Polygraphic study of vigilance states in the guinea pig fetus

The ontogenesis of the states of sleep in guinea pig foetus was studied by polygraphic method. Long-lasting records have been made in utero between the 40th and the 64th day of gestation. The ECoG activation pattern of paradoxical sleep (PS) and wakefulness appear from the 40th day (0,6 of term); the slow-wave sleep (SWS) appear about the 49th day (0,7 of term) and is characterized by cortical spindles. Between the 40th and the 47th day, cerebral maturation is accompanied by a progressive decrease of a discontinuous ECoG activity state. From 53 days (0,8 of term), the ECoG patterns of states of vigilance are similar to those of the newborn guinea pig. The percentage of time spent in PS is very high (80–90% at 48 days) before the SWS appearance. These observations prove the existence of a prenatal differentiation of the states of vigilance. The differentiation stages are similar to those observed after birth in immature newborn mammals. No relationship exists between the sleep of mother and foetus.     

Phasic activity in rats]

At the central level, in the rat, phasic activity has been recorded during paradoxical sleep and in acute conditions after injection of reserpine or parachlorophenylalanine. At the external level, during paradoxical sleep, the extraocular muscles lateral rectus, superior rectus and superior oblique are activated in both plastic and tonic manners. The muscles of the whiskers are also activated; these muscular activations are more often than not synchronous with the eye movements (80%). The time distribution of these ocular movements is homogenous. Reserpine induces phasic muscular activations of the extraocular muscles.     

Faut-il s’intéresser au sommeil des patients polyhandicapés ?

Far from superfluous, sleep recording is useful for diagnosing mechanical respiratory disorders such as Sleep Apneas. Those have an important impact on diurnal quality of life for patients with multiple disabilities: behaviour disorders, sleepiness, increased difficulty of concentration. Directed clinical examination and questioning are useful to decide whether to continue or not further investigations. Nocturnal pulse oxymetry recording is a good approach to the diagnosis. Confirmation can be achieved by sleep polygraphy. Only when doubt remains will polysomnography be considered. For the set-up of a ventilatory treatment, noninvasive PCO₂ monitoring is useful to differentiate pure OSA from global alveolar hypoventilation-associated OSA. Before setting-up a ventilatory treatment, a risk-benefit evaluation should be done: the OSA or alveolar hypoventilation treatment must improve enough quality of life sufficiently to balance the constraint of being ventilated every night.     

Sleep and wakefulness drugs and their indications

This paper is a review of the use of drugs in sleep and wakefulness disorders. Insomnia is more often a symptom than an autonomic disorder. Good knowledge of the clinical facts is required before prescribing hypnotics. Sedative drugs are potentially hypnotics; yet, melatonin is not sedative and may be considered to resynchronise of sleep phases. Stimulant drugs are prescribed in attention disorders; methylphenidate is the more frequently used. Narcolepsy, which is characterized by daytime sleepiness and irresistible episodes of sleep, is treated by an alpha1 noradrenergic stimulant modafinil which has no amphetaminic properties.     

Normal and disordered sleep

Normal sleep is a complex and reversible state of brain functioning, including reduced inputs and outputs, blunted reflexes, and metabolic and cognitive changes. Evidence supports a role for sleep in the consolidation of an array of learning and memory tasks. Sleep deprivation and fragmentation result in executive dysfunction, increased appetite/weight and cellular stress. Sleep is a vital, complex but plastic function that can be modulated depending on individual heritage and motivation. The major role of sleep in attention and memory raises about concern the reduction in sleep duration recently pointed in teenagers and young adults. Sleep disorders are numerous and various. Their mechanism is not always identified, but may result from a central dysfunction in sleep-wake (e.g. narcolepsy) or circadian (e.g. advanced sleep phase syndrome) systems, from the sleep-related loss of compensation of reflexes normally effective during wakefulness (breathing is the most vulnerable function during sleep), or from other diseases preventing sleep (e.g. psychiatric insomnia, restless legs syndrome).     

Troubles du sommeil et de l’éveil : mise au point

Insomnia is the most prevalent sleep disorders and affects severely 10% of adults worldwide. From poor sleep to insomnia, the severity of sleep disorders should be assessed clinically and by the use of validated questionnaires based on international consensual definitions. One main sign of insomnia is impaired daytime functioning. Insomnia may be treated with hypnotics only for a limited duration. Behavioural and cognitive therapies have been found efficient on chronic insomnia. Sleepiness is also a common sleep disorders due to altered sleep schedules, sleep deprivation, sleep disorders or as an adverse effect of some treatments. The risk of car accidents and the impaired quality of daytime functioning are the main consequences of sleepiness. The aim of this paper is to give some recommendations for the diagnosis and treatment of insomnia and sleepiness.     

Sommeil et nutrition chez le nourrisson et le jeune enfant

In infants, sleep/wake rhythms and the feeding pattern are closely related. Establishing stable night sleep depends on time givers. The decrease and later suppression of night feeds are part of the process. Breast fed infants keep waking up at night later than bottle fed peers, and they are fed more frequently during the nocturnal waking occasions. After the age of six months, night awaking is likely induced by environmental factors (sleep conditioning, night eating syndrome, sharing the parents’ bed, absence of limits) rather than by the composition of the mother's milk. Cow's milk intolerance as well as some dietary mistakes (low fat intake, excessive protein intake, low or high feed volumes) can induce true insomnias in infants.     

Propriospinal myoclonus at sleep onset

AIMS: To describe the clinical and polygraphic features of propriospinal myoclonus (PSM) at sleep onset. MATERIAL AND METHODS: PSM was first described in 1997 in patients with jerks occurring in the relaxation period preceding sleep. EMG showed jerks to arise in spinally innervated muscles, propagating thereafter to rostral and caudal muscles at a low speed, typical of propriospinal pathways. RESULTS: PSM arose when EEG alpha activity spread over the scalp and disappeared during either active wakefulness or actual sleep. In some patients EMG activity could sometimes remain localized to the abdominal muscles, propagating to other segments only in fully developed jerks. Neurological examination, brain and spinal MRI were usually normal and clonazepam afforded partial improvement. PSM has been recently observed also in restless legs syndrome, during relaxed wakefulness preceding falling asleep, coexisting with motor restlessness and sensory discomfort. PSM disappeared when spindles and K-complexes and typical Periodic Limb Movements appeared with EMG activity limited to leg muscles, without propriospinal propagation. CONCLUSIONS: Conceivably, PSM arises in axial muscles due to some spinal generator set into motion by facilitating influences characteristic of the wake-sleep transition and then undergoes multimeric propriospinal propagation. In the International Classification of Sleep Disorders (ICSD-2), PSM is listed in chapter VII, among the "Isolated symptoms, apparently normal variants and unresolved issues".