Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurologists are becoming increasingly aware of the frequency and clinical importance of sleep-related respiratory impairment. Sleep-induced narrowing of the upper airways underlies the widespread and supposedly trivial complaint of snoring, which may not only constitute a risk factor for the cardiocirculatory system, but in predisposed individuals, may lead to a sleep apnea syndrome, with its array of serious disturbances, including hypersomnia, systemic and pulmonary hypertension and ultimately heart failure. Idiopathic chronic alveolar hypoventilation, or Ondine's curse, is a fairly stereotyped clinical syndrome: sleep-related respiratory insufficiency in the absence of airways stenosis. Finally, sleep, and REM sleep in particular, significantly aggravates hypoventilation in patients with chronic obstructive pulmonary disease (COPD), kyphoscoliosis or chest musculoskeletal disorders.
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PMID:Sleep-related respiratory disorders. 408 59

Sleep and respiration during sleep were studied in patients with idiopathic Parkinson's disease, patients with Parkinsonism with autonomic disturbance, and normal age and sex matched controls. Patients with idiopathic Parkinson's disease showed significantly reduced REM sleep, and more frequent and prolonged waking throughout the night. Hypoventilation and sleep apnoea did not occur in the idiopathic Parkinson's disease or normal groups, but respiration was disorganised with frequent central and obstructive apnoeas in the autonomic disturbance group. Respiratory rate during non rapid eye movement sleep was similar in the idiopathic Parkinson's disease and normal groups, but patients with idiopathic Parkinson's disease showed tachypnoea awake and during REM sleep.
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PMID:Respiration and sleep in Parkinson's disease. 408 99

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

Polysomnographic recordings allow the recognition of three normal sleep stages: wakefulness, NREM and REM sleep. There are quantitative changes in these stages from childhood to old age. Most characteristic are progressive decreases in total sleep time, stage 4 NREM sleep and REM sleep. Insomnia can be defined as an alteration of both the quantity and quality of sleep. It can be associated with psychophysiological factors, psychiatric disorders, use of drugs and alcohol, sleep apnea, sleep-related myoclonus and restless legs, medical, toxic and environmental conditions, or REM sleep interruptions. At present, the benzodiazepines are the most frequently prescribed hypnotics. Their efficacy has been evaluated in the sleep laboratory and by means of sleep questionnaires (clinical studies). Their derivatives are grouped according to their pharmacokinetic profiles as short acting (triazolam), intermediate acting (flunitrazepam) and long acting (flurazepam). At the EEG level these compounds induce an increase in fast frequencies and in the number of sleep spindles. Slow wave activity is markedly decreased. All of the derivatives effectively and significantly induce and maintain sleep. Total sleep time increase is related to an imcrement of stage 2 sleep while REM sleep and stages 3 + 4 sleep are consistently reduced. Triazolam withdrawal is followed by a rebound insomnia. In contrast, under the same circumstances, flurazepam has a carry-over effect.
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PMID:Sleep laboratory and clinical studies of the effects of triazolam, flunitrazepam and flurazepam in insomniac patients. 612 Feb 70

Respiratory pauses (3-10 sec in duration), apnea (less than 10 sex in duration), and periodic respiration observed in thoracic respirograms were measured in 226 polysomnograms obtained on 17 normal infants during the first year of life. All subjects had one or more respiratory pauses in a majority of recordings; 35% had respiratory pauses in all recordings; 75% of respiratory pauses were associated with body movement. There is marked intersubject and even intrasubject variability in respiratory pause rates. The range of mean respiratory pause rates among subjects was 2.0 - 14.4/h, and for single recordings was 0.0 - 43.6/h. Their occurrence was directly related to the occurrence of periodic respiration. Rates were higher during REM and indeterminate sleep than during slow wave sleep. There was no significant trend toward increase or decrease in respiratory pause rate during the first year post term. Apnea occurred in only one of the 226 recordings (0.4%). Periodic respiration occurred in 8 of 17 subjects (47%), and in 25 of 226 recordings (11%). Its occurrence was unrelated to sleep stage. The following conclusions are considered valid on the basis of the data presented and reports in the literature: (1) Rates of respiratory interruption are higher before than after 40 weeks conceptional age. (2) There is considerable intersubject variability in rates of respiratory interruptions. (3) Respiratory pauses are common during sleep in normal human infants. (4) Respiratory pauses occur more frequently with movements than in their absence. (5) Respiratory pause rates are higher during REM sleep than during slow wave sleep. (6) Apneas of greater than 10-15 sec duration do occur in normal infants, but are rare. From the clinical viewpoint, respiratory pauses (less than 15 sec) of the central type, regardless of abundance, and periodic respiration cannot by themselves be used as evidence that a baby is at risk of anything. The occurrence of apneas (greater than 15 sec duration), especially if any are of the obstructive or mixed types (and perhaps respiratory pauses of the obstructive and mixed types), and/or if associated with bradycardia or decrease in oxygen saturation, indicate sleep apnea syndrome and suggest risk of sudden infant death.
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PMID:Respiratory pauses and apnea during daytime sleep in normal infants during the first year of life: longitudinal observations. 617

A 42-year-old patient is reported who presented with marked daytime sleepiness and in whom the only major nocturnal polysomnographic abnormality was intense fragmentary (partial) myoclonus occurring with equal frequency in all stages of NREM sleep associated with some degree of sleep fragmentation. The myoclonus was very brief (less than 150 msec duration), aperiodic and recurred in asynchronous and asymmetrical fashion over the legs, arms and face. It appears unrelated to the clinically similar physiological myoclonus of REM sleep. Other main sleep disorders such as periodic movements, restless leg syndrome, sleep apnea and narcolepsy-cataplexy were excluded by history and polysomnography.
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PMID:Fragmentary pathological myoclonus in NREM sleep. 620 Feb 93

15 subjects (mean age: 48.2 yr; 13 males, 2 females) with sleep apnea (12 obstructive, 3 central) were treated with an average dose of 2500 mg L-tryptophan (L-T) at bedtime. Comparison of pre- and post-drug polysomnograms showed significant improvement in obstructive sleep apnea but not with central sleep apnea. Most dramatic improvement is seen in subjects with obstructive sleep apnea in non-REM sleep only, but severity of apnea appears to be the most important factor determining improvement. L-T increased REM time and shortened REM latency but had no other significant effects on sleep architecture. Serotoninergic activity with a defect in feedback control of tryptophan-serotonin metabolism is postulated as a potential mechanism in the pathophysiology of obstructive sleep apnea. The enhanced usefulness of L-T in combination with protriptyline is predicted based on early preliminary work at the OSU Sleep Center. The Potential influence of dietary intake on respiratory automaticity is reviewed.
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PMID:L-tryptophan in the treatment of impaired respiration in sleep. 636 Feb 58

Nine men who were habitual snorers were studied during a control and a treatment night (in random order) to assess the effect of nasal continuous positive airway pressure (CPAP) on snoring, sleep-disordered breathing, and nocturnal oxygen desaturation. Four subjects had symptoms suggestive of the sleep apnea syndrome, but the other five were asymptomatic. Polysomnography and recordings of snores were obtained on both nights. On the treatment night, the subjects wore a customized infant anesthesia mask over their noses, and CPAP was applied and adjusted upward from 4 cm H2O to a level that obliterated snoring. Nasal CPAP (range 4 to 13 cm H2O) reduced the mean number of snores per night from 1,015 per subject to 23 per subject (p less than 0.01). Mean numbers of episodes of apnea, hypopnea, and desaturation were also significantly reduced. Analysis of sleep structure showed no significant differences in sleep period time, total sleep time, or the percentages of stages 3 and 4 sleep. The percentage of stages 1 and 2 was significantly greater on control nights, and the percentage of REM sleep was greater on treatment nights. On the control nights, snoring was common in stages 3 and 4 and least common during REM sleep.
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PMID:Positive nasal airway pressure eliminates snoring as well as obstructive sleep apnea. 636 May 71

To evaluate the effect of continuous positive airway pressure via nasal mask (nasal CPAP) on occlusive, mixed, and central apneas (OA, MA, and CA, respectively), we performed nocturnal polysomnography without and with nasal CPAP on 21 patients with sleep apnea. Three patients were unable to tolerate nasal CPAP. The remaining 18 patients had significant reductions in the overall apnea frequency when using nasal CPAP (52.9 +/- 5 per hour slept vs 3.3 +/- 1 per hour slept, mean +/- SE, p less than 0.001). The use of nasal CPAP significantly reduced the frequency of OAs during both nonrapid eye movement (non-REM) and REM sleep (p less than 0.001). It also reduced the frequency of MAs during both non-REM and REM sleep (p less than 0.05). Nasal CPAP did not increase the frequency of CAs in patients who had MAs when sleeping without nasal CPAP indicating that both the "central" and obstructive portions of MA were eliminated. In those patients who had CAs while sleeping without nasal CPAP, the CA frequency was unchanged by nasal CPAP although there was a good deal of interindividual variability. We conclude that nasal CPAP is well tolerated and effective in reducing the frequency of OAs and MAs. The variability of the response of CA to nasal CPAP suggests that the pathogenesis of CA may not be homogeneous.
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PMID:Nasal CPAP effect on patterns of sleep apnea. 638 32

Auditory middle-latency evoked potentials (AMEP) were recorded in 10 subjects with predominantly central sleep apnea. AMEP were recorded during: waking; non-rapid eye movement (non-REM) sleep between apneic episodes; first half of apneas; and second half of apneas. Latencies of vertex positive peaks Po and Pa were determined, and the effect of the apnea phase on these latencies was evaluated. The latencies measured did not reveal chronic or acute functional abnormality of central auditory structures, which may result from or cause apneic episodes during non-REM sleep. The normalcy and stability of AMEP during apneic sleep may indicate effective compensatory mechanisms in central auditory structures. Alternatively, the lack of changes may result from the variability of AMEP, which may obscure small functional changes.
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PMID:Auditory middle latency-evoked potentials during sleep apnea. 646 83


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