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Biomedical subjects

M Billiard

Publications and source records attributed to M Billiard.

At least 37 records · Page 2Linked to original sources
PubMed1999

Correlation dimension of EEG slow-wave activity during sleep in narcoleptic patients under bed rest conditions.

The calculation of the correlation dimension (D2) was applied to the study of the profiles of EEG slow-wave activity in nine narcoleptic subjects and nine sex- and age-matched control subjects who, following a baseline night recording, were maintained on 16 h of diurnal sleep deprivation and, thereafter, submitted to a 32-h bed rest protocol. The reversibility test allowed us to reject the null hypothesis that the time series considered in our study were generated by a static transformation of a linear Gaussian random process. Similarly, all profiles showed a positive largest Lyapunov exponent. Finally, the computation of D2 showed an average value of 5.27 (0.68 S.D.) in normal controls and 4.05 (1.49 S.D.) in narcoleptic patients (p = 0.067). Four of the narcoleptic patients showed values of D2 lower than 4, this was never observed in the normal controls (p = 0.0294). This study indicates that the mechanism of sleep-wake regulation in narcolepsy shows a somewhat lower degree of complexity as compared to normal controls. In particular, these data seem to confirm the already suggested different and simpler coupling between the homeostatic process of sleep regulation and the circadian and ultradian drives to sleep that occurs in bed rest condition in this disease.

Adult↗
PubMed1998

[Hypersomnia. Narcolepsy-cataplexy (Gélineau syndrome)].

SIGNS AND SYMPTOMS: Narcolepsy is the most prevalent of the primary disorders of vigilance. It is relatively easy to identify in presence of clearcut cataplexy and other REM-sleep related symptoms, i.e. sleep paralysis and hypnagogic hallucinations. Otherwise, one must rely on demonstration of sleep onsets in REM during night and daytime polygraphy, and on the very strong association with the HLA gene DQB1*0602. TREATMENT: With the advent of modafinil, treatment of narcolepsy has been substantially modified. New strategies are an improvement over amphetamines both in terms of side effects and long-term outcome. Most cataplectic attacks can be controlled by tricyclics or other antidepressants. PATHOGENESIS: Major advances in pathophysiology and etiology have been obtained through an animal model of the disease, canine narcolepsy. Pharmacological studies point to the importance of alpha-1 adrenergic mechanisms in cataplexy, while dopaminergic systems seem more involved in generating sleepiness. As concerns genetics of this autosomal recessive disease, there is an equivalent of the human HLA association in the form of an immunoglobulin gene (mu-switch) linkage. Narcolepsy research is now looking for other genes, for which familial cases may give clues.

Animals↗
PubMed1998

Homeostatic process and sleep spindles in patients with sleep-maintenance insomnia: effect of partial (21 h) sleep deprivation.

OBJECTIVES: A low level of process 5 at bed time would be responsible for a reduced amount of slow-wave activity (SWA) leading to increased alpha activity and awakenings at the end of the night. METHODS: Following a base-line night (BLN) recording, 7 sleep-maintenance insomnia (SMI) subjects and 7 sex- and age-matched controls were maintained on 21 h of sleep deprivation. Thereafter, a recovery night (RN) was performed from 2300 h until spontaneous awakening. SWA (power density of the EEG delta band between 0.75 and 4.5 Hz) was monitored by means of spectral analysis (FFT). Sleep spindles and the occupation ratio of Rechtschaffen and Kales EEG bands were observed by integrated digital filtering analysis. RESULTS: SWA was lower in SMI subjects than in controls during RN but was higher than in BLN indicating that the homeostatic process was operating, but weaker in SMI subjects. On the other hand in SMI subjects the sleep spindle index (SSI) did not decrease during slow-wave sleep and was significantly lower than in controls. Moreover during RN the SSI decreased significantly during the first sleep cycle in controls and not in SMI subjects. The existence of an inverse relationship between SWA and SSI was therefore not observed in insomniacs. Finally the mean duration of alpha frequency significantly increased in SMI subjects. CONCLUSIONS: It is hypothesised that in SMI subjects, an alteration of the homeostatic process is responsible for insufficient sleep pressure leading to an inability to maintain sleep for an extended period.

Adult↗
PubMed1998

Idiopathic hypersomnia.

Identification of idiopathic hypersomnia dates back 20 years only. It typically consists of prolonged nocturnal sleep, great difficulty waking up in the morning or at the end of a nap, and constant or recurrent excessive daytime sleepiness. Complete and incomplete forms are encountered. Twenty-three subjects fulfilling ICSD criteria are reported with clinical, polysomnographic and immunogenetic data. Considering differential diagnosis is an important step in the diagnosis of idiopathic hypersomnia. Idiopathic hypersomnia is much less frequent than narcolepsy. A strong genetic component is suggested by the high proportion of familial cases. No association with HLA has been evidenced to date.

Adolescent↗
PubMed1998

[Wake disorders. I. Primary wake disorders].

Primary wake disorders encompass various conditions of excessive daytime sleepiness and/or increased nighttime sleep, of unknown origin beginning most often in adolescence and of chronic or recurrent natural history. The best known of these conditions is narcolepsy associating two major clinical features, irresistible episodes of sleep, sleep onset REM periods and an almost constant association with HLA DR2-DQ1. The prevalence of the condition is close to the one of multiple sclerosis but positive diagnosis requires most often over 10 years to be made. The treatment of excessive daytime sleepiness has recently benefited from a new non-amphetamine awakening compound, modafinil, active in 60 to 70 p. 100 of the cases. The treatment of cataplexy still relies on antidepressants, tricyclics or selective serotonin reuptake blockers. Major advances in pathophysiology and pathogeny have been obtained through a natural model of the disease, canine narcolepsy. Pharmacological studies point to the importance of alpha-1 b adrenergic mechanisms in cataplexy, while dopaminergic systems seem more involved in excessive daytime sleepiness. As concerns genetics, the HLA DQB1*0602 gene predisposes to narcolepsy. In the canine model it is mirrored by an autosomal recessive gene showing a strong homology with the human immunoglobulin gene mu-switch. Familial studies have shown that besides typical phenotypes, attenuated forms of the condition characterized by isolated recurrent daytime naps and/or lapses into sleep do exist. In addition one or several other genes may be involved. Narcolepsy is multifactorial, including one or several genes as well as environmental factors. Idiopathic hypersomnia is noted for very long night sleep, difficulty waking up and more or less constant excessive daytime sleepiness. In contrast with narcolepsy sleep in not refreshing. There is no polysomnographic or immunogenetic special feature. Idiopathic hypersomnia is 10 times less frequent than narcolepsy. It is often overdiagnosed due to insufficient knowledge of other causes of excessive daytime sleepiness such as the upper airway resistance syndrome. Modafinil is also of great value in the treatment of idiopathic hypersomnia. In the absence of an animal model, pathophysiology and pathogeny are still poorly understood. Even rarer is the Kleine-Levin syndrome which is easily distinguishable through its recurrent character and its tendency to progressively disappear. It mainly occurs in early adolescent males. Its main features are episodes of sleep of a week duration recurring at a several months' interval along with disturbances of alimentary and sexual behavior. There is no satisfactory treatment of hypersomniac episodes. On the other hand a prophylactic treatment with carbamazepine or lithium may be active. Pathophysiology remains unsettled in spite of some evidence of a hypothalamic functional disturbance.

Animals↗
PubMed1997

[Clinical study of familial forms of amyotrophic lateral sclerosis. Review of the literature].

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder involving both upper and lower motor neurons. The disease is possibly due to several factors, including a genetic one. This is supported by the existence of 5 to 10 p. 100 familial cases. In these pedigrees, the transmission is autosomal dominant, with a high penetrance (> 90 p. 100). We studied the phenotypes of these familial cases, in reviewing the literature on familial ALS (FALS). It has been noted that FALS are heterogeneous, with different age of onset, site of onset and disease duration. Moreover, in FALS, onset is earlier than in the sporadic form (48 vs 60 years, as usually reported in the literature). We also frequently noted sensory disorders (20 p. 100), onset on the lower limbs (46 p. 100) and decreased or absent ankle-jerks (75 p. 100) in FALS patients.

Age Factors↗
PubMed1996

[Narcolepsy].

Narcolepsy is a rather unknown but not exceptional condition. Its prevalence, 2 to 6/10000, is ranging among this of multiple sclerosis. Narcolepsy is remarkable for clinical, polygraphic and immunogenetic features which make it a kind of model of disorders of alertness. It was first described in 1877. It has recently benefited from consistent pathophysiological progresses, which have been facilitated by the discovery of a natural canine model. The two main symptoms are irresistible and refreshing episodes of sleep and cataplexy a loss of muscle tone emotionally triggered. Polygraphically the sleep onset REM period is the major feature. Immunogenetically the condition is remarkable for an almost 100% association with HLA DR2-DQ1. Narcolepsy is a debilitating, chronic condition. Its treatment is threefold including stimulants against excessive daytime sleepiness and irresistible episodes of sleep, modafinil a new compound with awakening properties has just been introduced, antidepressants against cataplexy and associated symptoms and hypnotics against disrupted sleep.

Adolescent↗
PubMed1996

Hypersomnia in association with dysthymia in comparison with idiopathic hypersomnia and normal controls.

Polysomnographic studies in hypersomniac patients with mood disorders are rare. Previous studies investigated patients with a severe mood disorder, but our study was done in patients with dysthymia, who complained of sleepiness. Mean sleep latency test (MSLT) and continuous polysomnographic recording (CPR) were done in 12 dysthymic patients, in comparison with 12 idiopathic hypersomnia patients, and 12 normal controls. In dysthymic patients mean sleep latency on the MSLT (13 +/- 1) was normal, and when CPR was done during 24 hours, no hypersomnia was found (553 +/- 24). Dysthymic patients showed an abnormal macrostructure of sleep (characterised by an excess of sleep stage I and a decrease of stages 3 and 4), which could be related to their complaint of hypersomnia.

Adolescent↗
PubMed1996

Ultradian aspects of sleep in narcolepsy.

Following a baseline night recording, 9 narcoleptic subjects and 9 sex and age-matched control subjects were maintained on 16 hours of diurnal sleep deprivation. Thereafter subjects were submitted to a 32 hour bed rest protocol in a sound-light attenuated room. The EEG was recorded and processed using a Fast Fourier Transform. Narcoleptic patients did not differ from control subjects in total sleep time over the whole time-span. An ultradian tendency to sleep seems to be predominant in narcoleptic patients and evidence of a strong basic rest activity cycle is shown. The coupling between the homeostatic process of sleep regulation and an ultradian drive to sleep would explain the peculiar 4 hour distribution pattern of SWA in narcoleptic patients.

Activity Cycles↗
PubMed1996

Use of modafinil in the treatment of narcolepsy: a long term follow-up study.

One hundred and forty patients (104 male and 36 female) aged 42.26 +/- 19.19 (range = 8 to 79.5 years) with narcolepsy-cataplexy were given modafinil (200 to 400 mg) at the Montpellier sleep disorders center from 1984 onwards. The follow-up focused on the reduction of excessive daytime somnolence (EDS), side effects and duration of treatment. In order to determine if any clinical aspect of narcolepsy could be involved in modafinil discontinuation, patients were divided into two groups according to continued or interrupted treatment. When modafinil effect on EDS was evaluated according to a scale varying from 0 (no effect) to 3 (excellent effect), 64.1% of the subjects, scored good or excellent. The mean duration of treatment was 22.05 months +/- 24.9, ranging from 1 to 114 months. Dependency signs were never observed.

Adolescent↗
PubMed1996

Idiopathic hypersomnia.

Idiopathic hypersomnia is not as well delineated as narcolepsy and its history is much more recent. There are at least two forms of the disorder: (1) a polysymptomatic form, characterized by excessive daytime sleepiness, nocturnal sleep of abnormally long duration, and signs of sleep drunkenness on awakening, and (2) a monosymptomatic form that manifests only by excessive daytime sleepiness. The most widely used laboratory procedures are nocturnal polysomnographic recording following by an MSLT demonstrating a mean sleep latency of less than 10 minutes. At least in the polysymptomatic form, however, continuous polysomnography on an ad lib protocol deserves to be performed to catch the abnormally long major sleep episode and the long unrefreshing naps. Idiopathic hypersomnia is probably one of the most overdiagnosed sleep disorders. Several other disorders must be excluded before the diagnosis can be considered conclusive. Treatment of idiopathic hypersomnia relies on stimulants, which are frequently less effective and less well tolerated than in narcolepsy.

Adult↗
PubMed1996

[Circadian rhythm in normal and pathological sleep].

Different challenges, constraints for quality of sleep and wakefulness, sleep in extreme conditions, search for a better identification of disorders of sleep and wakefulness, spur researches on the circadian rhythm of sleep and on its disorders. Any advance in that field rests on the understanding of different physiologic phenomena: the intrinsic period of our internal clock is not 24-hours but a little less than 25-hours and it must be reset daily by the Zeitgebers. A sudden phase shift provokes an external desynchronisation. In addition not all rhythms resynchronize together resulting in an internal desyncronization. There is a close relationship between quantities of total sleep and REM sleep and the time of sleep onset within the 24-hours. The propensity to sleep follows a circasemidian rhythm with a major peak during the night and a secondary peak in the midafternoon. Disorders of the circadian rhythm of sleep are of two types: related to the misalignment of the sleep-wake schedule and the synchronizer-controlled rest-activity rhythm (shift work sleep disorder and time zone change syndrome) or related to an abnormal escape of the individual rest-activity rhythm from synchronizer control (delayed sleep phase syndrome, advanced sleep phase syndrome and non 24-hour sleep-wake syndrome.

Biological Clocks↗
PubMed1995

Dynamics of slow wave activity in narcoleptic patients under bed rest conditions.

Following a baseline night recording, 9 narcoleptic subjects and 9 sex- and age-matched control subjects were maintained on 16 h of diurnal sleep deprivation. Thereafter subjects were submitted to a 32 h bed rest protocol in a sound- and light-attenuated room. The EEG was recorded and processed by a Fast Fourier Transform. Narcoleptics did not differ from controls in total sleep time over the whole 32 h, but spent more time sleeping during the daytime (DT). In both groups slow wave activity (SWA) showed an exponential decaying trend during the first night (N1); a similar exponential trend during the second night (N2) was evident only in controls. In controls SWA showed a circadian-circasemidian distribution that was hardly detectable in nacroleptics. Narcoleptics showed an ultradian distribution of SWA with periodic emergence every 4 h during DT and N2. Our data confirm that a homeostatic mechanism is evident in narcolpetics when stimulated by diurnal sleep deprivation, while circadian and circasemidian mechanisms are less evident during DT and N2. These findings suggest a different coupling between homeostatic sleep regulating and circadian drives to sleep in narcoleptics. Ultradian drives to sleep seem to be predominant in these patients, thus probably acting as a means for the avoidance of stressful attempts to counteract a weaker waking state maintenance mechanism.

Adult↗
PubMed1995

Changing heat and moisture exchangers every 48 hours rather than 24 hours does not affect their efficacy and the incidence of nosocomial pneumonia.

Heat and moisture exchangers (HME) (Dar-Hygrobac II, Peters) can safely be used every 24 h for long-term mechanical ventilation and provide a cost-saving alternative to heated humidifiers. We have prospectively determined whether changing HMEs every 48 h only affects their clinical and bacteriological efficiency in a series of consecutive nonselected ICU patients requiring long-term mechanical ventilation. Two consecutive periods were compared. During period 1, HMEs were replaced every day; during period 2, they were changed every 48 h. Patients from the two periods were similar in terms of age and indication for and overall duration of MV (10 +/- 8.6 versus 10 +/- 9 d, p = 0.9). Minute ventilation and maximum values for peak airway pressure were identical during the two periods. These values were also identical after 1 and 2 d of HME use during period 2, indicating that HME resistance was not increased by prolonged use. Obstruction of the tracheal tube occurred only once in a period 1 patient. The results of quantitative cultures indicate that the maximum and mean levels of bacterial colonization during the two periods were similar for the pharynx, trachea, Y-connector, patient, and ventilator side of the HME. More importantly, the incidence of nosocomial pneumonia was similar during the two periods (6/61 versus 8/68, p = 0.7). Thus, prolonged HME use is safe and provides a substantial reduction in the cost of mechanical ventilation.

Adult↗
PubMed1995

Effects of zolpidem on the architecture and cyclical structure of sleep in poor sleepers.

Effects of zolpidem, a short acting non benzodiazepine hypnotic, have been studied in eight female poor sleepers, aged 25 to 54 years, documented during two consecutive adaptation nights. Subjects were recorded according to a 22 day single blind study. Placebo was given orally at bedtime on nights 2-4, zolpidem on nights 5-20 and finally placebo on nights 21-22. Polygraphic recordings (conventional analysis) were performed on nights 1-6; 12, 13; 19-22. Parameters of sleep continuity, sleep architecture and cyclical structure of sleep were studied. Zolpidem 10 mg showed a hypnotic effect on poor sleepers. It reduced sleep latency, increased total sleep time and decreased the number of awakenings during all recorded nights. During the first post-drug night a rebound insomnia was observed in two subjects only. Zolpidem did not increase specifically stage 2 to the detriment of stages 3 and 4 but it restored them during the first nights of administration. Study of the rapid eye movements-non rapid eye movements (REM-NREM) sleep cycles structure showed that the increase of stages 3 and 4 occurred only during the first part of the night. Finally, zolpidem had no effect on REM sleep temporal distribution.

Adult↗
PubMed1994

Objective and subjective sleep disturbances in patients with rheumatoid arthritis. A reappraisal.

OBJECTIVE: To assess objective and subjective evidence of sleep disturbances in patients with rheumatoid arthritis (RA) and to examine correlations between parameters of inflammatory activity and sleep pathology. METHODS: Nineteen RA patients and 19 age-matched healthy control subjects underwent all-night polysomnography on 2 consecutive nights. RA patients were also evaluated for daytime sleepiness by mean sleep latency test and responded to a self-report questionnaire on their first night. RESULTS: Whereas normal sleep architecture is conserved in RA, we confirmed former findings of severe sleep fragmentation and an enhanced presence of primary sleep disorders. No correlation exists between RA activity and the sleep disorders. Subjective assessment was not consistent with the objective evidence of sleep disruption, unlike the findings in patients with fibrositis. CONCLUSION: Sleep is severely disturbed in patients with RA, regardless of the inflammatory disease activity. The specificity of the sleep disorders assessed needs confirmation, as does specific sleep therapy for these patients.

Adult↗