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)

The authors studied sleep organization and modifications in ventilation in 20 healthy subjects (11 men, 9 women) with an average age of 65 years. There was a diminution (in relation to young adults) in the quantity of sleep with a relative increase in light slow wave sleep and reduction in deep slow wave and REM sleep phases. A reduction was also noted in the ventilation rate during slow wave and REM sleep phases in relation to calm awake periods, especially towards the end of the night. This was due to a reduction in tidal volume insufficiently compensated by an increased ventilation frequency. Hypopnea and apnea were noted in 19 of the 20 subjects, the latter occurring in the form of obstructive apnea during light slow wave sleep. The variable number of apnea can be used to divide the subjects into two sub-groups: one group of 14 of the subjects who had less than 50 apnea; the other group containing 6 subjects, all males, having more than 80 apnea during the night, and being identical to a group of patients with the sleep apnea syndrome.
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PMID:[Respiratory changes during sleep in healthy elderly subjects (author's transl)]. 720 80

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

Regional cerebral flow after inhalation of xenon 133 as well as polysomnography were recorded during daytime sleep and the awake state in patients with narcolepsy and sleep apnea. Brainstem-cerebellar (BSC) gray matter blood flow (Fg) values in the awake state were reduced below normal (p less than 0.05) in both narcolepsy and sleep apnea; in sleep apnea, bihemispheric Fg values were also reduced in the awake state. After sleep onset, Fg paradoxically increased in narcolepsy but decreased further in sleep apnea. Maximal regional Fg changes occurred in BSC regions in both groups of patients. Oral administration of methylphenidate hydrochloride (Ritalin) increased resting Fg values in awake narcoleptics, particularly in BSC regions, but attentuated Fg increases during sleep onset. Regional Fg values during visual dreaming or hypnagogic hallucinations in narcoleptics were maximally increased in right parietooccipital regions. In narcoleptics, impaired control of sleep-wake and REM mechanisms is attentuated by methylphenidate. In patients with sleep apnea, brainstem functional activity is low in the awake state but becomes critically reduced during sleep, culminating in apnea-stimulated arousal followed by repetitive cycles as sleep recurs.
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PMID:Sleep apnea, narcolepsy, and dreaming: regional cerebral hemodynamics. 739 26

As a follow-up to a previous assessment of complications of sleep-disturbed breathing in 265 patients, we have reevaluated measures of sleepiness and hypertension in patients with obstructive sleep apnea (OSA) (n = 518), central sleep apnea (n = 50), and subclinical sleep-disordered breathing (SDB) (n = 107). Both subjective and objective (multiple sleep latency test [MSLT]) measures indicated that OSA patients were sleepier than those with subclinical SDB. The OSA patients weighed significantly more than the patients with central sleep apnea or subclinical SDB. They had a higher proportion of men, described more habitual sleepiness, and had a higher likelihood of feeling unrefreshed in the morning compared with the group with subclinical SDB. Among the OSA patients, there was a significant correlation between subjective and objective assessment of sleepiness, but this relationship was quantitatively very small. A forward stepwise regression analysis revealed that weight, and to a lesser degree waking time after sleep onset, could account for 65.5% of the variance in subjective sleepiness. Seventy-five percent of the variance of the mean sleep latency in the MSLT could be accounted for by the mean minimum arterial oxygen saturation in non-REM sleep and the nocturnal sleep latency. Diastolic BP was significantly higher in OSA patients compared with the patients with central sleep apnea and subclinical SDB. When covarying for weight, age, and gender, this effect lost significance. Among OSA patients taken by themselves, 98.3% of the variance in diastolic blood pressure could be accounted for by the mean minimum arterial oxygen saturation in non-REM sleep, with very small additional contributions of apnea/hypopnea index, weight, and age. In summary, among patients across a spectrum of SDB, differences in diastolic BP were primarily associated with weight, age, and gender. Among OSA patients, perhaps because of a more limited variance in weight, diastolic BP was associated with measures of SDB.
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PMID:The relationship of sleepiness and blood pressure to respiratory variables in obstructive sleep apnea. 755 70

The prevalence of sleep apnea, sleep apneic activity, nocturnal myoclonus, and nocturnal myoclonic activity was assessed in 375 outpatient insomniacs and 150 normal controls. Only a small percentage of insomniacs (n = 8, 2.3%) and normal controls (n = 2, 1.3%) presented > or = 30 apneic events per night. Only one of these subjects, an insomniac, met the laboratory and clinical criteria of sleep apnea sufficient to recommend treatment. A limited amount of sleep apneic activity per subject (only 3-29 apneic events per night) was evenly distributed between insomniacs (n = 52, 13.9%) and normal controls (n = 22, 14.7%). Also, small percentages of insomniacs (n = 43, 11.5%) and normal controls (n = 11, 8.5%) displayed nocturnal myoclonus (five or more leg movements per hour) or nocturnal myoclonic activity (less than five movements per hour). Thus, these results do not support the claim that sleep apnea or nocturnal myoclonus are common causes of insomnia. In addition, different cutoff points of REM latency (based on first-night recordings) were associated with very low sensitivity and moderately high specificity resulting in inadequate levels of diagnostic accuracy in differentiating depressed insomniacs from non-depressed insomniacs. Finally, empirically optimized values for REM variables were less successful than similarly optimized MMPI values in differentiating depressed insomniacs from nondepressed ones. In conclusion, with our current level of knowledge, polysomnography has limited clinical usefulness in the differential diagnosis of insomnia.
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PMID:Usefulness of polysomnographic studies in the differential diagnosis of insomnia. 759 15

The nocturnal increases in blood pressure in cases of obstructive sleep apnea are discussed as causes in connection with increased cardiovascular mortality in sleep apnea. Previous antihypertension therapy studies revealed the antihypertensive action of the ACE inhibitor cilazapril averaged over NREM (NR) and REM sleep (R). In the present study, the effect of this drug on the blood pressure increase within the stress segment of obstructive apnea in NR and R was investigated in a double-blind randomized study versus placebo. Data were collected in digital form with the help of cardiorespiratory polysomnography and intra-arterial blood pressure measurements; a total of 640 apnea in 16 patients were evaluated. Relevant increases in blood pressure occurred during the apnea which were, as expected, more pronounced in R (150/74 mmHg) than in NR (135/69 mmHg). The antihypertensive action of cilazapril was also stronger in R (systole--11.9/diastole--6.4 mmHg) than in NR (systolic--9.0 mmHg/diastolic--5.7 mmHg). Placebo caused significantly lower decreases in blood pressure (systolic--3.7 mmHg/diastolic--2.4 mmHg in R, systolic--2.8 mmHg/diastolic--1.8 mmHg in NR). Thus, evidence is provided for a clinically relevant blood pressure lowering effect of the drug cilazapril on the stress-induced blood pressure increases accompanying obstructive apnea both in NREM and in REM sleep.
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PMID:[Nocturnal hypertension and sleep apnea: effect of the ACE inhibitor cilazapril on apnea-induced blood pressure increases during sleep]. 761 7

In COPD patients hypoxaemia does worsen during sleep and particularly during REM sleep. However, severe sleep-related O2 desaturation is only observed in patients who exhibit a marked daytime hypoxaemia. Nocturnal desaturation is due to the combination of alveolar hypoventilation and ventilation-perfusion mismatch; alveolar hypoventilation is the predominant mechanism, at least during REM sleep. Sleep-related hypoxaemia leads to peaks of pulmonary hypertension but also to cardiac arrhythmias. Hypoxaemia can be particularly severe when COPD is associated with a sleep apnoea syndrome (this association is rather frequent). A severe nocturnal desaturation needs a treatment with prolonged oxygen therapy, especially if daytime hypoxaemia (PaO2 < 55-60 mmHg) is present. The real benefit from oxygen therapy limited to sleep time in nocturnal desaturators who have not a significant daytime hypoxaemia, has not been yet demonstrated.
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PMID:[Sleep and COPD]. 765 71

Sleepiness is a common complaint in the epilepsy clinic, and sleep disturbances are frequently reported by seizure patients. Polysomnography was performed in 6 patients with complex partial seizures, with and without secondary generalization, who had not yet started anticonvulsant treatment or whose medication had been discontinued. Five patients sleep through the night, but 1 slept only 3 hours. Two patients had reduced sleep efficiency and slow wave sleep was reduced or absent in 4 patients. No REM sleep disturbances occurred. Two patients had almost no periodic leg movements of sleep (PLMS), 2 had few or no arousals and PLMS indices of 5 or less, and 2 had markedly elevated PLMS and arousal indices. No apneas or significant hypopneas were recorded, but snoring indices were elevated in 2 patients. These findings suggest that sleep apnea is infrequent in unmedicated seizure patients. Some patients may have exaggerated PLMS with arousals, possibly related to epileptiform discharge and perhaps exacerbated by medications, but apparently not due to nocturnal seizures.
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PMID:Sleep apnea and periodic leg movements in epilepsy. 781 95

The present study was designed to determine the effect of sleep on reflex pharyngeal dilator muscle activation by stimuli of negative airway pressure in human subjects. Intra-oral bipolar surface electrodes were used to record genioglossus electromyogram (EMG) responses to 500 ms duration pressure stimuli of 0 and -25 cmH2O applied, via a face-mask, in four normal subjects. Stimuli were applied during early inspiration in wakefulness and in periods of non-rapid-eye-movement (non-REM) sleep, defined by electroencephalographic (EEG) criteria. The rectified and integrated EMG responses to repeated interventions were bin averaged for the 0 and -25 cmH2O stimuli applied in wakefulness and sleep. Response latency was defined as the time when the EMG activity significantly increased above prestimulus levels. Response magnitude was quantified as the in ratio of the EMG activity for an 80 ms post-stimulus period to an 80 ms prestimulus period; data from after the subject's voluntary reaction time for tongue protrusion (range, 150-230 ms) were not analysed. Application of the -25 cmH2O stimuli caused genioglossus muscle activation in wakefulness and sleep, but in all subjects response magnitude was reduced in sleep (mean decrease, 61%; range, 52-82%; P = 0.011, Student's paired t test). In addition, response latency was increased in sleep in each subject (mean latency awake, 38 ms; range, 30-50 ms; mean latency asleep, 75 ms; range, 40-110 ms; P = 0.072, Student's paired t test). Application of the -25 cmH2O stimuli caused arousal from sleep on 90% occasions, but in all cases the reflex genioglossus muscle responses (maximum latency, 110 ms) always proceeded any sign of EEG arousal (mean time to arousal, 643 ms; range, 424-760 ms). These results show that non-REM sleep attenuates reflex genioglossus muscle activation by stimuli of negative airway pressure. Attenuation of this reflex by sleep may impair the ability of the upper airway to defend itself from suction collapse by negative pressures generated during inspiration; this may have implications for the pathogenesis of obstructive sleep apnoea.
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PMID:The effect of sleep on reflex genioglossus muscle activation by stimuli of negative airway pressure in humans. 804 29

Central apneas during sleep may arise as a result of reduction in PaCO2 below the apnea threshold. We therefore hypothesized that hyperventilation and arousals from sleep interact to cause hypocapnia and subsequent central apneas in patients with idiopathic central sleep apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from sleep, and the onset and duration of subsequent central apneas were examined during Stage 2 non-REM sleep in eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 central apneas and hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic breathing with central apneas were triggered by hyperventilation. Minute ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI during the ventilatory phase of the periodic breathing cycle increased progressively with increasing grades of associated arousals from Grade 0 (no arousal) (10.3 +/- 1.4 L/min) to Grade 1 (EEG arousal) (12.6 +/- 1.6 L/min) to Grade 2 (movement arousal) (14.1 +/- 1.6 L/min, p < 0.01). There was a corresponding progressive increase in central apnea length following the ventilatory period from no arousal (14.1 +/- 2.0) to EEG arousal (16.4 +/- 1.8) to movement arousal (18.1 +/- 2.0 s, p < 0.01). We conclude that arousals and hyperventilation interact to trigger hypocapnia and central apneas in ICSA.
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PMID:Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea. 804 35


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