Sleepiness in neurological disorders.

Sleepiness is a frequent and underrecognized symptom in neurological disorders, that impacts functional outcomes and quality of life. Multiple and potentially additive factors might contribute to sleepiness in neurological disorders, including sleep quality alterations, circadian rhythm disorders, drugs, and sleep disorders including sleep apnea or central disorders of hypersomnolence. Physician awareness of the possible symptoms of hypersomnolence, and associated causes is of crucial importance to allow proper identification and treatment of underlying causes. This review first provides a brief overview on clinical aspects of excessive daytime sleepiness, and diagnosis tools, then examines its frequency and mechanisms in various neurological disorders, including neurodegenerative disorders, multiple sclerosis, autoimmune encephalitis, epilepsy, and stroke.

Idiopathic hypersomnia and Kleine-Levin syndrome.

Idiopathic hypersomnia (IH) and Kleine-Levin syndrome (KLS) are rare disorders of central hypersomnolence of unknown cause, affecting young people. However, increased sleep time and excessive daytime sleepiness (EDS) occur daily for years in IH, whereas they occur as relapsing/remitting episodes associated with cognitive and behavioural disturbances in KLS. Idiopathic hypersomnia is characterized by EDS, prolonged, unrefreshing sleep at night and during naps, and frequent morning sleep inertia, but rare sleep attacks, no cataplexy and sleep onset in REM periods as in narcolepsy. The diagnosis requires: (i) ruling out common causes of hypersomnolence, including mostly sleep apnea, insufficient sleep syndrome, psychiatric hypersomnia and narcolepsy; and (ii) obtaining objective EDS measures (mean latency at the multiple sleep latency test≤8min) or increased sleep time (sleep time>11h during a 18-24h bed rest). Treatment is similar to narcolepsy (except for preventive naps), including adapted work schedules, and off label use (after agreement from reference/competence centres) of modafinil, sodium oxybate, pitolisant, methylphenidate and solriamfetol. The diagnosis of KLS requires: (i) a reliable history of distinct episodes of one to several weeks; (ii) episodes contain severe hypersomnia (sleep>15h/d) associated with cognitive impairment (mental confusion and slowness, amnesia), derealisation, major apathy or disinhibited behaviour (hypersexuality, megaphagia, rudeness); and (iii) return to baseline sleep, cognition, behaviour and mood after episodes. EEG may contain slow rhythms during episodes, and rules out epilepsy. Functional brain imaging indicates hypoactivity of posterior associative cortex and hippocampus during symptomatic and asymptomatic periods. KLS attenuates with time when starting during teenage, including less frequent and less severe episodes. Adequate sleep habits, avoidance of alcohol and infections, as well as lithium and sometimes valproate (off label, after agreement from reference centres) help reducing the frequency and severity of episodes, and IV methylprednisolone helps reducing long (>30d) episode duration.

Kleine-Levin syndrome: A neuropsychiatric disorder.

Kleine-Levin syndrome (KLS) is a rare, relapsing-remitting disease that affects mostly adolescents. It is characterized by episodes lasting from 1 to several weeks, and comprises neurological (hypersomnia, confusion, slowness, amnesia) and neuropsychiatric symptoms (derealization and apathy). Some psychiatric symptoms (megaphagia, hypersexuality, anxiety, depressed mood, hallucinations, delusions) arise during episodes, albeit less frequently, while patients are normal between episodes. However, sudden severe (>18h/day of sleep) and recurrent hypersomnia helps to differentiate KLS from other psychiatric mimics. Derealization, the striking feeling of unreality or of being in a dream-like environment, is strongly associated with hypoperfusion of the associative temporoparietal junction cortex, whereas apathy is almost complete loss of autoactivation: teenagers stop using their cell phones and their only spontaneous initiative is to sleep. The cause of KLS is not known, but evidence suggests it could be a recurrent inflammatory encephalitis. Up to 5% of cases are familial, although no abnormal gene has yet been found. Hypersomnia episodes tend to become less frequent and to disappear with advancing age. However, 28% of patients have long-lasting episodes (>30 days), and around 15% have no signs of recovery after >20 years of living with the disorder. Patients' cognitive and psychiatric status should be regularly checked during asymptomatic periods, as 20-40% develop long-term mild cognitive impairment or mood disorders. Lithium therapy is beneficial for reducing episode frequency, and intravenous steroids can reduce the duration of long episodes.

French consensus: Pharmacoresistant restless legs syndrome.

Dopaminergic agonists, α2δ ligands and opioids are, as single-drug therapy, the first line treatment for restless legs syndrome (RLS/Willis-Ekbom disease). However, despite treatment efficacy, exacerbations of RLS may occur with overall worsening in symptoms severity, development of pain and symptoms spreading to other parts of the body, without meeting augmentation syndrome criteria. This development of "drug-resistant" RLS can cause pain, severe insomnia and psychiatric disorders that affect considerably patients' quality of life. The lack of French recommendations for this form of RLS leave physicians with few options to help patients with physical and emotional distress. Our group of neurological experts and sleep specialists proposes a diagnostic and therapeutic strategy to provide better care and appropriate treatment through searching for the organic, psychiatric and/or iatrogenic causes of drug resistance. Once a drug-resistant RLS diagnosis has been confirmed, we recommend an obligatory work-up including: a video-polysomnogram, a biological evaluation including iron status, standard numeration and C-reactive protein level. Treatment will be comorbidity-dependent: dopaminergic agonist would be recommended in case of depression or associated periodic leg movements, α2δ ligand in case of insomnia, complaint of pain, or general anxiety, in association with low-dose opioids if necessary. Strong opioids should be preferred for multiresistant RLS.

French consensus. Management of patients with hypersomnia: Which strategy?

Central hypersomnias principally involves type 1 narcolepsy (NT1), type 2 narcolepsy (NT2) and idiopathic hypersomnia (IH). Despite great progress made in understanding the physiopathology of NT1 with low cerebrospinal fluid hypocretin-1 levels, current treatment remains symptomatic. The same applies to NT2 and IH, for which the physiopathology is still largely unknown. Controlling excessive daytime sleepiness (EDS), cataplexy, hypnagogic hallucinations, sleep paralysis and disturbed night-time sleep are key therapeutic targets in NT1. For IH and NT2, reducing EDS is the main objective. Based on European and American directives for the treatment of narcolepsy, we propose French recommendations for managing central hypersomnias as well as strategies in the case of drug-resistance. Stimulating treatments target EDS, and Modafinil is the first-line treatment. Other stimulants such as methylphenidate, pitolisant, and exceptionally dextro-amphetamine can be prescribed. Selective serotonin and noradrenaline reuptake inhibitor antidepressants are effective for the management of cataplexy in NT1. Sodium oxybate is an effective treatment for several symptoms, including EDS, cataplexy and disturbed night-time sleep. Treatment of central hypersomnia must also take into consideration frequent cardiovascular, metabolic and psychiatric comorbidities, particularly in NT1. New therapies are currently under study with the development of new stimulants and anti-cataplectics. The next few years will see innovative emerging therapies, based on a physiopathological approach, aiming to restore hypocretinergic transmission or to interrupt the autoimmune processes causing the loss of hypocretin neurons.

Earplugs and eye masks vs routine care prevent sleep impairment in post-anaesthesia care unit: a randomized study.

BACKGROUND: Post-anaesthesia care units (PACUs) with 24/7 activity and consequently artificial light and noise may disturb the sleep of patients who require prolonged medical supervision. After one postoperative night, we compared sleep quality in patients with and without noise (earplug) and light (eye mask) protection. METHODS: After ethical board approval, 46 patients without any neurological or respiratory failure undergoing major non-cardiac surgery were prospectively included. They were randomized to sleep with or without protective devices during the first postoperative night in the PACU. Sleep quality was simultaneously measured by sleep-quality scales (Spiegel score and Medical Outcomes Study Sleep), nurses' assessment, and through a wrist actigraph (Actiwatch). Secondary outcomes such as pain control and nocturnal activity were recorded. Comparisons between groups were made by Student's t-test or non-parametric test for repeated measures as appropriate (SPSS 10.0). A P-value <0.05 was considered significant. RESULTS: Data from 41 patients were analysed. Protective devices during the first postoperative night prevented a decrease in sleep quality compared with standard care, as evaluated by the Spiegel scale: 20 (4) vs 15 (5), P=0.006. These devices significantly decreased the need for a nap [50% 95% confidence interval (CI) (20-80) vs 95% 95% CI (85-100), P<0.001], but had no effect on sleep length evaluated by Actiwatch. The total consumption of morphine was significantly reduced in the first 24 h [respectively, 15(12) mg and 27(17) mg, P=0.02]. CONCLUSIONS: Earplugs and eye masks applied in the PACU during the first postoperative night significantly preserve sleep quality. Such non-invasive and cheap devices may be generalized in the PACU or in intensive care units.

Latency To N3 Interruption In Arousal Disorders.

STUDY OBJECTIVES: To help expert witnesses in criminal cases using the "sleepwalking defense", we studied the time of first and last interruptions from stage N3 in patients with arousal disorders, including sexsomnia, as well as their determinants. METHODS: The epochs of lights off, sleep onset, first N3 interruption (with and without behaviors), and last N3 interruption were determined by videopolysomnography on two consecutive nights in 163 adults with disorders of arousal, including 46 with and 117 without sexsomnia. RESULTS: The first N3 interruption (independently of concomitant behavior) occurred as early as 8 minutes after sleep onset and within 100 minutes of falling asleep in 95% of cases. The first motor arousal from N3 occurred as early as 25 min after lights off time, a timing more variable between participants (between 30 and 60 minutes after lights off time in 25% of participants and within 60 minutes of falling asleep in 50%). These latencies did not differ between the groups with and without sexsomnia. No correlation was found between these latencies and the young age, sex or clinical severity. The latency of motor arousals was shorter when they were associated with a fast-wave EEG profile and were not preceded by another type of N3 arousal. CONCLUSION: The first motor arousal may occur early in the night in patients with arousal disorders, with or without sexsomnia, suggesting that abnormal behaviors occurring as early as 25 min after lights off time in clinical and criminal cases can be a parasomnia manifestation.

[Potential teratogenicity of modafinil - Conflicting evidence, need for research]. / Tératogénicité potentielle du modafinil ­ des données contradictoires, un besoin de recherche.

Central disorders of hypersomnolence include narcolepsy type 1, narcolepsy type 2, idiopathic hypersomnia and hypersomnia associated with medical or mental disorders. Treatment is both non-pharmacological and pharmacological, including wake enhancing drugs and stimulants. One of the first-line treatment (modafinil, MODIODAL®) was the subject of a health authority alert in 2019 concerning a risk of major congenital malformations when taken during organogenesis. Since this date, three epidemiological studies have presented contradictory results. Given their methodological weaknesses, it is not possible at this stage to confirm or deny such a risk for the embryo and its nature if there is one. In clinical practice, because of these uncertainties, it is preferable if possible to suspend the treatment of a pregnant woman during the first 10 weeks from last menstrual period (organogenesis). There is an unmet clinical need for research to clarify the potential teratogenic impact of modafinil.

Residual sleepiness in obstructive sleep apnoea: phenotype and related symptoms.

The characteristics of residual excessive sleepiness (RES), defined by an Epworth score >10 in adequately treated apnoeic patients, are unknown. 40 apnoeic patients, with (n = 20) and without (n = 20) RES, and 20 healthy controls underwent clinical interviews, cognitive and biological tests, polysomnography, a multiple sleep latency test, and 24-h sleep monitoring. The marked subjective sleepiness in the RES group (mean ± sd score 16.4 ± 3) contrasted with moderately abnormal objective measures of sleepiness (90% of patients with RES had daytime sleep latencies >8 min). Compared with patients without RES, the patients with RES had more fatigue, lower stage N3 percentages, more periodic leg movements (without arousals), lower mean sleep latencies and longer daytime sleep periods. Most neuropsychological dimensions (morning headaches, memory complaints, spatial memory, inattention, apathy, depression, anxiety and lack of self-confidence) were not different between patients with and without RES, but gradually altered from controls to apnoeic patients without and then with RES. RES in apnoeic patients differs markedly from sleepiness in central hypersomnia. The association between RES, periodic leg movements, apathy and depressive mood parallels the post-hypoxic lesions in noradrenaline, dopamine and serotonin systems in animals exposed to intermittent hypoxia.

The 'scanning hypothesis' of rapid eye movements during REM sleep: a review of the evidence.

Rapid eye movements (REMs) and visual dreams are salient features of REM sleep. However, it is unclear whether the eyes scan dream images. Several lines of evidence oppose the scanning hypothesis: REMs persist in animals and humans without sight (pontine cats, foetus, neonates, born-blinds), some binocular REMs are not conjugated (no focus point), REMs occur in parallel (not in series) with the stimulation of the visual cortex by ponto-geniculo-occipital spikes, and visual dreams can be obtained in non REM sleep. Studies that retrospectively compared the direction of REMs to dream recall recorded after having awakened the sleeper yielded inconsistent results, with a concordance varying from 9 to 80%. However, this method was subject to methodological flaws, including the bias of retrospection and neck atonia that does not allow the determination of the exact direction of gaze. Using the model of RBD (in which patients are able to enact their dreams due to the absence of muscle atonia) in 56 patients, we directly determined if the eyes moved in the same directions as the head and limbs. When REMs accompanied goal-oriented motor behaviour during RBD (e.g., framing something, greeting with the hand, climbing a ladder), 90% were directed towards the action of the patient (same plane and direction). REMs were however absent in 38% of goal-oriented behaviours. This directional coherence between limbs, head and eye movements during RBD suggests that, when present, REMs imitate the scanning of the dream scene. Because REMs index and complexity were similar in patients with RBD and controls, this concordance can be extended to normal REM sleep. These results are consistent with the model of a brainstem generator activating simultaneously images, sounds, limbs movements and REMs in a coordinated parallel manner, as in a virtual reality.

[REM sleep behavior disorder: an overt access to motor and cognitive control during sleep]. / La motricité redevient-elle normale en sommeil paradoxal ? Le trouble comportemental en sommeil paradoxal.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by violent, or potentially violent, movements during REM sleep, corresponding to enacted dreams. During sleep monitoring, there is a partial or total loss of the normal muscle atonia during REM sleep. REM sleep behavior disorder predominantly affects elderly subjects without any other disease (idiopathic RBD, a precursor of Parkinson disease and Lewy body dementia) or suffering from various neurological and neurodegenerative diseases, mainly synucleinopathies. In addition to being a treatable cause of nocturnal injury of the patients or their bed-partners, RBD is a fantastic window into motor and cognitive control during REM sleep. Notably, parkinsonism transiently disappears during RBD. The patient's voice is louder and better articulated than when awake, and movements are rapid (but jerky) suggesting that the deleterious message from the basal ganglia to the primary motor cortex is reduced or bypassed. As we observed culturally-acquired behaviors, retired patients practicing their former work with mastered gestures, as well as sentences pronounced with appropriate prosody, gesturing, fluency, and syntax during the RBD, we suggest that these behaviors are generated by the same cortical areas as during wakefulness. This model also enables the demonstration that REM during REM sleep are coded in the same direction as the arm and hand movements, as if the dreamer were scanning the dream images. This online access to the motor and verbal dream scenario (through the video and audio monitoring), and the physiological measures (via the EEG, eye movements, muscle tone, respiration, heart rate), together with the offline access to the mental content (dream report after the awakening) constitute a triangulation for validating new hypotheses about REM sleep and dreams.

[Narcolepsy with cataplexy]. / Narcolepsie avec cataplexie.

Narcolepsy is a rare, disabling sleep disorder, with a prevalence of 20 to 30 per 100,000. Its onset, from childhood to the fifties, peaks in the second decade. The main features are excessive daytime sleepiness and cataplexy or sudden loss of muscle tone triggered by emotional situations. Other less consistent symptoms include hypnagogic hallucinations, sleep paralysis, sleep maintenance insomnia, REM sleep behavior disorders, attention deficit and weight gain at disease onset. Narcolepsy with cataplexy remains a clinical diagnosis but nighttime and daytime polysomnography (multiple sleep latency tests) are useful to document a mean sleep latency below 8 min and at least two sleep-onset REM periods. HLA typing shows an association with HLA DQB1*0602 in more than 92% of cases but was not included in the new diagnostic criteria. In contrast, a low hypocretin levels (values below 110 pg/ml) in the cerebrospinal fluid (CSF) was highly specific for narcolepsy with cataplexy. The deficiency of the hypocretin system is well-established in animal models of narcolepsy (murine and canine narcolepsy) but also in human narcoleptics with a 90% reduction of CSF hypocretin levels in relation with an early loss of hypocretin neurons. The cause of human narcolepsy remains unknown, however an autoimmune process is most probable. The treatment of narcolepsy includes stimulants against sleepiness (modafinil, methylphenidate), anticataplectic drugs (antidepressants) and sodium oxybate. The current therapeutic target is oriented towards hypocretine agonists, histamine (an arousal system) H3 antagonists and immunosuppressants.

[REM sleep behavior disorders and their characteristics in Parkinson's disease]. / Les comportements oniriques et leurs caractéristiques lors de la maladie de Parkinson.

REM sleep behavior disorders (RBD) are vigorous, complex movements corresponding to enacted dreams. They may disturb sleep, and injure the patients or their bed partner. RBD are frequently associated with neurodegenerative diseases, especially synucleopathies. They can precede parkinsonism or dementia by five to 10 years. These presymptomatic RBDs are frequently associated with EEG slowing, reduced olfaction, mild visuospatial cognitive impairment, and decreased dopamine transport in functional brain imaging. In Parkinson's disease, 15 to 60% patients speak, laugh, shout, kick, punch or fight invisible enemies during REM sleep. In contrast to sleepwalkers, patients with RBD rarely stand up or walk, but can fall out of bed. Sleep monitoring indicates an imperfect abolition of muscle tone during REM sleep in these patients. RBD are probably caused by nondopaminergic pontine lesions in the REM sleep atonia system. This condition may also expose patients with Parkinson's disease to a higher risk of daytime and nighttime hallucinations, and to more frequent cognitive impairment. Interestingly, several spouses reported that they observed a sharp contrast between the slow, limited movements, and poorly intelligible, low voice of their affected spouse when awake, and the fast, vigorous movements with loud voice that the very same patient exhibited during enacted dreams. We recently demonstrated that parkinsonism indeed disappears during RBD, in a large study combining the interview of 100 couples and the sleep and video monitoring of 50 patients. The mechanism of this improvement is now being explored.

[Restless-legs syndrome]. / Le syndrome des jambes sans repos.

Restless-legs syndrome (RLS) is a sensorimotor disorder, characterized by an irresistible urge to move the legs usually accompanied or caused by uncomfortable and unpleasant sensations. It begins or worsens during periods of rest or inactivity, is partially or totally relieved by movements and is exacerbated or occurs at night and in the evening. RLS sufferers represent 2 to 3% of the general population in Western countries. Supportive criteria include a family history, the presence of periodic-leg movements (PLM) when awake or asleep and a positive response to dopaminergic treatment. The RLS phenotypes include an early onset form, usually idiopathic with a familial history and a late onset form, usually secondary to peripheral neuropathy. Recently, an atypical RLS phenotype without PLM and l-DOPA resistant has been characterized. RLS can occur in childhood and should be distinguished from attention deficit/hyperactivity disorder, growing pains and sleep complaints in childhood. RLS should be included in the diagnosis of all patients consulting for sleep complaints or discomfort in the lower limbs. It should be differentiated from akathisia, that is, an urge to move the whole body without uncomfortable sensations. Polysomnographic studies and the suggested immobilization test can detect PLM. Furthermore, an l-DOPA challenge has recently been validated to support the diagnosis of RLS. RLS may cause severe-sleep disturbances, poor quality of life, depressive and anxious symptoms and may be a risk factor for cardiovascular disease. In most cases, RLS is idiopathic. It may also be secondary to iron deficiency, end-stage renal disease, pregnancy, peripheral neuropathy and drugs, such as antipsychotics and antidepressants. The small-fiber neuropathy can mimic RLS or even trigger it. RLS is associated with many neurological and sleep disorders including Parkinson's disease, but does not predispose to these diseases. The pathophysiology of RLS includes an altered brain-iron metabolism, a dopaminergic dysfunction, a probable role of pain control systems and a genetic susceptibility with nine loci and three polymorphisms in genes serving developmental functions. RLS treatment begins with the elimination of triggering factors and iron supplementation when deficient. Mild or intermittent RLS is usually treated with low doses of l-DOPA or codeine; the first-line treatment for moderate to severe RLS is dopaminergic agonists (pramipexole, ropinirole, rotigotine). In severe, refractory or neuropathy-associated RLS, antiepileptic (gabapentin, pregabalin) or opioid (oxycodone, tramadol) drugs can be used.

[Narcolepsy with cataplexy in the child: clinical evaluation and therapeutical management]. / Narcolepsie avec cataplexie chez l'enfant : particularités cliniques et approches thérapeutiques.

Narcolepsy with cataplexy is a rare but long lasting and disabling disorder where onset often occurs during childhood. Excessive daytime sleepiness, irresistible sleep attacks, partial or complete cataplexies leading to abrupt falls without loss of consciousness are the major symptoms of the disorder together with hypnagogic hallucinations and sleep paralysis. Narcolepsy cases with childhood onset are often severe. School and social life are affected in children suffering from this condition. Due to the permanence of the disorder, long-term treatment is often required targeting sleepiness. Anticataplectic treatments may be necessary early on in the course of the disease, when considering the potential handicap created by the cataplexies and the risk of falls. There is no medication available to this day to cure the disorder. Familial education, psychological and academic support play a crucial role in the management of the symptoms and in, combination with pharmacological treatment, the quality of life in children with narcolepsy and their outcome in adulthood should lead to an improvement.

[Kleine-Levin syndrome: state of the art]. / Le syndrome de Kleine-Levin.

INTRODUCTION: Kleine-Levin syndrome is a rare neurological disorder (1-2 cases per million inhabitants) primarily affecting young subjects. It is characterized by relapsing-remitting episodes of hypersomnia in association with cognitive and behavioral disturbances. Case-reports, small series, meta-analysis and a recent large, prospective trio study are consistent with a homogeneous, genuine disease entity. STATE OF THE ART: Patients are mostly male (68-78%) and adolescents (81%), with mean onset at 15 years (range 4-82 years). The first episode is triggered by an infection in 72% of patients. Patients experience an average of 7-19 episodes of 10-13 days each, relapsing every 3.5 months. Episodes recur more quickly in patients with childhood onset. The median disease course is 8-14 years, with longer course in men, in patients with hypersexuality, and when onset is after age 20. During episodes, all patients have hypersomnia (with sleep lasting 15-21 heures per day), cognitive impairment (apathy, confusion, slowness, amnesia) and a specific feeling of derealization (dreamy state, altered perception). Less frequently, patients experience hyperphagia (66%), hypersexuality (53%, principally men) and depressed mood (53%, predominantly women). Patients are remarkably similar to controls between episodes regarding sleep, vigilance, mood, and eating attitude, but have increased body mass index. Structural brain imaging, evaluation of the cerebrospinal fluid and serological inflammatory markers are unremarkable. EEG slowing is notable in 70% of cases during episodes, without epileptic activity. Sleep structure varies from harmonious hypersomnia to hypo-arousal with low sleep efficiency. The brain scintigraphy may show hypoperfusion, mostly focused on the thalamic, hypothalamic and fronto-temporal areas, especially when contrasted to images obtained between episodes. Newly identified factors include increased birth and developmental problems, Jewish heritage, genetics (5% multiplex families, suggesting autosomal recessive transmission). The association of KLS with HLA-DQ2, found in a small series, is not replicated in a larger independent sample. There is no increased family history for neuropsychiatric disorders. Some stimulants (amantadine, but more rarely modafinil or amphetamins) and mood stabilizers (lithium, valproate, but not carbamazepine) have marginal efficacy. In the 10% KLS cases secondary to various genetic, inflammatory, vascular or paraneoplasic conditions, patients are older, have more frequent and longer episodes, but their clinical symptoms, disease course and treatment response are similar to primary cases. PERSPECTIVE: The most promising findings are the familial clustering and a potential Jewish founder effect, supporting a role for genetic susceptibility factors. CONCLUSION: KLS is a puzzling and disabling disease. Until its cause will be identified, disease management should be primarily supportive and educational.

A multicentre trial of education strategies at CPAP induction in the treatment of severe sleep apnoea-hypopnoea syndrome.

BACKGROUND AND PURPOSE: Compliance with continuous positive airway pressure (CPAP) treatment in obstructive sleep apnoea syndrome (OSAS) may be difficult. Patient education is important but strategies and their outcomes are not clear. PATIENTS AND METHODS: We studied the effects of four education strategies on compliance and quality of life changes with CPAP treatment in seven centres in the French ANTADIR homecare network. Patients received from prescribers either a simple oral explanation (SP) or an oral and written explanation (RP) of CPAP use. In addition, they received from homecare technicians either a single home visit (SH) at CPAP onset or repeated home visits at CPAP onset and at 1 week, 1 month and 3 months after (RH). Compliance and quality of life were evaluated at CPAP onset, and at 3, 6 and 12 months after initiation of treatment. RESULTS: One hundred twelve patients with severe OSAS (mean age 58+/-11 year, apnoea-hypopnoea index 58+/-25/h) were allocated randomly to groups (SP+SH; SP+RH; RP+SH; RP+RH) with no initial differences. Quality of life, evaluated by the generic SF-36 questionnaire, improved in the combined emotional domains. Compliance was over 5h in all four education groups. These effects were sustained over 12 months and were not different between the four groups. We conclude that standard education strategies for CPAP induction in France are sufficient for good compliance and improved quality of life with CPAP. Education with reinforced input should be focussed on identified subgroups prone to problems.

[Normal and disordered sleep]. / Le sommeil normal et pathologique.

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).