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 1,062 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Excessive daytime sleepiness is a complaint characterizing many disorders of the wakefulness--sleep cycle. This paper addresses the complaint of sleepiness objectively by an attempt to differentiate a group of control subjects from a group of patients with unambiguous narcolepsy. Fourteen control and 27 narcoleptic subjects were evaluated by one of three protocols involving nocturnal recordings, detailed interviews, and 5 or more 20-min opportunities to sleep offered at 2-h intervals beginning at 10.00 o'clock, +/- 30 min. Each 20-min opportunity to sleep was given to subjects lying in a darkened quiet room and asked to try to fall asleep. Polysomnographic variables were monitored and sleep was scored in 30-sec epochs by standard criteria. The interval from the start of each test to the first epoch of NREM (including stage 1 sleep) or REM sleep was called sleep latency. In two of the protocols, the subjects were awakened immediately after sleep onset. In the third protocol, the subjects were awakened after 10 min of sleep. Narcoleptics consistently fell asleep much more readily than did control subjects. We conclude that the Multiple Sleep latency test, in addition to providing opportunities to clinically document sleep onset REM sleep periods, can demonstrate pathological sleepiness. Based on these data, we suggest that an average sleep latency less than 5 min be set as the minimum cutoff point for pathological sleepiness.
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PMID:Excessive daytime sleepiness in man: multiple sleep latency measurement in narcoleptic and control subjects. 8 64

Polysomnographic studies were performed in 6 patients with obstructive sleep apnoea syndrome (OSA). The sleep study consisted of: electroencephalography, electromyography, electrooculography, electrocardiography, pulse oximetry and observation of respiration. During day multiple sleep latency tests were performed. In all patients fragmentation of sleep with prevalent stages 1. and 2. of NREM and occasionally deep sleep and REM phase were observed. Concomitantly with the appearance of electrophysiologic sleep stages the muscle tone decreased and episodes of obstructive apnoea occurred. The periods of sleep and apnoea alternated with wakefulness and breathing. In MSLF the mean latency was 3 +/- 2 min. In OSA syndrome episodes of obstructive sleep apnoea cause sleep fragmentation and prevalence of light sleep stages. Excessive daytime somnolence observed in this syndrome is caused by sleep disturbances. MSLT demonstrated pathologic hypersomnolence in OSA syndrome.
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PMID:[Electrophysiological recording of nocturnal sleep and the multiple sleep latency test in obstructive sleep apnea syndrome]. 196 75

First described as a separate entity by Gelineau in 1880 and later considered as a symptom, narcolepsy has eventually been recognized as a disease on clinical and polygraphic grounds. Its prevalence stays between 0.04 and 0.06 percent. Age at onset varies from 5 to 50 with a peak in the second decade. Clinical symptoms include excessive daytime somnolence, overwhelming daytime sleep episodes, attacks of cataplexy, hypnagogic hallucinations, sleep paralysis and disturbed nocturnal sleep; sleep onset REM episodes are the main polygraphic feature. Natural history varies with the different symptoms. Excessive daytime somnolence never subsides completely. Cataplexy may disappear spontaneously. Hypnagogic hallucinations and sleep paralysis are not present in all patients and tend to be more transitory. A positive diagnosis of narcolepsy requires a minimum of one major symptom, daytime sleep episodes or cataplexy, together with documented sleep onset REM episodes. Prolonged polygraphic recordings or multiple sleep latency test are of special interest in difficult cases. Clinical variants can be grouped under three headings, incomplete, symptomatic and associated narcolepsies. The etiology of narcolepsy is not well understood. However the discovery of natural animal models of narcolepsy, mainly dogs, has prompted genetic, pharmacological and biochemical studies. The breeding of narcoleptic canine colonies has led to the evidence of a possible autosomal recessive model of inheritance in some species. Pharmacological and neurochemical analysis has shown an imbalance between monoaminergic and cholinergic mechanism. In man, extensive family studies suggest either a two-threshold multifactorial model of inheritance or a dominant mode of inheritance and immunologic studies have recently shown a strong association between HLA-DR2 and narcolepsy. Assays of CSF biogenic amines suggest a decreased bioavailability of dopamine to explain sleepiness and an imbalance between monoamines and acetylcholine to explain cataplexy. A disturbance of circadian rhythms has not been evidenced in narcoleptics. Treatment is still purely symptomatic. Amphetamines and tricyclic antidepressants have been extensively used. However they are not free of side-effects hence the need for alternative treatments.
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PMID:[Narcolepsy]. 286 18

Uvulopalatopharyngoplasty (UPPP) was performed in 12 patients with obstructive sleep apnea. Pre-surgical clinical and polysomnographic data were compared with those one to three months after surgery. Excessive daytime sleepiness was partially improved in 4 cases and completely abolished in 8. Total sleep time, sleep efficiency, number of arousals and sleep latency were similar in both evaluations. REM latency to stage 2 markedly increased on the follow-up. Stage distributions were similar in both nights except for stage 4 which was more frequently absent on the first recording. SaO2 levels below 80% were seen in 10 cases before UPPP and in 4 after it. Apnea index decreased in all cases but it reached normal levels only in 4.
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PMID:[Polysomnographic follow-up of sleep apneas after uvulopalatopharyngoplasty]. 383 37

Two cases of myotonic dystrophy with excessive daytime somnolence are described. All-night polysomnographic studies were performed revealing high number of central sleep apnea which triggered micro-arousals and awakenings leading to decrease of sleep efficiency as well as of stage 3, 4 and REM. Obstructive and mixed apneas were found in the normal range. Hypoxia was not present in both recordings. Central sleep apneas and its secondary excessive daytime sleepiness may indicate early signs of the central nervous system impairment related to myotonic dystrophy, as a multi-organ disease.
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PMID:[Excessive daytime sleepiness, central type sleep apnea and myotonic dystrophy]. 383 40

Multiple sleep latency tests (MSLT) performed on 144 patients with excessive daytime somnolence were examined for the diagnostic reliability of a short sleep latency (SL less than 5 min) and the presence of sleep-onset REM periods (SOREMPs). Based on clinical criteria, 61 patients (42%) were diagnosed as having narcolepsy. Thirty-five narcoleptic patients and five nonnarcoleptic patients exhibited a mean SL less than 5 min, yielding a sensitivity of 57% and a specificity of 94% for this criterion for pathological drowsiness. The occurrence of two or more SOREMPs was found in 52 narcoleptic patients but in only one nonnarcoleptic patient (sensitivity of 84% and specificity of 99%). Those narcoleptic patients with cataplexy demonstrated a shorter SL and more frequent SOREMPs than their noncataplectic counterparts. It was concluded that the MSLT is a highly reliable laboratory tool for the confirmation of the diagnosis of narcolepsy based on the SOREMP criterion. The criterion value for SL in pathological drowsiness may depend on laboratory conditions as well as the patient population selected.
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PMID:Diagnosis of narcolepsy using the multiple sleep latency test: analysis of current laboratory criteria. 388 Jan 72

Narcolepsy is not a rare disease. Age of onset varies from childhood to the 5th decade. Evidence for a genetic basis stems from the overall rate of narcolepsy and/or disorder of excessive somnolence among first degree relatives. The clinical features include overwhelming episodes of sleep, excessive daytime somnolence, hypnagogic hallucinations, disturbed nocturnal sleep; manifestations of dissociated REM sleep inhibitory process, cataplexy and sleep paralysis; and a special polygraphic pattern: the sleep onset REM episode. Not all symptoms are necessarily present at the onset or even during the course of narcolepsy. Excessive daytime somnolence never disappears completely while other symptoms may. Narcolepsy is a disabling condition. Its aetiology is still poorly understood but the use of natural animal models, namely dogs and horses, has been an important contribution in the areas of genetic, pharmacological and direct neurochemical analysis. Treatment of excessive daytime somnolence is still primarily based upon CNS stimulants while treatment of cataplexy and other related symptoms rests on chlorimipramine. However, new treatments are being tested, which could be of significant value.
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PMID:Narcolepsy. Clinical features and aetiology. 390 16

The objective of this study was to evaluate polysomnographic data, and especially the sudden onset of REM periods that occur after spontaneous awakenings during the night as characteristics of narcolepsy. We evaluated 148 consecutive patients with excessive daytime somnolence, except for those with sleep apnea. After clinical evaluation, all-night polysomnographic recording and multiple sleep latency test, 55 were diagnosed as narcoleptics and 93 were grouped as non-narcoleptics. The mean age of narcoleptics was 42.9 +/- 14.4 years old and the non-narcoleptics were 40.3 +/- 13.5 years old. Polysomnographic variables were compared between both samples using unpaired t test. Non-significant differences were found for: sex; total time in bed; total sleep time; time in stages 3, 4 and REM; number of arousals (less than 30 sec); number of body movements; REM density. The following significant differences were found: number of sleep onset REM periods during the night was higher for narcoleptics (p less than 0.001); total sleep time was lower for narcoleptics (p = 0.02); sleep latency was shorter for narcoleptics (p less than 0.001); REM latency to stage 1 was shorter for narcoleptics (p less than 0.001); time in stage 1 was higher for narcoleptics (p less than 0.001); time in stage 2 was lower for narcoleptics (p less than 0.001); number of full awakenings (greater than 30 sec) was higher for narcoleptics (p less than 0.001); number of awakenings longer than 5 minutes was higher for narcoleptics (p = 0.002). In conclusion, there were marked differences in the sleep architecture between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Narcolepsy and sudden onset of REM periods after nocturnal awakenings]. 409 34

Twenty-five children, age range 2 to 14 years (mean age = 7), were referred to the Stanford University Sleep Disorders Clinic for various clinical symptoms, including excessive daytime somnolence, heavy nocturnal snoring, and abnormal daytime behavior. All children (10 girls and 15 boys) were polygraphically monitored during sleep. No sleep apnea syndrome or oxygen desaturation was revealed. However, each child presented significant respiratory resistive load during sleep associated with electrocardiographic R-R interval and endoesophageal pressure swings. The most laborious breathing occurred during REM sleep. Second degree atrioventricular blocks were also noted. Tonsillectomy and/or adenoidectomy was performed in every case and resulted in a complete disappearance or substantial amelioration of the reported symptoms. Objective evaluation by Multiple Sleep Latency Test and Wilkinson Addition Test confirmed the beneficial effect of surgery.
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PMID:Children and nocturnal snoring: evaluation of the effects of sleep related respiratory resistive load and daytime functioning. 716 Apr 5

A consecutive series of 100 sleep apnea free patients with the complaint of excessive daytime somnolence (EDS) were evaluated; data from medical histories, physical examination, personality inventories, and polysomnography [nocturnal polysomnography (NPSG) and daytime multiple sleep latency testing (MSLT)] were tabulated. Significant differences were found between narcoleptic and non-narcoleptic patients in a number of parameters, including EDS severity, mean sleep latency on MSLT, sleep latency on NPSG, latency to REM sleep at night, number of REM sleep at night, number of REM sleep segments throughout the night, the total number of nocturnal myoclonic jerks (as well as the number occurring per hour of NREM and REM sleep), and the number of arousals and wake periods preceded by a myoclonic jerk. Significant differences in sleep latency during MSLT and NPSG testing were found between different EDS diagnostic groups of non-narcoleptic patients. The majority of patients in the MSLT group with long sleep latencies were in the diagnostic groups of EDS associated with psychophysiological and/or psychiatric problems or with drug abuse; patients with a diagnosis of idiopathic central nervous system hypersomnia or EDS associated with disturbed nocturnal sleep formed the majority of the MSLT group with short sleep latencies. The non-narcoleptic patients in a MSLT group with short sleep latencies had significantly shorter sleep latencies at night, more sleep cycles, higher sleep efficiency, and earlier REM sleep than patients with long sleep latencies.
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PMID:Disorders of excessive daytime somnolence: polygraphic and clinical data for 100 patients. 723 69


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