921 research outputs found
Raphael Emmanuel Verhaeren, Partir ? Une théorie économique des migrations internationales
No full textCaire Guy. Raphael Emmanuel Verhaeren, Partir ? Une théorie économique des migrations internationales. In: Tiers-Monde, tome 35, n°138, 1994. Technologies de communication et d'information au Sud : la mondialisation forcée, sous la direction de Yvonne Mignot-Lefebvre. pp. 473-474
Characteristics of Maintenance of Wakefulness Test (MWT) in drug-naïve patients with narcolepsy type 1 and type 2, and relationship with other measures of sleepiness
No full textStudy objectives: We aimed to describe the characteristics of standard maintenance of wakefulness test (MWT), outside of clinical trials, in a sample of drug-na & iuml;ve patients with narcolepsy type 1 (NT1) and type 2 (NT2). Methods: Consecutive drug-na & iuml;ve patients with narcolepsy underwent two days of continuous PSG recording, the multiple sleep latency test (MSLT), then night-PSG and, on the following day, MWT. MWT results were correlated with MSLT and Epworth Sleepiness Scale (ESS). Patients in the two lower tertiles of MWT mean sleep latency (mSL) were compared to those in the upper tertile. Results: Seventy-eight NT1 (30.6 +/- 11.4 years, 35 males) and 19 NT2 (31.0 +/- 9.9 years, 12 males) were included. MWT results showed a bimodal distribution with a large peak with reduced mSL and a small peak with values towards 40 minutes. MWT mSL was lower in NT1 than in NT2 (10.7 +/- 10.8 min vs 23.9 +/- 11.5 min, p<.001). In the entire sample, lower MWT mSL was moderately correlated with lower MSLT mSL (Rho = 0.347, p=.001) and higher ESS (Rho = -0.398, p<.001). Patients with NT1 with MWT mSL in the two lower tertiles (<= 11.2 min) had higher ESS than those in the upper tertile, without any difference in other clinical or neurophysiological features. In NT2, no significant correlations emerged between MWT, MSLT, and ESS. Conclusions: MWT mSL is reduced in drug-naive narcolepsy, more severely in NT1 than in NT2. However, a minority of patients show normal MWT results. MSLT, MWT, and ESS measure different aspects of sleepiness in narcolepsy, and none can be considered a comprehensive measure of its severity
Dataset for paper "Flow Resistance for a Varying Density of Obstacles on Smooth and Rough Beds"
No full textThis dataset contains the experimental data that supports the paper:
Guillén-Ludeña, S., Lopez, D., Mignot, E., & Riviere, N. (2019). Flow Resistance for a Varying Density of Obstacles on Smooth and Rough Beds. Journal of Hydraulic Engineering, 146(2), 04019059.
The file Readme.txt contains al explanations regarding the data organization
Sleep Problems in Narcolepsy and the Role of Hypocretin/Orexin Deficiency
No full textSince its description in the 19th century, narcolepsy type 1 (NT1) has been considered as a model sleep disorder, and after the discovery of rapid eye movement (REM) sleep onset in the disorder, a gateway to understanding REM sleep. The discovery that NT1 is caused by hypocretin/orexin deficiency, together with neurochemical studies of this system, has helped to establish how this neuropeptide regulates the organization of sleep and wake in humans. Current analyses suggest that the main functions of the hypocretin/orexin system are (1) maintenance of wakefulness in the face of moderate sleep deprivation; (2) passive wake promotion, especially in the evening, driven by the circadian clock; (3) inhibition of REM sleep, with possible differential modulating effects on various subcomponents of the sleep-stage, explaining REM sleep dissociation events in NT1. Narcolepsy is also associated with an inability to consolidate sleep, a more complex phenotype that may result from secondary changes or be central to the role of hypocretin in coordinating the activity of other sleep- and wake-promoting systems. Novel technologies, such as the use of deep learning analysis of electroencephalographic signals, is revealing a complex pattern of sleep abnormalities in human narcolepsy that can be used diagnostically. The availability of novel devices measuring sleep 24 h per day also holds promise to provide new insights into how brain electrical activity and muscle tone are regulated by hypocretin
Sympathetic and cardiovascular activity during cataplexy in narcolepsy
No full textAutonomic nervous system activity changes have been described during cataplexy as playing a role in triggering it. To confirm these previous findings, we investigated the time course of sympathetic and cardiovascular activities during cataplexy. We made for the first time microneurographic recordings of 10 cataplectic episodes in three patients with hypocretin-deficient narcolepsy. During microneurography, muscle sympathetic nerve activity (MSNA) was recorded simultaneously with heart rate (HR), respiratory movements, arterial finger blood pressure (BP), electroencephalography, electro-oculogram and superficial electromyogram. Results showed no significant autonomic changes before the onset of the cataplectic episodes. Cataplexy was associated with a significant increase in MSNA and BP compared with baseline, whereas HR was markedly decreased. An irregular breathing pattern mainly characterized by apnea typically occurred during the attacks. In conclusion, our findings did not show significant changes in autonomic activity prior to cataplexy onset, ruling out a triggering role of the autonomic system. However, cataplexy was associated with co-activation of sympathetic and parasympathetic autonomic systems, a pattern reminiscent of that reported during the vigilance reaction in animals
Behavioural and neurophysiological correlates of human cataplexy: A video-polygraphic study
No full textCardiovascular autonomic dysfunction, altered sleep architecture, and muscle overactivity during nocturnal sleep in pediatric patients with narcolepsy type 1
No full textSTUDY OBJECTIVES: arterial blood pressure (ABP) decreases during sleep compared to wakefulness and this change is blunted in mouse models of and adult patients with narcolepsy type 1 (NT1). We tested whether: 1) pediatric patients with NT1 have similar cardiovascular autonomic abnormalities during nocturnal sleep; and 2) these abnormalities can be linked to hypocretin-1 cerebrospinal fluid concentration (CSF HCRT-1), sleep architecture or muscle activity. METHODS: laboratory polysomnographic studies were performed in 27 consecutive drug-naïve NT1 children or adolescents and in 19 matched controls. Nocturnal sleep architecture and submentalis (SM), tibialis anterior (TA), and hand extensor (HE) electromyographic (EMG) activity were analyzed. Cardiovascular autonomic function was assessed through the analysis of pulse transit time (PTT) and heart period (HP). RESULTS: PTT showed reduced lengthening during total sleep and REM sleep compared to nocturnal wakefulness in NT1 patients than in controls, whereas HP did not. NT1 patients had altered sleep architecture, higher SM EMG during REM sleep, and higher TA and HE EMG during N1-N3 and REM sleep when compared to controls. PTT alterations found in NT1 patients were more severe in subjects with lower CSF HRCT-1, but did not cluster or correlate with sleep architecture alterations or muscle overactivity during sleep. CONCLUSION: our results suggest that pediatric NT1 patients close to disease onset have impaired capability to modulate ABP as a function of nocturnal wake-sleep transitions, possibly as a direct consequence of hypocretin neuron loss. The relevance of this finding for cardiovascular risk later in life remains to be determined
Sleep-related hippocampo-cortical interplay during emotional memory recollection.
No full textpeer reviewedEmotional events are usually better remembered than neutral ones. This effect is mediated in part by a modulation of the hippocampus by the amygdala. Sleep plays a role in the consolidation of declarative memory. We examined the impact of sleep and lack of sleep on the consolidation of emotional (negative and positive) memories at the macroscopic systems level. Using functional MRI (fMRI), we compared the neural correlates of successful recollection by humans of emotional and neutral stimuli, 72 h after encoding, with or without total sleep deprivation during the first post-encoding night. In contrast to recollection of neutral and positive stimuli, which was deteriorated by sleep deprivation, similar recollection levels were achieved for negative stimuli in both groups. Successful recollection of emotional stimuli elicited larger responses in the hippocampus and various cortical areas, including the medial prefrontal cortex, in the sleep group than in the sleep deprived group. This effect was consistent across subjects for negative items but depended linearly on individual memory performance for positive items. In addition, the hippocampus and medial prefrontal cortex were functionally more connected during recollection of either negative or positive than neutral items, and more so in sleeping than in sleep-deprived subjects. In the sleep-deprived group, recollection of negative items elicited larger responses in the amygdala and an occipital area than in the sleep group. In contrast, no such difference in brain responses between groups was associated with recollection of positive stimuli. The results suggest that the emotional significance of memories influences their sleep-dependent systems-level consolidation. The recruitment of hippocampo-neocortical networks during recollection is enhanced after sleep and is hindered by sleep deprivation. After sleep deprivation, recollection of negative, potentially dangerous, memories recruits an alternate amygdalo-cortical network, which would keep track of emotional information despite sleep deprivation
Clinical, electroencephalographic and biological parameters to optimise narcolepsy diagnostic criteria
No full textLa narcolepsie est une maladie rare, touchant une personne sur 2000. Elle se caractérise par l'association d'une somnolence diurne excessive, d'épisodes de cataplexie, de paralysies du sommeil, d'hallucinations hypnagogiques. et d'une fragmentation du sommeil. La narcolepsie sans cataplexie constitue un sous-type hétérogène. Le diagnostic de narcolepsie peut être clinique, mais bien souvent un Test Itératif de Latence d'Endormissement (T1LE), précédé d'une polysomnographie nocturne (NPSG). sont utilisés pour porter le diagnostic.La cause de la plupart des cas de narcolepsie avec cataplexie a été découverte au début des années 2000: la destruction, probablement d'origine auto-immune. des neurones à hypocrétine de l'hypothalamus. Un déficit en hypocrétine à la ponction lombaire constitue désormais un test de référence pour établir le diagnostic, ce qui offre l'opportunité d'optimiser les critères actuels et de tester de nouvelles hypothèses diagnostiques en regard de ce test de référence. Peu d'études ont à ce jour spécifiquement porté sur la narcolepsie sans cataplexie et son diagnostic. Nous avons donc cherché à identifier les prédicteurs du déficit en hypocrétine dans la narcolepsie sans cataplexie. De plus, dans la narcolepsie-cataplexie, l'utilisation comme critère diagnostique d'une latence courte d'apparition du sommeil paradoxal à la NPSG n'a jamais été évaluée en utilisant comme test de référence le déficit en hypocrétine, et nous avons donc cherché à en déterminer l'utilité diagnostic et la valeur-seuil optimale.Afin de mener à bien ces projets de recherche, nous avons initié et participé au développement du logiciel d'analyse ROC (Receiver Operating Characteristic) SoftROC. Dans la narcolepsie sans cataplexie. nous avons montré que les paramètres électrophysiologiques, plus que cliniques, différaient entre les patients avec un taux bas d'hypocrétine et ceux avec un taux normal. Dans la narcolepsie avec cataplexie. nous avons établi qu'une latence courte (< 15 minutes) d'apparition du sommeil paradoxal à la NPSG était un test diagnostique spécifique, mais peu sensible, pour la narcolepsie avec déficit en hypocrétine. Nos résultats ont contribué à la révision des classifications internationales des troubles du sommeil.Narcolepsy is characterised by excessive diurnal sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations andsleep fragmentation. Narcolepsy without cataplexy is a heterogeneous subtype. Diagnosis can be established clinically,but a Mulitple Sleep Latency Test (MSLT) following a Nocturnal PolySomnoGraphy (NPSG), is used most of the time.Auto-immune loss of hypocretin cells is responsible for narcolepsy with cataplexy. Hypocretin deficiency at lumbarpuncture is a gold standard for diagnosis.Few studies have focused specifically on narcolepsy without cataplexy. Our aim was to identify predictors of hypocretindeficiency in this condition. Moreover, in narcolepsy with cataplexy, a short REM sleep latency at NPSG has never beenevaluated as a diagnostic test using hypocretin deficiency as a gold standard, and we therefore have aimed at assessing itsdiagnostic utility and optimal cut-off.In order to conduct our research, we have contributed to developing a ROC analysis software (SoftROC).In narcolepsy without cataplexy- objective (NPSG and MSLT) more than clinical parameters were predictors ofhypocretin-deficiency. In narcolepsy-cataplexy, a short (< 15 mins) REM latency at NPSG was a specific, but notsensitive. diagnostic test. Our results contributed to the revision of international diagnostic classifications
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