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.

[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.

Parkinson's disease and sleepiness: an integral part of PD.

OBJECTIVE: To investigate the potential causes of excessive daytime sleepiness in patients with PD-poor sleep quality, abnormal sleep-wakefulness control, and treatment with dopaminergic agents. METHODS: The authors performed night-time polysomnography and daytime multiple sleep latency tests in 54 consecutive levodopa-treated patients with PD referred for sleepiness, 27 of whom were also receiving dopaminergic agonists. RESULTS: Sleep latency was 6.3 +/- 0.6 minutes (normal >8 minutes), and the Epworth Sleepiness score was 14.3 +/- 4.1 (normal <10). A narcolepsy-like phenotype (> or = 2 sleep-onset REM periods) was found in 39% of the patients, who were sleepier (4.6 +/- 0.9 minutes) than the other 61% of patients (7.4 +/- 0.7 minutes). Periodic leg movement syndromes were rare (15%, range 16 to 43/h), but obstructive sleep apnea-hypopnea syndromes were frequent (20% of patients had an apnea-hypopnea index >15/h; range 15.1 to 50.0). Severity of sleepiness was weakly correlated with Epworth Sleepiness score (r = -0.34) and daily dose of levodopa (r = 0.30) but not with dopamine-agonist treatment, age, disease duration, parkinsonian motor disability, total sleep time, periodic leg movement, apnea-hypopnea, or arousal indices. CONCLUSIONS: In patients with PD preselected for sleepiness, severity of sleepiness was not dependent on nocturnal sleep abnormalities, motor and cognitive impairment, or antiparkinsonian treatment. The results suggest that sleepiness-sudden onset of sleep-does not result from pharmacotherapy but is related to the pathology of PD.

High levels of nocturnal activity in children with attention-deficit hyperactivity disorder: a video analysis.

Sleep disturbances can lead to symptoms of attention-deficit hyperactivity disorder (ADHD) in children. In the present study, we compared the sleep patterns of 30 children with ADHD, with those of 19 controls matched for age (5-10 years) and sex. Sleep patterns were recorded during one night, using polysomnography (PSG) and a video system in the sleep laboratory. Both ADHD children and controls were medication free and showed no clinical signs of sleep and alertness problems. An infrared camera was used to record all types of movement, which were scored and analyzed using specific software (Observer(R) 3.0; Noldus International, The Netherlands). No significant differences in sleep variables were found between ADHD children and controls. Polysomnography data showed no significant difference between the two groups. Attention-deficit hyperactivity disorder children moved more often than controls (upper limbs, P < 0.04; lower limbs, P < 0.03; all types, P < 0.003). The duration of movements was significantly longer in ADHD children (upper limbs, P < 0.03; all types, P < 0.02). The results of the video analysis were consistent with previous findings that ADHD children have higher levels of nocturnal activity than controls. This activity concerned mostly upper and lower limb movements. Futher studies are required to determine why noctural activity does not affect sleep continuity in a more significant way and whether it should be treated specifically.

Sleep and alertness in children with ADHD.

OBJECTIVE: To evaluate sleep and alertness and to investigate the presence of possible underlying sleep/wake disorders in children with attention-deficit/hyperactivity disorder (ADHD). METHOD: After 3 nights of adaptation in a room reserved for sleep studies in the department of child psychiatry, children underwent polysomnography (PSG) followed by the Multiple Sleep Latency Test (MSLT) and reaction time tests (RT) during the daytime. Thirty boys diagnosed as having ADHD (DSM-IV), aged between 5 and 10 years, and 22 age- and sex-matched controls participated in the study. All children were medication-free and showed no clinical signs of sleep and alertness problems. RESULTS: No significant differences in sleep variables were found between boys with ADHD and controls. The mean latency period was shorter in children with ADHD. Significant differences were found for MSLT 1, 2 and 3 (p < .05). Mean reaction time was longer in children with ADHD, with significant differences in all tests (p < .05). Number and duration of sleep onsets measured by the MSLT correlated significantly with the hyperactivity-impulsivity and inattentive-passivity indices of the CTRS and CPRS. CONCLUSION: Children with ADHD were more sleepy during the day, as shown by the MSLT, and they had longer reaction times. These differences are not due to alteration in the quality of nocturnal sleep. The number of daytime sleep onsets and the rapidity of sleep-onsets measured as MSLT were found to be pertinent physiological indices to discriminate between ADHD subtypes. These results suggest that children with ADHD have a deficit in alertness. Whether this deficit is primary or not requires further studies.