagnosis. METHODS Thirteen de novo apathetic and 13 nonapathetic PD patients were recruited in a longitudinal double-tracer positron emission tomography cohort study. We quantified the progression of presynaptic dopaminergic and serotonergic pathology using [11 C]PE2I for dopamine transporter and [11 C]DASB for serotonin transporter at baseline and 3 to 5���years later, using linear mixed-effect models and mediation analysis to compare the longitudinal evolution between groups for clinical impairment and region-of-interest-based analysis. RESULTS After the initiation of dopamine replacement therapy, apathy, depression, and anxiety improved at follow-up in patients with apathy at diagnosis (n��=��10) to the level of patients without apathy (n��=��11). Patients had similar progression of motor impairment, whereas mild impulsive behaviors developed in both groups. Striato-pallidal and mesocorticolimbic presynaptic dopaminergic loss progressed similarly in both groups, as did serotonergic pathology in the putamen, caudate nucleus, and pallidum. Contrastingly, serotonergic innervation selectively increased in the ventral striatum and anterior cingulate cortex in apathetic patients, contributing to the reversal of apathy besides dopamine replacement therapy. CONCLUSION Patients suffering from apathy at diagnosis exhibit compensatory changes in limbic serotonergic innervation within 5���years of diagnosis, with promising evidence that serotonergic plasticity contributes to the reversal of apathy. The relationship between serotonergic plasticity and dopaminergic treatments warrants further longitudinal investigations. �� 2022 International Parkinson and Movement Disorder Society.

Published
2022
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42. Maladaptive One-Leg Balance Control in Parkinson’s Disease

Author

Chevrier, Eric, Moro, Elena, Pelissier, Pierre, Castrioto, Anna, Krack, Paul, Fraix, Valérie, and Debû, Bettina

Subjects
Physics and Astronomy (miscellaneous), Chemistry (miscellaneous), General Mathematics, Computer Science (miscellaneous), 610 Medicine & health
Abstract

Balance disorders are very frequent in Parkinson’s disease (PD). One-leg stance performance is a predictor of fall risk. We investigated one-leg stance strategies in people with PD. We hypothesized that patients would choose, and better perform on, the leg on the least affected body side. Fifty participants with 2 to 19 years of PD duration stood on one leg while ON medication. The leg spontaneously chosen was recorded. Performance was compared between the spontaneously chosen vs. contralateral, and most vs. least stable legs. Influence of disease duration, severity, age, cognition, and motor fluctuations was analyzed. Twenty-eight patients spontaneously stood on the leg of the least affected body side, which was not always the most stable one. The chosen standing leg was influenced by disease duration with a switch between the least vs. most affected body side after seven years of disease duration. Fourteen patients (28%) spontaneously stood on their least stable leg. Thus, some patients with PD choose the least stable leg when asked to perform one-leg stance. It is important to identify these patients since they may be at greater risk of falls and/or gait difficulties. Specific rehabilitation may help prevent such maladaptive strategy.

Published
2022
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43. Relevance of corpus callosum splenium versus middle cerebellar peduncle hyperintensity for FXTAS diagnosis in clinical practice

Author

Renaud, Mathilde, Perriard, Julien, Coudray, Sarah, Sévin-Allouet, Mathieu, Marcel, Christophe, Meissner, Wassilios G., Chanson, Jean-Baptiste, Collongues, Nicolas, Philippi, Nathalie, Gebus, Odile, Quenardelle, Véronique, Castrioto, Anna, Krack, Paul, N’Guyen, Karine, Lefebvre, François, Echaniz-Laguna, Andoni, Azulay, Jean-Philippe, Meyer, Nicolas, Labauge, Pierre, Tranchant, Christine, and Anheim, Mathieu

Published
2015
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44. Limbic Serotonergic Plasticity Contributes to the Compensation of Apathy in Early Parkinson's Disease

Author

Prange, Stéphane, primary, Metereau, Elise, additional, Maillet, Audrey, additional, Klinger, Hélène, additional, Schmitt, Emmanuelle, additional, Lhommée, Eugénie, additional, Bichon, Amélie, additional, Lancelot, Sophie, additional, Meoni, Sara, additional, Broussolle, Emmanuel, additional, Castrioto, Anna, additional, Tremblay, Léon, additional, Krack, Paul, additional, and Thobois, Stéphane, additional

Published
2022
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