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Michel Billiard

Publications and source records attributed to Michel Billiard.

15 recordsLinked to original sources
PubMed2006

Kleine-Levin syndrome in a 14-year-old girl: CSF hypocretin-1 measurements.

CSF hypocretin-1 measurements were performed during a period of hypersomnia and during an asymptomatic interval in a 14-year-old girl affected with severe Kleine-Levin syndrome. A twofold decrease in hypocretin-1 was evidenced during the period of hypersomnia in comparison with the asymptomatic interval. Together with previous data, this result is in favour of recurrent dysfunction at the hypothalamic level in Kleine-Levin syndrome.

Adolescent↗
PubMed2005

No effect on cognitive function from daily mobile phone use.

The increasing use of mobiles phones (MP) has raised the problem of the effects of daily electromagnetic fields (EMF) exposure on human health. To date several studies have been published concerning the effects of acute MP exposure on psychomotor performances. This study investigated the effects of daily exposure to GSM 900 type MP on cognitive function. Fifty-five subjects (27 male and 28 female) were divided into two groups: a group with MP switched on and a group with MP switched off. The two groups were matched according to age, gender, and IQ. This double blind study lasted for 45 days and was divided in three periods: baseline (BLP, 2 days), exposure (EP, 27 days), and recovery (RP, 13 days). Subjects were exposed during EP and sham exposed during RP for 2 h/day, 5 days/week. The neuropsychological test battery composed of 22 tasks screened four neuropsychological categories: information processing, attention capacity, memory function, and executive function. This neuropsychological battery was performed four times on day 2 (BLP), day 15 (EP), day 29 (EP), and day 43 (RP). Our results indicate that daily MP use has no effect on cognitive function after a 13-h rest period.

Adolescent↗
PubMed2005

Family studies in insomnia.

OBJECTIVE: Several predisposing factors to insomnia have been hypothesized, including a familial component; however, few studies have focused on this topic. The aim of this study is to evaluate the prevalence of insomnia among first-degree relatives of chronic insomniacs and to compare the symptoms between sporadic and familial insomnia. METHODS: Two hundred fifty-six consecutive chronic insomniacs completed a clinical interview, psychometric questionnaires, a questionnaire on the family history of insomnia and, when indicated, a polysomnography. A control group was performed to estimate a base-rate incidence of insomnia in their families. RESULTS: Patients with primary (n=77) and psychiatric (n=104) insomnia were definitely included. Of those with primary insomnia, 72.7% reported familial insomnia compared with 24.1% in the noninsomnia control group. Among the psychiatric insomniacs, 43.3% reported familial insomnia. The mother was the relative most frequently affected. Comparisons between the family prevalence rates of insomnia assessed by the probands and by first-degree relatives show high concordance. A tendency to a younger age at onset was observed in familial and primary insomnia. CONCLUSION: This study reports a significant increase of familial aggregation of insomnia, warranting further genetic studies in primary insomnia with early age at onset.

Adolescent↗
PubMed2005

[Methadone and sleep apnea syndrome].

BACKGROUND: Sleep apnea syndrome occurs when, during sleep, breathing stops for 10 seconds or longer, with an index of 5 times or more an hour. It is clinically characterized by loud snoring at night, continuous or interrupted by pauses followed by loud breathing. Sleep is fitful, broken by arousals, and yields little rest. There is daytime excessive sleepiness with repeated involuntary falling asleep, often unknown by the subject. CLINICAL DESCRIPTION: In this article, we describe an observation of central sleep apnea syndrome in a female patient receiving an opiate replacement therapy. METHOD: An analysis of the before and after methadone withdrawal polysomnograhic tracing was done for this patient. RESULTS: This diagnosis etiology and physiopathology are critically approached. Clinicians should be careful in treating induced sleep disorders in such patients. CONCLUSION: Prescribing benzodiazepines during an opiate withdrawal of the methadone type is not recommended when central apnea occurs.

Adult↗
PubMed2004

[Narcolepsy, from Westphal to hypocretin].

CLINICAL DATA: Narcolepsy is a poorly known disease, though not exceptional, with a prevalence of 25 to 35 per 100,000 according to various surveys. Its onset can be anytime from childhood to the fifties with a peak in the second decade. It is characterized by two cardinal symptoms, irresistible sleep episodes and cataplexy or sudden loss of muscle tone triggered by emotional situations. The other symptoms, referred to as accessory due to their inconstancy, are hypnagogic hallucinations, sleep paralysis and disturbed nocturnal sleep. Its diagnosis relies on the identification of the cardinal symptoms. Laboratory tests are required to confirm the diagnosis before initiation of a life-long treatment. Theses test include: all-night and daytime polysomnography documenting sleep-onset REM periods, HLA typing, showing the association with HLA DQB1*0602, and, in unclear cases only, measurement of cerebro-spinal fluid (CSF) hypocretine-1 showing values below 110pg/ml, highly specific of narcolepsy with cataplexy. Pathophysiology owes a lot to the existence of a natural canine model, the narcoleptic dog. Irresistible sleep episodes and cataplexy exhibit different pharmacological control, the former depending on dopaminergic systems and the latter on noradrenergic systems. The most remarkable findings of the last twenty years are the close association with HLA DQB1*0602, the identification of a mutation of hypocretin receptor 2 in the narcoleptic dog and the absence of CSF hypocretin-1 in 90% of patients. An autoimmune mechanism is suggested but not evidenced. THREE-FOLD TREATMENT: First line treatment of irresistible sleep episodes in modafinil, Cataplexy or tricyclic antidepressants or sodium oxybate, and disturbed nocturnal sleep by hypnotics or sodium oxybate. Current therapeutic research is oriented towards hypocretin agonists and immunosuppressors.

Animals↗
PubMed2004

A narcolepsy susceptibility locus maps to a 5 Mb region of chromosome 21q.

The genetic basis of human narcolepsy remains poorly understood. Multiplex families with full-blown narcolepsy-cataplexy are rare, whereas families with both narcolepsy-cataplexy and excessive daytime sleepiness without cataplexy are more common. We performed a genomewide linkage analysis in a large French family with four members affected with narcolepsy-cataplexy and 10 others with isolated recurrent naps or lapses into sleep. Only three regions showed logarithm of odds (LOD) scores greater than 1 in two-point linkage analysis (D6S1960, D11S2359, and D21S228). Genotyping additional markers provided support for linkage to 9 markers on chromosome 21 (maximum two-point LOD score, 3.36 at D21S1245). The multipoint linkage analysis using SimWalk2 provided further evidence for linkage to the same region (maximum parametric LOD score, 4.00 at 21GT26K). A single haplotype was shared by all affected individuals and informative crossovers indicated that the elusive gene that confers susceptibility to narcolepsy is likely to be located between markers D21S267 and ABCG1, in a 5.15 Mb region of 21q.

Child↗
PubMed2004

Is insomnia best categorized as a symptom or a disease?

Insomnia, defined by difficulty falling asleep or remaining asleep, early morning awakening and/or non-restorative sleep, and daytime consequences, is an important public health issue with a significant negative impact on individuals' physical and social performance, ability to work and quality of life, as well as on society as a whole. Chronic insomnia warrants treatment in the majority of cases, but it is often under-treated. Primary insomnia occurs independently of other factors, and is possibly related to a general psychophysiologic hyperarousal. Other types of insomnia occur in association with various conditions such as psychiatric disorders, medical disorders (e.g., chronic pain, dysfunction and movement disorders), circadian rhythm disorders and medication or substance use. These types of insomnia are diagnosed more frequently in the clinic. As a result, insomnia is traditionally viewed and treated as a symptom rather than a disease, with the majority of therapies aimed at resolving underlying medical factors. However, it is important to clearly establish whether co-morbidities are causative for or simply co-exist with insomnia, in order to recommend the most appropriate treatment and optimize treatment outcomes. Difficulties still arise when categorizing insomnia subtypes. Here, we highlight some of the major challenges for future research in classifying both primary insomnia and insomnia related to or associated with various conditions, and their relevance to primary care.

Brain↗
PubMed2004

Effect of cognitive behavioural therapy for insomnia on sleep architecture and sleep EEG power spectra in psychophysiological insomnia.

There is now an overwhelming preponderance of evidence that cognitive behavioural therapy for insomnia (CBT-I) is effective, as effective as sedative hypnotics during acute treatment (4-8 weeks), and is more effective in long term (following treatment). Although the efficacy of CBT-I in the treatment of chronic insomnia is well known, however there is little objective data on the effects of CBT-I on sleep architecture and sleep EEG power densities. The present study evaluated, first, subjective change in sleep quality and quantity, and secondly the modifications occurring in polysomnography and EEG power densities during sleep after 8 weeks of CBT-I. Nine free drug patients with psychophysiological insomnia, aged 33-62 years (mean age 47 +/- 9.7 years), seven female and two male participated in the study. Self-report questionnaires were administered 1 week before and 1 week after CBT-I, a sleep diary was completed each day 1 week before CBT-I, during CBT-I and 1 week after CBT-I. Subjects underwent two consecutive polysomnographic nights before and after CBT-I. Spectral analysis was performed the second night following 16 h of controlled wakefulness. After CBT-I, only scales assessing insomnia were significantly decreased, stages 2, REM sleep and SWS durations were significantly increased. Slow wave activity (SWA) was increased and the SWA decay shortened, beta and sigma activity were reduced. In conclusion CBT-I improves both subjective and objective sleep quality of sleep. CBT-I may enhance sleep pressure and improve homeostatic sleep regulation.

Adult↗
PubMed2003

Clinical aspects and pathophysiology of narcolepsy.

UNLABELLED: Narcolepsy is a chronic debilitating sleep disorder first described in the late 19th century. It is characterized by two major symptoms, excessive daytime sleepiness and cataplexy, and two so-called auxiliary symptoms, hypnagogic hallucinations and sleep paralysis. The final diagnosis relies on polysomnography showing the presence of sleep onset rapid eye movement periods (SOREMPs) during the multiple sleep latency test. The presence of HLA DQA1*0102-DQB1*0602 is supportive of the diagnosis. The pathophysiology of the disorder is still unknown but an imbalance between monoamines and acetylcholine is generally accepted. Recent findings in narcoleptic dogs, a natural model of narcolepsy, and in knockout mice revealed that a mutation of type 2 hypocretin receptor plays a major role in the etiology of narcolepsy. Up to now, no mutation has been found in humans except a case of early onset and atypical narcolepsy. However, a marked reduction of hypocretin type 1 has been found in the cerebrospinal fluid (CSF) of a majority of patients and a global loss of hypocretins was noted in post-mortem brain tissue of narcoleptic subjects. Conversely, no hypocretin neuron degeneration has been observed in the genetic form of narcolepsy in dogs but no trace of hypocretin was seen in the brain or the CSF in cases of sporadic canine narcolepsy. This suggests that different hypocretinergic mechanisms are involved in sporadic and genetic forms of canine narcolepsy. Treatment has not evolved significantly over the last few years. However, new drugs, such as hypocretin agonists, are currently being developed. SIGNIFICANCE: After the discovery of the type 2 hypocretin receptor mutation in canine narcolepsy and the finding of a CSF hypocretin-1 deficiency in human narcolepsy, the major stream of research has involved the hypocretinergic system. However, other lines of research deserve to be pursued simultaneously, in view of comprehensive advancements in the understanding of narcolepsy.

Animals↗
PubMed2003

Month of birth as a risk factor for narcolepsy.

STUDY OBJECTIVES: A loss of hypocretin neurons has been observed in human narcolepsy; however, the cause of this disorder is still unknown. While family history and genetic factors are important individual risk factors for narcolepsy, environmental factors also contribute to the pathogenesis of the disease. The aim of the study was to find out whether there is a seasonality of month of birth in narcoleptic patients. DESIGN: Diagnosis of narcolepsy with cataplexy was based on International Classification of Sleep Disorders criteria with clinical, standard polysomnographic, and Multiple Sleep Latency Test features. PATIENTS AND SETTING: The birth dates of 886 patients with a clear-cut diagnosis of narcolepsy with cataplexy from 3 large narcolepsy databases (352 from Montpellier-France, 157 from Montreal-Canada, and 377 from Stanford-United States of America) were compared with those of 35,160,522 subjects from the general population. MEASUREMENTS AND RESULTS: Patients with narcolepsy had a significantly different seasonality of month of birth compared to that of the general population. The monthly distribution of birth yielded a peak in March with a maximal odds ratio at 1.45 and a trough in September with a minimal odds ratio at 0.63. No gender or country of origin differences were observed. CONCLUSIONS: A birth seasonality in the development of narcolepsy suggests the presence of environmental factors acting in combination with genetic factors during the fetal or perinatal period, in terms of an autoimmune process targeting the hypocretin system.

Birth Rate↗
PubMed2002

Severity of narcolepsy among French of different ethnic origins (south of France and Martinique).

STUDY OBJECTIVES: The aim of the study was to describe the clinical and polygraphical characteristics of narcoleptics, with and without cataplexy and to assess HLA predisposition across two different ethnic populations. DESIGN AND SETTING: Patients were 126 men and 58 women referred to the Montpellier Sleep Disorders Center (Mtp) and 12 men and 8 women referred to the Fort-de-France Sleep Disorders Center (FdF) (Martinique, a French West Indy island) with symptoms of narcolepsy. PARTICIPANTS: Narcoleptics were included if they had both excessive daytime sleepiness and clear-cut cataplexy (for the group with cataplexy), a mean sleep latency of less than 8 minutes and at least two sleep onset REM periods. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Narcolepsy without clear-cut cataplexy was rare (12/172) in the Mtp population whereas it was as frequent as full-blown narcolepsy (10/10) in the FdF population. Comparison between narcoleptics with cataplexy from the Mtp and FdF populations revealed a younger age of onset, a trend towards more severe sleepiness and lower frequency of cataplexy in Martinicans. Comparison between narcoleptics without cataplexy from the Mtp and FdF population revealed a higher frequency of hypnagogic hallucinations and sleep paralysis and a trend towards more severe sleepiness in Martinicans. 4.2% of the Mtp and 15% of the FdF patients were negative for HLA DR2. However all of them were positive for HLA DQ1. Moreover, a tight association with HLA DRB1*1503 was observed in Martinicans in contrast with DRB1*1501 in the Mtp population. Association with HLA DQB1*0602 was observed in 99.4% of narcoleptics with cataplexy and in 89.5% of those without cataplexy. CONCLUSIONS: Narcolepsy is a heterogeneous clinical syndrome, the more so as ethnic origins are considered. A modulating effect of HLA and non-HLA genes on symptoms disease may explain these differences.

Adult↗
PubMed2002

Awakening from sleep.

Awakening is a crucial event for the organism. The transition from sleep to waking implies physiological processes which lead to a new behavioural state. Spontaneous awakenings have varying features which may change as a function of several factors. The latter include intrasleep architecture, circadian phase, time awake, age, or disordered sleep. Despite its clear theoretical and clinical importance, the topic of awakening (in humans) has received little attention so far. This contribution focuses on major issues which relate to awakening from both basic (experimental) and clinical research. Recent knowledge on neurophysiological mechanisms is reported. The experimental data which provide in the human suggestions on the regulation of awakening are discussed, mainly those concerning sleep architecture and homeostatic/circadian factors also in a life-span perspective, since age is a powerful factor which may influence awakening. Clinical contributions will examine two main sleep disorders: insomnia and hypersomnia. Daytime functioning is shown in insomniac patients and compared to other pathologies like sleep apnea. A final section evokes links between some types of night waking and psychological factors.

Adrenocorticotropic Hormone↗
PubMed2002

Arousal reactions in sleepwalking and night terrors in adults: the role of respiratory events.

STUDY OBJECTIVES: The aim of the study was to determine the role of respiratory events, assessed by means of esophageal pressure monitoring, during arousals from slow wave sleep in adult patients with parasomnias. DESIGN: N/A. SETTING: N/A. PATIENTS: Ten patients with parasomnias (sleepwalking, night terrors, or both) and 10 control subjects matched for gender and age underwent 3 consecutive nights of polysomnography. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: By increasing sleep fragmentation, esophageal pressure monitoring has a deleterious effect on sleep architecture in patients with parasomnias and in control subjects. Respiratory events occur more frequently in parasomniacs than in controls. Respiratory effort seems to be responsible for the occurrence of a great number of arousal reactions in parasomniacs and is involved in triggering the parasomnia episodes. CONCLUSION: Sleep-disordered breathing seems to be frequently associated with parasomnias during slow wave sleep, emphasizing the utility of performing esophageal pressure monitoring in cases of sleep walking or night terrors.

Adult↗