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2 raisons identifiées
Praticien-chercheur
6 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
146.3 rhumatos / 100 000 hab. — département bien doté
2ans d'exercice (thèse 2024)·22 publications sur 5 ans↗
✨ Génération du profil synthétique IA en cours…
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
Source : catalogue national des thèses theses.fr (ABES). Ne couvre que les doctorats / HDR — les thèses d'exercice (DES) sont archivées dans les SCD universitaires.
Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.
Influence scientifique
5
5 articles ont été cités au moins 5fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.
h-index
Total citations reçues
133
Nombre de fois où d'autres équipes ont mentionné ses publications dans leurs propres travaux.
Publications totales
25
Articles, revues et chapitres référencés dans les bases académiques internationales.
Articles influents
3
Publications ayant marqué leur domaine — chacune citée au moins 10 fois par d'autres chercheurs.
i10-index
Thématiques principales
Affiliations FR : Inserm · Assistance Publique – Hôpitaux de Paris · Centre Hospitalier Régional et Universitaire de Nancy
Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.
Articles déposés en accès libre sur l'archive ouverte des universités françaises (HAL) — gage d'activité de recherche en France.
Non-motor Subtypes in Candidates for Subthalamic Deep Brain Stimulation for Parkinson’s Disease
2025ArticleParkinsonism & Related Disorders
Troubles des métabolismes des monocarbones dans la maladie de Huntington
2024Thèse
Amantadine use in the French prospective NS-Park cohort
2024ArticleJournal of Neural Transmission
Epilepsy in early onset Alzheimer’s disease
2022ArticleJournal of Alzheimer's Disease
Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).
CHRU NANCY - HOPITAL CENTRAL
29 AV DE LATTRE DE TASSIGNY CO 60034, 54035 NANCY CEDEX
Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).
Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
Journal of Alzheimer's disease : JAD · 2022
Background: Epilepsy seems to be an important comorbidity in patients with early onset Alzheimer’s disease (EOAD). Currently, seizures are still underestimated in this population. However, seizures may interact with AD evolution with possible acceleration of cognitive decline. Objective: To better define the epileptic disorders observed in patients with EOAD. Methods: All patients diagnosed as EOAD in our hospital between 2013 and 2019 with positive CSF biomarkers for AD were selected. The usual follow-up was extended with a 3-h EEG and a consultation with an epilepsy expert. Information on epilepsy and AD were collected and analyzed. Results: Among the 25 included patients, 10 (40%) were classified as epileptic. Seizure types were tonic-clonic (25%), typical temporal seizures (25%), myoclonus (25%), focal extra-temporal seizures (8%), and other seizure types (17%). AD-E patients had a significant lower MMSE (15.3±8.4 AD-E versus 22.1±5.1 AD-NE, p = 0.036) and a lower autonomy (IADL 4.1±2.7 AD-E versus 6.4±1.9 AD-NE, p = 0.046) at AD diagnosis with comparable ages between AD-E and AD-NE. Epileptic patients seemed to present a faster cognitive decline ([ΔMMSE per year 1.7±1.3 AD-E versus 0.9±1.4 AD-NE; p = 0.09). All patients with severe cognitive impairment (MMSE ≤ 10) had an epileptic comorbidity. Conclusion: Epilepsy is a frequent comorbidity in EOAD patients, with a percentage of 40%in our study. This comorbidity may be associated with a severe form of EOAD. The role of epilepsy in the acceleration of cognitive decline and the positive impact of antiepileptic drugs on cognition need further research.
Brain communications · 2025
Abstract Autosomal dominant spastic paraplegia type 4 (SPG4, SPAST gene) is commonly described as a pure phenotype, with progressive spastic weakness of the lower limbs. Some cognitive disorders have been reported but remain difficult to characterize. Brain flurodesoxyglucose (18F-FDG) PET is a sensitive biomarker of glycolytic metabolism and shows loss of neuronal activity. Our objective was to describe the cognitive impairment of SPG4 patients, supported by brain 18F-FDG PET, to characterize the cognitive pattern and its localization. Twenty subjects from the Grand Est region, with a pathogenic variant in the SPAST gene, were included. Each patient had to undergo a neuropsychological assessment, a brain 18F-FDG PET scan, and a SPATAX-EuroSpa clinical assessment, including the Spastic Paraplegia Rating Scale (SPRS). Brain 18F-FDG PET was analyzed semiquantitatively after comparison with age and sex-matched control subjects. The study population was 65% (13/20) female, with an average age of 50 years (19–75 years). The median SPRS was 15/52 (12–45). Forty-six percent (7/15) of patients had a deficient Montreal Cognitive Assessment (MoCA) score (score <26) without any severe impairment (score <10). Assessments with a pathological score of <1.65 standard deviations or at the 5th percentile included verbal episodic memory in 16-item Free and Cued Recall Test (16-FCRT; 63%, 10/16), facial emotion recognition (56%, 9/16), and executive functions (Trail Making Test A and B; 47%, 7/15; the Stroop; 47%, 7/15; digit span of Weschler Adult Intelligence Scale 4; 38%, 6/16). Compared with those of control subjects, 18-FDG PET images of the brains of SPG4 subjects revealed frontotemporal and precuneus hypometabolism, principally in the prefrontal cortex, which was mainly mesial (P voxel value <0.001, corrected for the size of the familywise error (FWE) cluster, k = 1464). Frontal hypometabolism was correlated with age at onset (k = −0.475, P = 0.046) and the time to perform the Trail Making Test B test (k = −0.597, P = 0.019). Here, we describe a mild cognitive disorder clinically in SPG4 patients, associated with an hypometabolism on 18F-FDG PET imaging, which mainly corresponded to frontotemporal localization. Mild cognitive dysfunction should be screened in SPG4, as it can have a significant impact on socioprofessional life. Brain 18F-FDG PET, combined with neuropsychological assessment appears to be a good screening and follow-up examination for cognitive disorders.
Parkinsonism & related disorders · 2025
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Brain communications · 2025 · Journal Article
Miroglio R, Hocquel A, Ravel JM, Clément G, et al.
European journal of medical genetics · 2025 · Case Reports
Ducatel P, Verger A, Selton M, Renaud M, et al.
Parkinsonism & related disorders · 2025 · Journal Article
Ducrocq H, Puisieux S, Hopes L, Frismand S, et al.
Journal of Alzheimer's disease : JAD · 2022 · Journal Article
Haoudy S, Jonveaux T, Puisieux S, Epstein J, et al.
Journal of neurology · 2025 · Letter
Hocquel A, Pellerin D, Méreaux JL, Huin V, et al.
The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques · 2024 · Journal Article
Clément G, Puisieux S, Ashton C, Pellerin D, et al.