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M Billiard

Publications and source records attributed to M Billiard.

133 records · Page 8Linked to original sources

[Arousal of respiratory origin and upper airway resistance syndrome: pathophysiological and diagnostic aspects].

INTRODUCTION: The description of Upper Airway Resistance Syndrome (UARS) let us to recognize the importance of the pair 'respiratory effort-arousal' on sleep-disordered breathing pathophysiology. DEVELOPMENT: First part of this paper reviews knowledge about respiratory arousal pathophysiology. Arousal response is normally needed to end obstructive respiratory episodes, but it is also the cause of sleep fragmentation. Among respiratory stimuli able to provoke arousal (respiratory effort, hypoxemia and hypercapnia), respiratory effort is the most constant. Neurophysiological mechanisms involved in arousal, sleep and vegetative consequences, and the possible role of non visible arousals, are also discussed. In UARS, because of the absence of apnea/hypopnea and significative O2 desaturations, arousals are induced by the increased respiratory effort. Diagnosis needs the simultaneous recording of polysomnography and esophageal pressure. Some symptoms and signs of UARS are similar to those of Obstructive Sleep Apnea Syndrome. However, UARS shows any differences: a lower Body Mass Index, less constant snoring, males and females are similarly affected or higher frequency of craniofacial abnormalities. Diagnostic difficulties may be due to confusion between hypopneas and episodes of increased resistance of upper airway, or to the lack of definitive diagnostic criteria. Finally, differential diagnosis needs a broad knowledge of disorders of excessive daytime sleepiness.

Body Mass Index↗

Circadian patterns of growth hormone and cortisol secretions in narcoleptic patients.

Narcolepsy, a disorder which is clinically characterized by recurring episodes of sleep during the day, frequently associated with nocturnal disrupted sleep and polygraphically by sleep onset REM periods, has been studied in regard to the relationships between GH, cortisol secretion and sleep. Ten narcoleptics were polygraphically recorded during 24 h after one night's adaptation. Blood samples were taken every 20 min for GH and cortisol immuno-assays. Three narcoleptics were recorded twice 2 months later and 2 normal subjects served as controls. The following results were obtained: GH secretory pattern was different in narcoleptics and controls; two groups were identified: the first one showed a very low basal GH secretion with rare and small secretory peaks not clearly linked with sleep. One subject of this group recorded twice showed a similar pattern. The second group exhibited a higher basal secretion with many peaks without any well-defined relationship to sleep stages. The pattern was again consistent in two recordings of 2 subjects in this group. Furthermore GH secretion rose significantly (p less than 0.01) between 2100 and 0000 with no apparent relationship to sleep stages. The cortisol secretory pattern showed a significant rise (p less than 0.01) between 0400 and 1000 and was not different in narcoleptics and controls. In narcolepsy the monophasic sleep-wakefulness cycle is disrupted. The GH secretion pattern is modified whereas the circadian pattern of cortisol secretion is normal and independent of the sleep-wakefulness cycle of the narcoleptic patient.

Adult↗