Michel Tiberge
University of Toulouse
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Publication
Featured researches published by Michel Tiberge.
Journal of Clinical and Experimental Neuropsychology | 2008
Agnès Daurat; Jean Foret; Jean-Luc Bret-Dibat; Carole Fureix; Michel Tiberge
This study evaluated episodic memory, with an emphasis on the recollection of spatial and temporal contexts, in 28 patients suffering from obstructive sleep apnea syndrome and 29 healthy controls. Recollection was assessed by means of the R/K paradigm and the process-dissociation procedure. Attentional abilities were also evaluated. A polysomnographic assessment, including nocturnal oxygen saturation and daytime sleepiness, was conducted. Recollection was strongly disturbed in patients, the number of microarousals being the best predictor of the memory deficit. Attention was only slightly disturbed. Results suggest a link between episodic memory deficit and those areas of the brain that are particularly sensitive to sleep fragmentation, in particular the hippocampus.
Brain | 2011
Valérie Cochen De Cock; Rachel Debs; Delphine Oudiette; Smaranda Leu; Fatai Radji; Michel Tiberge; Huan Yu; Sophie Bayard; Emmanuel Roze; Marie Vidailhet; Yves Dauvilliers; Olivier Rascol; Isabelle Arnulf
Multiple system atrophy is an atypical parkinsonism characterized by severe motor disabilities that are poorly levodopa responsive. Most patients develop rapid eye movement sleep behaviour disorder. Because parkinsonism is absent during rapid eye movement sleep behaviour disorder in patients with Parkinsons disease, we studied the movements of patients with multiple system atrophy during rapid eye movement sleep. Forty-nine non-demented patients with multiple system atrophy and 49 patients with idiopathic Parkinsons disease were interviewed along with their 98 bed partners using a structured questionnaire. They rated the quality of movements, vocal and facial expressions during rapid eye movement sleep behaviour disorder as better than, equal to or worse than the same activities in an awake state. Sleep and movements were monitored using video-polysomnography in 22/49 patients with multiple system atrophy and in 19/49 patients with Parkinsons disease. These recordings were analysed for the presence of parkinsonism and cerebellar syndrome during rapid eye movement sleep movements. Clinical rapid eye movement sleep behaviour disorder was observed in 43/49 (88%) patients with multiple system atrophy. Reports from the 31/43 bed partners who were able to evaluate movements during sleep indicate that 81% of the patients showed some form of improvement during rapid eye movement sleep behaviour disorder. These included improved movement (73% of patients: faster, 67%; stronger, 52%; and smoother, 26%), improved speech (59% of patients: louder, 55%; more intelligible, 17%; and better articulated, 36%) and normalized facial expression (50% of patients). The rate of improvement was higher in Parkinsons disease than in multiple system atrophy, but no further difference was observed between the two forms of multiple system atrophy (predominant parkinsonism versus cerebellar syndrome). Video-monitored movements during rapid eye movement sleep in patients with multiple system atrophy revealed more expressive faces, and movements that were faster and more ample in comparison with facial expression and movements during wakefulness. These movements were still somewhat jerky but lacked any visible parkinsonism. Cerebellar signs were not assessable. We conclude that parkinsonism also disappears during rapid eye movement sleep behaviour disorder in patients with multiple system atrophy, but this improvement is not due to enhanced dopamine transmission because these patients are not levodopa-sensitive. These data suggest that these movements are not influenced by extrapyramidal regions; however, the influence of abnormal cerebellar control remains unclear. The transient disappearance of parkinsonism here is all the more surprising since no treatment (even dopaminergic) provides a real benefit in this disabling disease.
American Journal of Medical Genetics Part A | 2011
V. Cochen De Cock; G. Diene; C. Molinas; V. Dauriac-Le Masson; I. Kieffer; E. Mimoun; Michel Tiberge; M. Tauber
Excessive daytime sleepiness is a frequent and a highly disruptive symptom to the daily routine of children with Prader–Willi Syndrome (PWS) and their families. The objective of the study was to evaluate the efficacy of modafinil, a central stimulant, on excessive daytime sleepiness in children and adolescents with PWS. The efficacy of modafinil was evaluated in this open label pilot study comparing the Epworth sleepiness scale before and after treatment. Ten patients with molecularly confirmed PWS and a complaint of excessive daytime sleepiness underwent a night‐time sleep recording and multiple sleep latency tests. One patient was excluded because of severe obstructive sleep apnea syndrome. Nine patients (4 males) with median age of 16 years (8–21) received modafinil at a starting dose of 100 mg/day. We found that all patients had excessive daytime sleepiness with an Epworth sleepiness scale at 14 (11–20) and mean sleep latency on multiple sleep latency tests at 5 (3–6) minutes. Moreover, six patients had at least two sleep‐onset rapid eye movement periods showing a narcolepsy‐like phenotype. Modafinil significantly improved sleepiness in all patients on the Epworth sleepiness scale from 14 (11–20) to 4 (3–12), (P = 0.007). Body mass index of the patients did not change significantly under treatment. No side effects were reported, and the drug was well‐tolerated. We posit that this open label case series shows good efficacy of modafinil in nine children and adolescents with PWS.
Journal of Neuropsychology | 2013
Agnès Daurat; Matthieu Ricarrère; Michel Tiberge
We assessed decision making in 20 patients newly diagnosed with obstructive sleep apnoea (OSA) and 20 healthy controls with the Iowa Gambling Task (IGT), which evaluates the ability to learn to sacrifice immediate rewards in favour of long-term gains. A standard neuropsychological battery was administered. Switching scores tended to be lower in patients. Patients persisted in selecting risky decks throughout the IGT, whereas controls behaved normally. Performance was correlated with hypoxaemia. Brain regions underlying decision making may be affected by OSA-related hypoxaemia.
Memory | 2014
Agnès Daurat; Nathalie Huet; Michel Tiberge
Patients with obstructive sleep apnoea syndrome exhibit memory deficit. The present study looked at whether this deficit is related to impaired memory monitoring and/or memory control. Here 25 patients and 26 healthy controls performed a paired-associate learning task. After participants had made a judgement of learning for each pair and performed an initial recall test they were free to restudy any items they wished, for as long or little as they wished, within a 5-minute period. They then performed a second recall test. Monitoring and control processes were assessed on the basis of judgements of learning, item selection, and study-time allocation. In spite of their memory impairment, patients accurately predicted their recall. For the restudy phase patients preferentially selected the judged-easy items, while controls selected the judged-difficult items. However, all the participants allocated more restudy time to the judged-difficult items than to the judged-easy ones. There were no significant correlations between memory performance, metamemory processes, and clinical measures (i.e., subjective sleepiness, subjective sleep quality, anxiety, and depression scores). Results suggested that both memory monitoring and memory control were preserved in our sample of patients with obstructive sleep apnoea.
Journal of cognitive psychology | 2014
Majdouline Sarhane; Isabelle Etcheverry; Michel Tiberge; Agnès Daurat
We assessed the propensity for false memories among patients with obstructive sleep apnoea syndrome (OSAS). Twenty-one patients with OSAS and 21 controls matched for sex, age and education were recruited. At encoding, an adaptation of the Deese-Roediger-McDermott paradigm was used to induce false memories. At retrieval, participants completed a forced-choice recognition task to distinguish memories based on verbatim traces from those based on gist traces. When the task encouraged retrieval based on either gist or verbatim traces, the groups performed similarly. However, when the task required retrieval based solely on verbatim traces, OSAS patients exhibited poor discrimination and produced more false memories. Our finding that OSAS leads to an increased propensity to produce false memories is discussed within the framework of both fuzzy-trace theory and activation-monitoring theory.
Neurophysiologie Clinique-clinical Neurophysiology | 2016
Agnès Daurat; Majdouline Sarhane; Michel Tiberge
Obstructive sleep apnea syndrome (OSAS) is a sleep-related breathing disorder characterized by repetitive episodes of airflow cessation, resulting in brief arousals and intermittent hypoxemia. OSAS is associated with a number of adverse health consequences, and cognitive difficulties. The overall pattern of cognitive impairment in OSAS is complex, and research in this field is mixed. On balance, OSAS have negative effects on cognition, most likely in the domain of attention/vigilance, verbal and visual delayed long-term memory, and executive functions. A still unanswered question is whether these deficits are primarily a consequence of sleep fragmentation and/or hypoxemia, or whether they coexist independently from OSAS. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment of OSAS. No consistent effect of CPAP use on cognitive performance was evident. This may be due, in part, to variability in study design and sampling methodology across studies. Structural changes have been reported in different brain regions, particularly in hippocampus and frontal cortex. Recent evidence suggests that the OSAS-related structural changes may improve with CPAP treatment. However, one of the challenges is to interpret the findings in light of comorbid conditions that also cause neural lesions. Animal models will be specifically useful to disentangle the different potential contributors to cognitive impairment in OSAS. The purpose of this article is to provide a review of the literature on cognition and neuroimaging in OSAS patients before and after CPAP treatment. We also discuss the mechanisms that have been proposed to explain cognitive deficits in OSAS patients.
Neurophysiologie Clinique-clinical Neurophysiology | 2016
Agnès Daurat; Majdouline Sarhane; Michel Tiberge
Obstructive sleep apnea syndrome (OSAS) is a sleep-related breathing disorder characterized by repetitive episodes of airflow cessation, resulting in brief arousals and intermittent hypoxemia. OSAS is associated with a number of adverse health consequences, and cognitive difficulties. The overall pattern of cognitive impairment in OSAS is complex, and research in this field is mixed. On balance, OSAS have negative effects on cognition, most likely in the domain of attention/vigilance, verbal and visual delayed long-term memory, and executive functions. A still unanswered question is whether these deficits are primarily a consequence of sleep fragmentation and/or hypoxemia, or whether they coexist independently from OSAS. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment of OSAS. No consistent effect of CPAP use on cognitive performance was evident. This may be due, in part, to variability in study design and sampling methodology across studies. Structural changes have been reported in different brain regions, particularly in hippocampus and frontal cortex. Recent evidence suggests that the OSAS-related structural changes may improve with CPAP treatment. However, one of the challenges is to interpret the findings in light of comorbid conditions that also cause neural lesions. Animal models will be specifically useful to disentangle the different potential contributors to cognitive impairment in OSAS. The purpose of this article is to provide a review of the literature on cognition and neuroimaging in OSAS patients before and after CPAP treatment. We also discuss the mechanisms that have been proposed to explain cognitive deficits in OSAS patients.
Revue Neurologique | 2012
V. Cochen De Cock; Rachel Debs; Delphine Oudiette; Smaranda Leu; F. Radgi; Michel Tiberge; Huan Yu; Sophie Bayard; Emmanuel Roze; Marie Vidailhet; Yves Dauvilliers; Olivier Rascol; Isabelle Arnulf
Introduction La plupart des patients atteints d’atrophie multisystematisee (AMS), developpent des troubles du comportement en sommeil paradoxal (TCSP). Nous avons recemment demontre que le syndrome parkinsonien etait ameliore pendant les TCSP au cours de la maladie de Parkinson (MP). Objectif Nous avons recherche si cette amelioration existe aussi dans la MSA alors que ce syndrome parkinsonien est moins dopasensible. Methode Nous avons interroge 49 patients atteints d’AMS, et 49 patients atteints de MP apparies en âge et en sexe ainsi que leurs 98 partenaires de lit sur la presence de TCSP et sur la qualite de mouvement pendant les TCSP par rapport a la veille. Nous avons realise un enregistrement video- polysomnographique chez 22 patients atteints d’AMS et 19 de MP. Resultats Nous avons retrouve des TCSP, a l’interrogatoire, chez 43/49 patients (88 %) atteints d’AMS. Parmi les 31 conjoints qui etaient capables de juger la qualite des mouvements de leur partenaire, 81 % d’entre eux rapportaient une amelioration de cette qualite. Celle- ci comprenait une amelioration du mouvement (73 % des patients ; plus rapides, 67 % ; plus forts, 52 % ; et plus souples, 26 %), une amelioration de la parole (59 % des patients ; plus forte, 55 % ; plus intelligible, 17 % ; et mieux articulee, 36 %), et une disparition de l’amimie (50 % des patients). Chez 7 patients, l’enregistrement video a confirme l’amelioration du mouvement. Ces mouvements etaient « haches » mais pas parkinsoniens ni cerebelleux. Conclusions Le syndrome parkinsonien est donc ameliore pendant les TCSP dans l’AMS malgre sa faible dopa- sensibilite Il est donc probable que l’amelioration du mouvement pendant les TCSP soit donc independante d’une restauration de la transmission dopaminergique.
Sleep | 2010
Yves Dauvilliers; Jacques Montplaisir; Valéerie Cochen; Alex Desautels; Mali Einen; Ling Lin; Minae Kawashima; Sophie Bayard; Christelle Monaca; Michel Tiberge; Daniel Filipini; Asit Tripathy; Bich Nguyen; Suresh Kotagal; Emmanuel Mignot