32 results on '"Leboyer, Marion"'
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2. De « Psychose maniaco-dépressive » à « Troubles bipolaires » : une histoire des représentations sociales et de la stigmatisation en rapport avec la nosographie
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Pignon, Baptiste, Tebeka, Sarah, Leboyer, Marion, and Geoffroy, Pierre-Alexis
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- 2017
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3. Une entité clinique aux implications thérapeutiques majeures : le trouble bipolaire à début précoce
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Geoffroy, Pierre Alexis, Etain, Bruno, Leboyer, Marion, and Bellivier, Frank
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- 2012
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4. Autisme, la piste génétique se confirme
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Bourgeron, Thomas, Leboyer, Marion, and Delorme, Richard
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- 2009
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5. Élaboration et évaluation d’un programme de gestion du stress pour patients souffrant de troubles bipolaires
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Dusser, Isabelle, Romo, Lucia, and Leboyer, Marion
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- 2009
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6. Hypovitaminosis D is associated with depression and anxiety in schizophrenia: results from the national FACE-SZ cohort. Running title: hypovitaminosis D, depression and anxiety in schizophrenia
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Fond, Guillaume, Godin, Ophelia, Schurhoff, Franck, Berna, F., Bulzacka, Ewa, Andrianarisoa, Meja, Brunel, Lore, Aouizerate, Bruno, Capdevielle, Delphine, Chereau, Isabelle, Coulon, Nathalie, d'Amato, Thierry, Dubertret, Caroline, Dubreucq, Julien, Faget, Catherine, Lancon, Christophe, Leignier, Sylvain, Mallet, Jasmina, Misdrahi, David, Passerieux, Christine, Rey, Romain, Schandrin, Aurélie, Urbach, Mathieu, Vidailhet, Pierre, Leboyer, Marion, Boyer, L., Llorca, Pierre Michel, Aix Marseille Université (AMU), Assistance Publique - Hôpitaux de Marseille (APHM), Centre d'études et de recherche sur les services de santé et la qualité de vie (CEReSS), Fondation FondaMental [Créteil], Institut Pierre Louis d'Epidémiologie et de Santé Publique (iPLESP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Molecular virology and immunology – Physiopathology and therapeutic of chronic viral hepatitis (Team 18) (Inserm U955), 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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Neuro-Psycho Pharmacologie des Systèmes Dopimanégiques sous-corticaux (NPsy-Sydo), CHU Clermont-Ferrand-Université Clermont Auvergne [2017-2020] (UCA [2017-2020]), Université de Bordeaux (UB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre de recherche en neurosciences de Lyon - Lyon Neuroscience Research Center (CRNL), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet [Saint-Étienne] (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Diderot - Paris 7 (UPD7), Centre Référent de Réhabilitation Psychosociale [CH Alpes Isère], Centre Hospitalier Alpes Isère, Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Laboratoire de recherches cliniques et en santé publique sur les handicaps psychique, cognitif et moteur (HANDIReSP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Université de Strasbourg (UNISTRA), ANR-11-IDEX-0004,SUPER,Sorbonne Universités à Paris pour l'Enseignement et la Recherche(2011), ANR-10-COHO-0010,Psy-COH,FondaMental-Cohortes(2010), Université de Lyon, Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), 2011 Programme Hospitalier de Recherche Clinique National and the French Ministry of Health (Direction Générale de la Santé), as well as grants from Janssen Pharmaceutical Companies and the Fondation de France (PHRC-12-024-0278, Afssaps B110684-50, Comité de Protection des Personnes 2011-A00668-33), Assistance Publique-Hôpitaux de Marseille (AP-HM), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Centre de recherche en neurosciences de Lyon (CRNL)
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Depression ,[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health ,Schizophrenia ,Vitamin D ,Anxiety ,Metabolic syndrome - Abstract
International audience; ObjectiveHypovitaminosis D has been associated with respectively major depressive disorder, schizophrenia (SZ) and cognitive disorders in the general population, and with positive and negative symptoms and metabolic syndrome in schizophrenia. The objectives were (i) to determine the prevalence of hypovitaminosis D and associated factors (with a focus on depression and cognition) in a national non-selected multicentric sample of community-dwelling SZ subjects (ii) to determine the rate of SZ patients being administered vitamin D supplementation and associated factors.MethodsA comprehensive 2 daylong clinical and neuropsychological battery was administered in 140 SZ subjects included between 2015 and 2017 in the national FondaMental Expert Center (FACE-SZ) Cohort. Hypovitaminosis D was defined by blood vitamin D level 0.05), however, a trend toward significance has been found for metabolic syndrome (p = 0.06). Vitamin D supplementation has been administered during the previous 12 months in only 8.5% of the subjects but was associated with lower depressive symptoms (aOR = 0.67 [0.46–0.98], p = 0.04) and lower rate of current anxiety disorder (aOR = 0.06 [0.01–0.66], p = 0.02) compared to patients with hypovitaminosis D.ConclusionHypovitaminosis D is frequent and associated with depressive symptoms and anxiety disorders in schizophrenia. Vitamin D supplementation is associated with lower depressive and anxiety symptoms, however patients with hypovitaminosis D remain insufficiently treated.
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- 2018
7. Les conséquences psychiatriques du Covid-19 sont devant nous…
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Leboyer, Marion and Pelissolo, Antoine
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- 2020
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8. Dépression résistante : les autres stratégies thérapeutiques
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Saba, Ghassen, Nieto, Isabel, Bation, Rémy, Allaïli, Najib, Bennabi, Djamila, Moliere, Fanny, Richieri, Raphaëlle, Holtzmann, Jérôme, Bubrovszky, Maxime, Camus, Vincent, Charpeaud, Thomas, Courtet, Philippe, Courvoisier, Pierre, Haesebaert, Frédéric, Doumy, Olivier, El-Hage, Wissam, Garnier, Marion, D'Amato, Thierry, Bougerol, Thierry, Lançon, Christophe, Haffen, Emmanuel, Llorca, Pierre-Michel, Vaiva, Guillaume, Bellivier, Frank, Leboyer, Marion, Aouizerate, Bruno, Pôle de Psychiatrie [Hôpital Henri Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital H. Mondor - A. Chenevier, Fondation FondaMental [Créteil], Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre Hospitalier le Vinatier [Bron], Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Hôpital de la Conception [CHU - APHM] (LA CONCEPTION), Pôle Psychiatrie et Neurologie [Grenoble], Centre Hospitalier Universitaire [Grenoble] (CHU), Service de Psychiatrie [CHRU Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Hôpital Michel Fontan 1, Clinique Psychiatrique Universitaire [Tours], Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), CHU Clermont-Ferrand, Neuropsychiatrie : recherche épidémiologique et clinique (PSNREC), Université Montpellier 1 (UM1)-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Charles Perrens, and Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)
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Depressive Disorder ,S-Adenosylmethionine ,Monoamine Oxidase Inhibitors ,Drug Resistance ,Antidepressive Agents ,Food-Drug Interactions ,Folic Acid ,Double-Blind Method ,Dietary Supplements ,Dopamine Agonists ,Fatty Acids, Omega-3 ,Humans ,Central Nervous System Stimulants ,Drug Interactions ,Drug Therapy, Combination ,Ketamine ,Adrenergic alpha-Agonists ,Excitatory Amino Acid Antagonists ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology ,Randomized Controlled Trials as Topic - Abstract
International audience; Non-selective and irreversible MAOI have become as third or fourth-line strategy for the management of treatment-resistant depression. Non-selective and irreversible MAOI requires careful monitoring of drug interactions and dietary restrictions. Nutritional supplements such as omega-3 have been found to produce beneficial effects in the management of treatment-resistant depression when administered in combination with the ongoing antidepressant treatment. The glutamate antagonist ketamine has been found to produce beneficial effects in the management of treatment-resistant depression while administered alone. Dopamine and/or norepinephrine agonists, such as methylphenidate, modafinil or pramipexole, have been found to produce beneficial effects in the management of treatment-resistant depression when administered in combination with the ongoing antidepressant treatment.
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- 2016
9. [Predicting bipolar disorder: What can we learn from prospective cohort studies?]
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Geoffroy, Pierre Alexis, Leboyer, Marion, Scott, Jan, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Pôle de Psychiatrie [Lille], Université Lille Nord (France)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Service de Psychiatrie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, Fondation FondaMental [Créteil], Academic Psychiatry, Newcastle University [Newcastle]-Institute of Neuroscience, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), and Geoffroy, Pierre Alexis
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Adult ,bipolar disorder ,Adolescent ,screening ,[SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health ,Prodromal Symptoms ,risk assessment ,Syndrome ,in strategy ,Cohort Studies ,early recognition ,Young Adult ,Early Diagnosis ,[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health ,Humans ,at ,Prospective Studies ,Age of Onset ,close ,prodromal features ,risk - Abstract
International audience; INTRODUCTION: Bipolar disorder (BD) is a life course illness; and there is increasing awareness of the many personal, social and economic consequences of the illness in older adults. However, it is important to emphasize that BD usually begins in late adolescence or early adulthood and 75 % cases have a first episode in this age period. This early onset and the associated level of disability mean that BD is the 4th leading cause of global disease burden in adolescents and young adults. Internationally, mental health services are increasingly striving to diagnose and treat BD as early as possible to try to prevent poor outcomes. In addition, researchers are using methods employed previously in psychosis studies as these may help us to recognise the earliest manifestations of BD. If it is possible to identify sub-threshold and 'ultra high risk' syndromes for BD, this might lead to new interventions that could target the prevention of first episodes of mania. One approach to understanding these risk syndromes is to examine prospective community cohort studies and BD offspring studies. METHODS: This paper reviews prospective cohort studies that identify robust risk factors in early illness onset, which was defined as age at onset of BD between 15-25 years. RESULTS: We found that although > 50 % of individuals who developed BD had developed a putative BD prodrome prior to 14 years of age, this usually began with non-specific symptoms that overlap with similar presentations for those who later develop psychosis or severe depression. However, there are some features that seem to better identify groups with a BD "at-risk" syndrome. This syndrome is frequently composed of several factors such as mood lability, depressive episodes, prior anxiety, sleep and/or conduct disorders, attention and concentration impairment, altered energy patterns, and a family history of mania and/or depression. The course of these early predictors suggests the precursor syndromes are composed of mini-clusters of symptoms many of which are episodic and change over time. During the early phases of BD, most of the affective disturbances reported were depressive in polarity and started during adolescence, there were few manic or mixed or psychotic episodes with an onset before puberty. The pathogenesis of BD demonstrates a gradual progression from non-specific to more specific symptoms and then to frank BD features. CONCLUSION: Prospective community and offspring BD cohort studies are approaches that together can help us understand the evolution of BD and allow us to define the developmental pathways. Further, identifying subjects with BD "at-risk" syndrome using a clinical staging model may allow benign interventions to be used as first-line treatment - such as neuroprotective agents like essential fatty acids; second line treatments, with a less benign risk to benefit ratio should be reserved for severe or resistant cases.
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- 2013
10. Mémoire de source – présentation générale et revue des études dans la schizophrénie. [Source monitoring: general presentation and review of literature in schizophrenia]
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Ferchiou, Abdelaziz, Schürhoff, Franck, Bulzacka, E., Mahbouli, M., Leboyer, Marion, Szöke, Andrei, 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), Université Paris-Est Marne-la-Vallée (UPEM), Service de psychiatrie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, and Guellaen, Georges
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memory ,schizophrenia ,Mémoire de source ,schizophrénie ,mémoire de réalité ,reality monitoring ,auditory hallucinations ,positive symptoms ,hallucinations auditives ,[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] ,[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] ,symptômes positifs ,Source monitoring - Abstract
International audience; SOURCE MONITORING FRAMEWORK: Source monitoring refers to the ability to remember the origin of information. Three source monitoring processes can be distinguished: external source monitoring, internal or self-monitoring and reality monitoring (i.e. discrimination between internal and external sources of information). Source monitoring decisions are based on memory characteristics recorded such as perceptions, contextual information or emotional reactions and heuristic or more controlled judgement processes. BRAIN STRUCTURES: Several studies suggested that specific structures in the prefrontal and the mediotemporal lobes are the main areas implicated in source monitoring. ASSESSMENT: A typical source monitoring paradigm includes an items generation stage and a second stage of recognition of items (old versus new) and identification of their sources: external (usually the examiner) or internal (the subject). Several indices can be calculated based on the raw data such as the number of false alarms, attribution biases or discrimination indexes. To date, there is no standardized source monitoring task and differences in the type of items used (words, pictures), in the cognitive or emotional effort involved or in the delay between the two test stages, contribute to the heterogeneity of results. FACTORS INFLUENCING SOURCE MONITORING: Factors such as age (either very young or very old) and emotions influence source monitoring performances. Influence of gender was not properly explored, whereas the role of IQ and selective attention is still debated. SOURCE MONITORING DEFICITS IN NEUROLOGICAL DISORDERS: Source monitoring deficits are observed mainly in disorders affecting frontotemporal areas, such as frontal trauma, Alzheimer's disease or frontotemporal dementia. SOURCE MONITORING AND SCHIZOPHRENIA: Source monitoring errors (e.g. external misattribution of self-generated information) are observed in schizophrenia and seem to correlate with positive symptomatology, in particular auditory hallucinations, thought intrusion and alien control symptoms. These results are of particular interest in clinical research because source monitoring is one of the rare cognitive tests showing a correlation with the positive dimension. Source monitoring deficits have been proposed as a potential explanation for the positive symptoms and some, but not all studies lent support to this hypothesis. Heterogeneity of studied samples, in particular different criteria to define hallucinating subjects (e.g. currently versus anytime during their lives), could explain the discordant results. SOURCE MONITORING IN PSYCHIATRIC DISORDERS WITHIN THE SCHIZOPHRENIC SPECTRUM: Source monitoring impairments were observed in pharmacological models of psychosis, in first degree relatives of schizophrenic patients, and also in the general population associated with schizotypal dimensions. These results support a relationship between source monitoring deficits and some of the symptomatic dimensions of the schizophrenic spectrum but still await replication. SOURCE MONITORING AND OTHER PSYCHIATRIC DISORDERS: Some studies found source monitoring deficits in other psychiatric conditions such as mania or obsessive-compulsive disorder. Thus, those studies suggest that source monitoring deficits may be not specific to schizophrenia. CONCLUSION: Source monitoring competencies are critical for good (i.e. adapted) everyday functioning. Source monitoring deficits have been suggested as a potential explanation for some (or all) positive psychotic symptoms. However, to date, methodological inconsistencies (especially with regard to test design and choice of subjects' samples) have precluded firm, definite conclusions.
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- 2010
11. [Alterations in synapsis formation and function in autism disorders]
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Durand, Christelle, Chaste, Pauline, Fauchereau, Fabien, Betancur, Catalina, Leboyer, Marion, Bourgeron, Thomas, Betancur, Catalina, Génétique Humaine et Fonctions Cognitives, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Génétique de l'autisme = Genetics of Autism (NPS-01), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), 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)-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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), 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)-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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Neurobiologie et Psychiatrie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Groupe Henri Mondor-Albert Chenevier, and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier
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[SDV.GEN]Life Sciences [q-bio]/Genetics ,MESH: Humans ,MESH: Mutation ,Models, Neurological ,MESH: Autistic Disorder ,MESH: Carrier Proteins ,Nerve Tissue Proteins ,[SDV.GEN] Life Sciences [q-bio]/Genetics ,MESH: Cell Adhesion ,MESH: Synapses ,MESH: Models, Neurological ,Mutation ,Synapses ,Cell Adhesion ,Humans ,MESH: Nerve Tissue Proteins ,Autistic Disorder ,Carrier Proteins ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience; No abstract available
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- 2008
12. [Psychometric properties of the French version of the signs and symptoms of psychotic illness (SSPI) scale]
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Houenou, Josselin, Szöke, Andrei, Méary, Alexandre, Loze, Jean-Yves, Mathieu, Flavie, Leboyer, Marion, Schürhoff, Franck, Service de psychiatrie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, Neurobiologie et Psychiatrie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Guellaen, Georges
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Adult ,Male ,MESH: Psychiatric Status Rating Scales ,Psychometrics ,MESH: Psychotic Disorders ,psychose ,MESH: Psychometrics ,[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,SSPI ,Language ,psychométrie ,Psychiatric Status Rating Scales ,MESH: Humans ,Reproducibility of Results ,MESH: Adult ,MESH: Male ,MESH: France ,MESH: Reproducibility of Results ,Psychotic Disorders ,échelle ,schizophrénie ,MESH: Language ,Female ,France ,MESH: Female - Abstract
International audience; OBJECTIVE: This report describes the psychometric evaluation of the French translation of the Signs and Symptoms of Psychotic Illness (SSPI) scale. The SSPI scale was designed to assess the five main clusters of symptoms of people suffering from psychotic disorders (psychomotor poverty, reality distortion, disorganisation, depression, and psychomotor excitation) across diagnostic entities. This new tool has been built by Liddle because, in the existing scales assessing psychotic symptoms, individual items cover symptoms that belong to different pathophysiological processes. The SSPI scale comprises 20 items. Its interview is semi-standardised and typically lasts around 25 min. The English version of this scale has shown good psychometric properties (inter-rater reliability, factor structure). METHOD: We used the SSPI ratings of 81 patients with psychotic symptoms to assess its factor structure and concurrent validity with the Clinical Global Impressions (CGI) scale. Twenty-eight videotaped ratings were used to calculate the intra-class correlation coefficient (ICC) as a measure of inter-rater reliability. RESULTS AND DISCUSSION: The sample was composed of 46 schizophrenic subjects, 14 with schizoaffective disorder, three with major depressive episode with psychotic features, nine with manic episode with psychotic features and nine with other psychotic disorders. A principal component analysis was conducted to determine the factor structure. Using the Cattell test, we retained a five-factor solution. This solution explained 56.9% of the variance. After varimax rotation, 18 items were attributed to a unique factor. The five factors were: a psychomotor poverty factor, a reality distortion factor, a disorganised factor, an anxious/depressive factor and a psychomotor excitation factor. This structure is close to the original one. The inter-rater reliability of the French version of the SSPI was satisfactory for 18 items, with a mean ICC of 0.64 for the individual items, and an ICC of 0.76 for the global scale. Only two items had an unsatisfactory ICC. This scale showed a good correlation with the CGI scale, with a correlation coefficient between CGI score and SSPI global score of 0.64. Among the factor scores, reality distortion, disorganisation and depression factor scores exhibited a significant correlation with the CGI score. CONCLUSIONS: The French version of the SSPI scale has good psychometric properties, similar to the English version. Furthermore, its factor structure is similar to the English one. This scale is a robust instrument to rate psychotic symptoms and dimensions across diagnosis entities.
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- 2007
13. [The schizotypal personality disorder: historical origins and current status]
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Leboyer, Marion, Schurhoff, Franck, Laguerre, Audrey, Service de psychiatrie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Hôpital Albert Chenevier, Institut Mondor de recherche biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), and Guellaen, Georges
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Bipolar Disorder ,[SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health ,Personality Assessment ,Nosological approach ,Dimensional approach ,Diagnostic and Statistical Manual of Mental Disorders ,Schizotypal Personality Disorder ,International Classification of Diseases ,[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health ,[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Schizophrenia ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Genetic Predisposition to Disease ,Schizophrenic Psychology - Abstract
BACKGROUND: The schizotypal personality disorder is a recent psychiatric nosological concept developed by Spitzer at the end of the 1970s, based on the analysis of the characteristics of relatives of schizophrenic subjects included in the adoption studies carried out in the same decade by Kety, Wender and Rosenthal. HISTORICAL ASPECTS: However, this entity is based on older observations, at the beginning of the past century, showing common behavioural characteristics in relatives of schizophrenics. Its status within our current nosography remains dubious, sometimes classified among personality disorders, sometimes in the schizophrenia spectrum disorders. It is interesting to present the origins of this concept that stem from two complementary approaches: a family approach and a clinical approach of sporadic cases and then to redefine the framework within which the diagnostic approach was based and its continuity, up until our current classifications, the DSM and CIM. CURRENT STATUS: The historical origins cannot summarize the disorder and it appears important to redefine the multidimensional characteristics of the schizotypal personality disorder, generally a three-factor model. Indeed, dimensional models of psychosis are becoming established as conceptually and clinically useful. Recent studies on the dimensionality of psychosis show an evolution of the schizotypal concept, initially defined as being part of the schizophrenia spectrum and which now appears to be more broadly linked to a concept of unitary psychosis, including the bipolar disorder. CONCLUSION: Dimensions of psychosis seem to be associated with different familial aggregation and risk of psychosis, suggesting that they are underlined by different physiopathological processes. Hence, the dimensional approach can help to disentangle the genetic heterogeneity of the disease.
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- 2006
14. Les rétrovirus endogènes humains, une implication dans la schizophrénie et le trouble bipolaire.
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Ellul, Pierre, Groc, Laurent, and Leboyer, Marion
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- 2017
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15. Genetics of autism: from genome scans to candidate genes
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Jamain, Stéphane, Betancur, Catalina, Giros, Bruno, Leboyer, Marion, Bourgeron, Thomas, Génomique fonctionnelle et développement, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Génétique Humaine et Fonctions Cognitives, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Neurobiologie et Psychiatrie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département de Psychiatrie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Albert Chenevier, INSERM, Assistance Publique–Hôpitaux de Paris (DRC) (CRC 932413 et AOM 95076), Fondation France Télécom, Fondation de France, Paris Autism Research International Sibpair (PARIS) Study, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)
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Chromosome Aberrations ,[SDV.GEN]Life Sciences [q-bio]/Genetics ,Genome ,MESH: Humans ,MESH: Pedigree ,MESH: Twins, Dizygotic ,DNA Mutational Analysis ,MESH: Autistic Disorder ,MESH: Genetic Predisposition to Disease ,Chromosome Mapping ,Chromosomes ,Pedigree ,Twins, Dizygotic ,Humans ,MESH: Chromosome Aberrations ,Genetic Predisposition to Disease ,MESH: Chromosomes ,MESH: Genome ,Autistic Disorder ,MESH: DNA Mutational Analysis ,MESH: Chromosome Mapping - Abstract
The autistic disorder was firstly described by Leo Kanner sixty years ago. This complex developmental disability is characterized by social and communicative impairments and repetitive and stereotyped behaviours and interests. The prevalence of autism in the general population is about 1 in 1,000, with four males affected for one female. In approximately 15% of the cases, autism is associated with known genetic disorders, such as fragile X syndrome, tuberous sclerosis or Rett syndrome. Nevertheless, a recognised medical etiology can only be identified in a minority of cases. A higher recurrence risk in families with autistic subjects (45 times greater than the prevalence in the general population) and higher concordance for autism among monozygotic (60-90%) than dizygotic (0-10%) twins argue for a genetic predisposition to idiopathic autism. The past decade has been marked by an increased interest in the genetic basis of autism, with a series of multiple independent whole genome scans and chromosomal abnormalities studies. These analyses have pointed out several candidate regions on chromosomes 2q, 7q, 6q, 15q and sex chromosomes. These regions possess candidate genes that have been screened for mutations or association with autism. However, a clear involvement of a major susceptibility gene (or genes) in autism remains far from clear. The results from linkage studies and the clear drop in the concordance rates between monozygotic and dizygotic twins suggests that the genetic aetiology of autism is certainly heterogeneous (different genes in different families) and polygenic (more than one affected gene per individual). The almost finished sequence of the human genome and the generation of haplotype maps will shed light on the inter-individual genetic variability and will certainly increase the power and reliability of association studies for complex traits, such as autism.; Soixante ans après sa caractérisation par Léo Kanner puis par Hans Asperger, les causes majeures du syndrome autistique restent toujours inconnues. Bien qu’un quart des cas d’autisme soit associé à des affections connues, les trois quarts restants demeurent idiopathiques.Cependant, les études sur les couples de jumeaux, réalisées durant les années 1970-1980, ont permis de déceler une forte influence géné-tique dans l’apparition de ce syndrome. En outre, le développement de nouvelles techniques d’analyse génétique, les nombreuses analyses de gènes candidats et l’amélioration de la définition du diagnostic ont permis au fil du temps de diri-ger les recherches sur plusieurs régions du génome comme les bras longs des chromosomes 2, 6, 7 et 15 ou les chromosomes sexuels. Cet article a donc pour but de retracer les dernières avancées dans la recherche de la prédisposition génétique au syndrome autistique.
- Published
- 2003
16. Autisme et psychopharmacologie : l’hypothèse opiacée
- Author
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Chabane, N., Tardif, Carole, Bouvard, Manuel-Pierre, Leboyer, Marion, Mouren-Simeoni, Marie Christine, Centre de Recherche en Psychologie de la Connaissance, du Langage et de l'Émotion (PsyCLÉ), Aix Marseille Université (AMU), Service de pédopsychiatrie, Université Bordeaux Segalen - Bordeaux 2-Hôpital Charles Perrens, Neurobiologie et Psychiatrie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de psychopathologie de l'enfant et de l'adolescent, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7), Université Bordeaux Segalen - Bordeaux 2-Centre hospitalier Charles Perrens [Bordeaux], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)
- Subjects
[SCCO.PSYC]Cognitive science/Psychology ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience
- Published
- 1998
17. Anticorps anti-NR1 dans l'encéphalite anti-récepteur N-méthyl- D-aspartate et la schizophrénie.
- Author
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Guen, Emmanuel Le, Doukhan, Raphaël, Hamdani, Nora, Tamouza, Ryad, Groc, Laurent, Honnorat, Jérôme, and Leboyer, Marion
- Published
- 2015
- Full Text
- View/download PDF
18. Trouble bipolaire à début précoce : validation par les études de mélange et les biomarqueurs.
- Author
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Geoffroy, Pierre Alexis, Etain, Bruno, Jamain, Stéphane, Bellivier, Frank, and Leboyer, Marion
- Subjects
DIAGNOSIS of bipolar disorder ,THERAPEUTICS ,BIPOLAR disorder ,AFFECTIVE disorders ,MENTAL depression ,BIOMARKERS - Abstract
Copyright of Canadian Journal of Psychiatry is the property of Sage Publications Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2013
- Full Text
- View/download PDF
19. POINT DE VUE: « Il faut absolument informer le grand public du lien entre infection et maladie mentale ».
- Author
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LEBOYER, Marion
- Published
- 2022
20. [Psychiatric consequences of Covid-19 are in front of us…].
- Author
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Leboyer M and Pelissolo A
- Published
- 2020
- Full Text
- View/download PDF
21. [Seclusion and mechanical restraints in psychiatric care: Prescriptions procedures, pharmacological management, and monitoring].
- Author
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Tezenas du Montcel C, Kowal C, Leherle A, Kabbaj S, Frajerman A, Le Guen E, Hamdani N, Schürhoff F, Leboyer M, Pelissolo A, and Pignon B
- Subjects
- Aggression psychology, France, Humans, Monitoring, Physiologic methods, Prescriptions, Patient Isolation methods, Psychomotor Agitation therapy, Restraint, Physical
- Abstract
We will briefly summarize the French recommendations concerning the use of seclusion and mechanical restraint. Acute agitation and aggression or self-injurious activity during psychotic and manic episodes are the main indication of prescription of the coercive measures. Their prescriptions respect specific modalities that will be explained. Although they proved to be efficient, seclusion and restrain need to stay a last resort option, considering the risk of physical complications and psychological consequences. Specific pharmacological prescription will necessarily be associated with coercive measures and we present prescription guidelines. Finally, physical complications need to be prevented and we submit specific protocol concerning constipation and thromboembolic risk management., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)
- Published
- 2018
- Full Text
- View/download PDF
22. [Implication of human endogenous retroviruses in schizophrenia and bipolar disorder].
- Author
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Ellul P, Groc L, and Leboyer M
- Subjects
- Animals, Bipolar Disorder pathology, Bipolar Disorder virology, Endogenous Retroviruses pathogenicity, Humans, Schizophrenia pathology, Schizophrenia virology, Virus Activation physiology, Bipolar Disorder genetics, Endogenous Retroviruses physiology, Schizophrenia genetics
- Abstract
Schizophrenia and bipolar disorder are neuropsychiatric disorders of unknown origin. It seems that these two disorders share some common etiopathogenic mechanisms including genetic, environmental and inflammatory ones. Reactivation of the human endogenous retrovirus type W (HERV-W) can be a shared element in the pathophysiology of schizophrenia and bipolar disorder, linked to immuno-genetic and environment risk factors. We will present studies that have highlighted the presence of HERV-W in schizophrenic and bipolar disorder patients. We will then describe a two-hit model which could explain the common pathophysiological mechanism of affective and non-affective psychosis. Identification of immuno-inflammatory mediated subgroup of schizophrenia and bipolar disorder associated to HERV-W reactivation might open the way for the development of diagnostic biomarker and more targeted treatments. These new tools pave the way towards personalized psychiatry for a better care of patients., (© 2017 médecine/sciences – Inserm.)
- Published
- 2017
- Full Text
- View/download PDF
23. [Switching and combining strategies of antidepressant medications].
- Author
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Charpeaud T, Moliere F, Bubrovszky M, Haesebaert F, Allaïli N, Bation R, Nieto I, Richieri R, Saba G, Bellivier F, Bennabi D, Holtzmann J, Camus V, Courtet P, Courvoisier P, d'Amato T, Doumy O, Garnier M, Bougerol T, Lançon C, Haffen E, Leboyer M, Llorca PM, Vaiva G, El-Hage W, and Aouizerate B
- Subjects
- Antidepressive Agents adverse effects, Antidepressive Agents classification, Antidepressive Agents pharmacokinetics, Drug Administration Schedule, Drug Interactions, Drug Resistance, Drug Substitution, Drug Therapy, Combination, Humans, Practice Guidelines as Topic, Antidepressive Agents therapeutic use, Depressive Disorder drug therapy
- Abstract
Switching antidepressant medication may be helpful in depressed patients having no benefit from the initial antidepressant treatment. Before considering switching strategy, the initial antidepressant treatment should produce no therapeutic effect after at least 4 weeks of administration at adequate dosage. Choosing an antidepressant of pharmacologically distinct profile fails to consistently demonstrate a significant superiority in terms of effectiveness over the switching to another antidepressant within the same pharmacological class. Augmenting SSRI/SNRIs with mirtazapine/mianserin has become the most recommended strategy of antidepressant combinations. Augmenting SSRI with tricyclic drugs is now a less recommended strategy of antidepressant combinations given the increased risk for the occurrence of pharmacokinetic drug-drug interactions and adverse effects., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
24. [How to define treatment-resistant depression?].
- Author
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Holtzmann J, Richieri R, Saba G, Allaïli N, Bation R, Moliere F, Nieto I, Bellivier F, Bennabi D, Bubrovszky M, Camus V, Charpeaud T, Courvoisier P, Haesebaert F, Doumy O, Courtet P, El-Hage W, Garnier M, d'Amato T, Lançon C, Leboyer M, Llorca PM, Vaiva G, Bougerol T, Aouizerate B, and Haffen E
- Subjects
- Antidepressive Agents classification, Antidepressive Agents pharmacokinetics, Antidepressive Agents therapeutic use, Avitaminosis diagnosis, Chronic Pain diagnosis, Comorbidity, Depressive Disorder classification, Depressive Disorder epidemiology, Diagnosis, Differential, Drug Interactions, Drug Resistance, Drug Substitution, Electroconvulsive Therapy, Endocrine System Diseases diagnosis, Humans, Mental Disorders diagnosis, Patient Compliance, Psychometrics, Quality of Life, Recurrence, Socioeconomic Factors, Stress, Psychological epidemiology, Stress, Psychological psychology, Depressive Disorder diagnosis
- Abstract
The most largely used definition of the treatment-resistant depression relies on the failure of two successive trials of antidepressant treatment at an adequate dose and duration. The absence of response to previous antidepressant treatments should be assessed using specific and appropriate clinical instruments enabling a correct staging of the therapeutic resistance. A wide range of socio-demographic and clinical factors (i.e. psychiatric/somatic comorbidities) are classically associated with the therapeutic resistance. The aim of the treatment of major depression is to achieve a complete clinical remission. The presence of residual symptoms increases the risk for the subsequent occurrence of relapses and recurrences, hence facilitating the development of therapeutic resistance. The treatment-resistant depression has a deleterious impact on the social, familial or professional functioning, thereby leading to an impaired quality of life with serious socioeconomic consequences and costs., (Copyright © 2016. Published by Elsevier Masson SAS.)
- Published
- 2016
- Full Text
- View/download PDF
25. [Potentiation strategies].
- Author
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Doumy O, Bennabi D, El-Hage W, Allaïli N, Bation R, Bellivier F, Holtzmann J, Bubrovszky M, Camus V, Charpeaud T, Courvoisier P, d'Amato T, Garnier M, Haesebaert F, Bougerol T, Lançon C, Moliere F, Nieto I, Richieri R, Saba G, Courtet P, Vaiva G, Leboyer M, Llorca PM, Aouizerate B, and Haffen E
- Subjects
- Anticonvulsants pharmacokinetics, Anticonvulsants therapeutic use, Antidepressive Agents classification, Antidepressive Agents pharmacokinetics, Antipsychotic Agents adverse effects, Antipsychotic Agents pharmacokinetics, Antipsychotic Agents therapeutic use, Bipolar Disorder drug therapy, Double-Blind Method, Drug Resistance, Drug Synergism, Drug Therapy, Combination, Humans, Lithium Carbonate pharmacokinetics, Lithium Carbonate therapeutic use, Meta-Analysis as Topic, Practice Guidelines as Topic, Randomized Controlled Trials as Topic, Thyroid Hormones pharmacokinetics, Thyroid Hormones therapeutic use, Thyrotropin blood, Treatment Outcome, Antidepressive Agents therapeutic use, Depressive Disorder drug therapy
- Abstract
Lithium is among the most classically recommended add-on therapeutic strategy for the management of depressive patients showing unsuccessful response to standard antidepressant medications. The effectiveness of the add-on strategy with lithium requires achieving plasma levels above 0.5 mEq/L. Mood-stabilizing antiepileptic drugs such as carbamazepine, valproate derivatives or lamotrigine have not demonstrated conclusive therapeutic effects for the management of depressive patients showing unsuccessful response to standard antidepressant medications. Thyroid hormones are considered among the currently recommended add-on therapeutic strategy for the management of depressive patients showing unsuccessful response to standard antidepressant medications. The effectiveness of the add-on strategy with thyroid hormones requires achieving plasma concentration of TSH close to the lower limits at the normal range (0.4 μUI/L) or even below it. Second-generation antipsychotics such as aripiprazole or quetiapine have consistently demonstrated significant therapeutic effects for the management of depressive patients showing unsuccessful response to standard antidepressant medications. Second-generation antipsychotics however require the careful monitoring of both cardiovascular and metabolic adverse effects., (Copyright © 2016. Published by Elsevier Masson SAS.)
- Published
- 2016
- Full Text
- View/download PDF
26. [Other therapeutic strategies].
- Author
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Saba G, Nieto I, Bation R, Allaïli N, Bennabi D, Moliere F, Richieri R, Holtzmann J, Bubrovszky M, Camus V, Charpeaud T, Courtet P, Courvoisier P, Haesebaert F, Doumy O, El-Hage W, Garnier M, d'Amato T, Bougerol T, Lançon C, Haffen E, Llorca PM, Vaiva G, Bellivier F, Leboyer M, and Aouizerate B
- Subjects
- Antidepressive Agents pharmacokinetics, Double-Blind Method, Drug Interactions, Drug Resistance, Drug Therapy, Combination, Fatty Acids, Omega-3 therapeutic use, Folic Acid therapeutic use, Food-Drug Interactions, Humans, Monoamine Oxidase Inhibitors pharmacokinetics, Randomized Controlled Trials as Topic, S-Adenosylmethionine therapeutic use, Adrenergic alpha-Agonists therapeutic use, Antidepressive Agents therapeutic use, Central Nervous System Stimulants therapeutic use, Depressive Disorder drug therapy, Dietary Supplements, Dopamine Agonists therapeutic use, Excitatory Amino Acid Antagonists therapeutic use, Ketamine therapeutic use, Monoamine Oxidase Inhibitors therapeutic use
- Abstract
Non-selective and irreversible MAOI have become as third or fourth-line strategy for the management of treatment-resistant depression. Non-selective and irreversible MAOI requires careful monitoring of drug interactions and dietary restrictions. Nutritional supplements such as omega-3 have been found to produce beneficial effects in the management of treatment-resistant depression when administered in combination with the ongoing antidepressant treatment. The glutamate antagonist ketamine has been found to produce beneficial effects in the management of treatment-resistant depression while administered alone. Dopamine and/or norepinephrine agonists, such as methylphenidate, modafinil or pramipexole, have been found to produce beneficial effects in the management of treatment-resistant depression when administered in combination with the ongoing antidepressant treatment., (Copyright © 2016. Published by Elsevier Masson SAS.)
- Published
- 2016
- Full Text
- View/download PDF
27. [The potential role of microbiota in major psychiatric disorders: Mechanisms, preclinical data, gastro-intestinal comorbidities and therapeutic options].
- Author
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Fond G, Chevalier G, Eberl G, and Leboyer M
- Subjects
- Animals, Gastrointestinal Diseases complications, Gastrointestinal Diseases therapy, Humans, Mental Disorders complications, Mental Disorders therapy, Gastrointestinal Microbiome, Mental Disorders microbiology
- Abstract
While forecasts predict an increase in the prevalence of mental health disorders in the worldwide general population, the response rate to classical psychiatric treatment remains unsatisfactory. Resistance to psychotropic drugs can be due to clinical, pharmacological, pharmacokinetic, and pharmacodynamic factors. Among these factors, recent animal findings suggest that microbiota may have an underestimated influence on its host's behavior and on drug metabolism that may explain ineffectiveness or increased side effects of psychiatric medications such as weight gain. The following issues were identified in the present review: (i) microbiota dysbiosis and putative consequences on central nervous system functioning; (ii) chronic microbiota dysbiosis-associated illnesses in humans; (iii) microbiota-oriented treatments and their potential therapeutic applications in psychiatry., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
28. [Anti-NR1 antibodies in anti-N-methyl-D-aspartate receptor encephalitis and schizophrenia].
- Author
-
Le Guen E, Doukhan R, Hamdani N, Tamouza R, Groc L, Honnorat J, and Leboyer M
- Subjects
- Anti-N-Methyl-D-Aspartate Receptor Encephalitis epidemiology, Anti-N-Methyl-D-Aspartate Receptor Encephalitis immunology, Anti-N-Methyl-D-Aspartate Receptor Encephalitis therapy, Humans, Schizophrenia epidemiology, Schizophrenia immunology, Anti-N-Methyl-D-Aspartate Receptor Encephalitis blood, Autoantibodies blood, Receptors, N-Methyl-D-Aspartate immunology, Schizophrenia blood
- Abstract
The recent discovery of anti-NMDA receptor antibodies and proof of their pathogenic effects in limbic encephalitides raised many questions among neuroscientist and physicians working in the field of schizophrenia. Indeed, this two conditions share several major clinical, pathophysiological or etiological aspects and some authors tend to consider some forms of schizophrenia as mild-encephalitis cases. Some studies have reported the presence of these antibodies in schizophrenic patient's sera without neurological symptoms. These findings suggest new therapeutic perspectives in some schizophrenic patients, despite a low seroprevalence and pathogenic effects that remain to be demonstrated., (© 2015 médecine/sciences – Inserm.)
- Published
- 2015
- Full Text
- View/download PDF
29. [Early onset bipolar disorder: validation from admixture analyses and biomarkers].
- Author
-
Geoffroy PA, Etain B, Jamain S, Bellivier F, and Leboyer M
- Subjects
- Age of Onset, Anxiety Disorders epidemiology, Anxiety Disorders psychology, Biomarkers metabolism, Bipolar Disorder epidemiology, Bipolar Disorder metabolism, Comorbidity, Humans, Substance-Related Disorders epidemiology, Substance-Related Disorders psychology, Suicide, Attempted psychology, Suicide, Attempted statistics & numerical data, Bipolar Disorder psychology
- Abstract
Objectives: Bipolar affective disorder (BD) is a multifactorial disorder with heterogeneous clinical presentations, in particular according to age at onset (AAO). The relevance of such an indicator has been discussed as a potential specifier in future nosographical classification., Method: We summarize available evidence of admixture analyses and biomarkers in early onset BD., Results: Numerous clinical arguments have led us to conclude that the early onset BD subgroup is clinically homogeneous, with particular, recurrent, and severe characteristics.Eight admixture studies have demonstrated the existence of 3 subgroups of patients with BD according to AAO (early, intermediate, and late AAO), with 2 cut-off points of 21 (21.33) [SD 1.41]) and 35 years (34.67 [SD 5.52]). Differential clinical features and outcome measures characterize the early onset subgroup: higher rate of suicide attempts, rapid cycling, alcohol and drugs misuse, psychotic symptoms, and comorbid anxiety disorders. This may partially explain the delayed diagnosis and late initiation of mood stabilizers. Genetic, biological, imaging, and cognitive arguments may be considered as potential markers in providing external validity of the existence of this early onset subgroup. Implementation of AAO in the algorithms of treatment may be discussed, although the level of proof for focused medication strategies remains to be consolidated., Conclusion: Given the high frequency (44.80%) of early onset BD, awareness of clinicians should be stimulated to provide an early and accurate detection, preventive strategies, and possibly specific treatments.The forthcoming DSM-5 should include AAO as a specifier, given its relevance for course and outcome.
- Published
- 2013
- Full Text
- View/download PDF
30. [Autism: more evidence of a genetic cause].
- Author
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Bourgeron T, Leboyer M, and Delorme R
- Subjects
- Child, Humans, Nerve Tissue Proteins, Synapses physiology, Autistic Disorder genetics, Carrier Proteins genetics
- Abstract
Autism spectrum disorders (ASD) affect at least 1/200 individuals. They are characterized by impaired communication skills and social interaction, as well as restricted, repetitive and stereotyped behaviours. Recent studies point to a role of a synaptic pathway, including synaptic cell adhesion molecules (neuroligins and neurexins) and scaffolding proteins (SHANK3). Abnormal synapse formation/maintenance and an imbalance between GABAergic and glutamatergic synaptic currents seem to be involved in the etiology of ASD.
- Published
- 2009
31. [Pathogenesis of bipolar disorders: genetic vulnerability and environmental factors].
- Author
-
Leboyer M and Henry C
- Subjects
- Environment, Genetic Predisposition to Disease, Humans, Bipolar Disorder etiology
- Abstract
It is now well-established that there is a genetic vulnerability for developing bipolar disorders. For instance, the rate of bipolar disorders in first degree relatives of bipolar probands (19%) is higher than in the general population (1%); monozygote twins have higher concordance rates for bipolar diseases (67%) than dizygote (19%); finally affective disorders are more frequent in biological parents than in adoptive parents in adopted bipolar patients. However, currently genes predisposing for the disease are not known, in part because bipolar disorders are very heterogeneous. New research strategies should be developed based on more homogeneous groups of patients defined by the presence of "candidate symptoms" or by the evidence of endophenotypes in healthy relatives. However, it is clear now that there is an interaction between the genetic vulnerability and environmental factors in the aetiology and course of the disorder. Environmental factors have been neglected for a long time because bipolar disorder was considered an endogenous disease. Thus, very recently, studies have shown that early trauma could contribute to the occurrence or the severity of the disease. During a lifetime, many environmental components (stressful life events, changes in daily schedules, drug abuse, some medications) could also trigger the onset of the pathology or the occurrence of new episodes. It is very important to recognize these factors in order to develop preventive strategies for limiting their impact.
- Published
- 2005
32. [Genetics of autism: from genome scans to candidate genes].
- Author
-
Jamain S, Betancur C, Giros B, Leboyer M, and Bourgeron T
- Subjects
- Chromosome Aberrations, Chromosome Mapping, Chromosomes, DNA Mutational Analysis, Humans, Pedigree, Twins, Dizygotic, Autistic Disorder genetics, Genetic Predisposition to Disease, Genome
- Abstract
The autistic disorder was firstly described by Leo Kanner sixty years ago. This complex developmental disability is characterized by social and communicative impairments and repetitive and stereotyped behaviours and interests. The prevalence of autism in the general population is about 1 in 1,000, with four males affected for one female. In approximately 15% of the cases, autism is associated with known genetic disorders, such as fragile X syndrome, tuberous sclerosis or Rett syndrome. Nevertheless, a recognised medical etiology can only be identified in a minority of cases. A higher recurrence risk in families with autistic subjects (45 times greater than the prevalence in the general population) and higher concordance for autism among monozygotic (60-90%) than dizygotic (0-10%) twins argue for a genetic predisposition to idiopathic autism. The past decade has been marked by an increased interest in the genetic basis of autism, with a series of multiple independent whole genome scans and chromosomal abnormalities studies. These analyses have pointed out several candidate regions on chromosomes 2q, 7q, 6q, 15q and sex chromosomes. These regions possess candidate genes that have been screened for mutations or association with autism. However, a clear involvement of a major susceptibility gene (or genes) in autism remains far from clear. The results from linkage studies and the clear drop in the concordance rates between monozygotic and dizygotic twins suggests that the genetic aetiology of autism is certainly heterogeneous (different genes in different families) and polygenic (more than one affected gene per individual). The almost finished sequence of the human genome and the generation of haplotype maps will shed light on the inter-individual genetic variability and will certainly increase the power and reliability of association studies for complex traits, such as autism.
- Published
- 2003
- Full Text
- View/download PDF
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