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 multiple sleep latency test (MSLT) has proved to be a useful diagnostical tool for patients complaining of excessive daytime sleepiness (EDS). The intention of the present study was to investigate the structure of MSLT naps and in particular sleep spindle and k-complex density in three different groups of EDS patients. MSLT was performed at 8 a.m., 10 a.m. 12 a.m., 2. p.m. and 4 p.m.. Each recording lasted 20 minutes and was not stopped even if sleep occurred before 20 min. Sleep was scored visually. Spindle and k-complex density was determined per minute of S2 sleep. Statistical analysis used ANOVA. Each of the three groups consisted of 15 patients. Diagnosis of narcolepsy, sleep apnea, of EDS due to a psychiatric disorder has been confirmed subsequently. There were 5 female and 10 male narcoleptics (mean age: 43.9 +/- 10.9 years), 2 female and 13 male obstructive sleep apnea patients (mean age: 53.9 +/- 10.9 years) and 7 female and 8 male patients complaining of EDS, in whom a psychiatric disorder was diagnosed (mean age: 38.8 +/- 13.8 years). Narcoleptics sent more than half of the recording time of 100 min asleep (52.9%). Apnea patients slept 41.3% and psychogenic EDS patients 22.7%. The proportion of sleep stages 1 and 2 in narcoleptics (S2/S1 = 1:1) was clearly different from the other two (apnea patients: S2/S1 = 4:1; psychogenic EDS patients: S2/S1 = 3:1). 18.5% of the naps contained stage REM and during the afternoon naps 0.9% of S3 in the narcoleptics. Neither REM nor S3 was observed in the others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Quality of day time sleep in the multiple sleep latency tests in patients with narcolepsy, obstructive sleep apnea and psychogenic hypersomnia]. 148 26

An impaired ability to concentrate, loss of intellectual performance, and changes in personality are frequently-mentioned psychological symptoms of sleep apnoea. Apnea-associated disturbances of sleep structure as well as nocturnal cerebral hypoxia are possible causes. Twenty men and two women with an average age of 51.5 years underwent psychological testing. The average apnea index was 36 (range 11 to 92). The following psychodiagnostic procedures were used for screening; attention-strain test (d2) to measure short term concentration ability, numbers-connecting test (ZVT) for the evaluation of cognitive processing speed as an indication of intellectual performance, the Freiburg Personality Inventory FPI-R for assessing personality traits. As compared with the standard random sample of the d2, our patients' ability to concentrate over a period of five minutes does not seem to be impaired. Deficits in patients with sleep apnea are more likely to be found in the care of long-term concentration, especially in monotonous situations. The mean IQ score of our sample (93) is rather low as compared with the mean value of the age-matched sample (100). Patients with an Apnea index greater than 30 tended to have lower IQ-values (87.4) than those with less severe sleep apnea (97). Older patients had significantly lower age-corrected figures (87.2) than younger patients (98). Younger patients with high apnea activity (greater than median) had significantly (ANOVA: interaction alpha = 0.01) lower IQ scores (84.8) than younger patients with less severe sleep apnea (107). Sleep apnea seems to impair cognitive processing speed. Our sample turned out to be normal with respect to the twelve personality traits measured by means of the FPI-R.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Psychological aspects of sleep related disorders of respiratory control]. 260 56

Previous animal studies support the presence of an upper airway reflex mechanism that when blocked by topical anesthesia of the upper airway results in upper airway occlusion. We sought a similar reflex mechanism in humans. Nine normal male volunteers 20 to 28 yr of age underwent 3 successive overnight sleep studies: a control study (C); a study in which selective topical oropharyngeal anesthesia (OPA) was achieved prior to sleep using a 10% lidocaine spray and 0.25% bupivocaine solution; a study in which selective nasal anesthesia (NA) was achieved prior to sleep using a mixture of 2% lidocaine and 0.25% bupivocaine solutions instilled into the nose while the nasal airway was positioned as the most dependent part of the upper airway. Total sleep times were similar during the 3 study nights as were the amounts of slow-wave and rapid-eye-movement (REM) sleep. Obstructive apneas and hypopneas (OAH) differed significantly between the 3 study nights [13(3.8), mean (SEM), during OPA as compared to 3(1.8) during C and 7(2.5) during NA; p less than 0.01 by ANOVA] and were most frequent during REM sleep. Total apneas and hypopneas also differed significantly between the 3 study nights [19(3.9) during OPA as compared to 8(2.1) during C and 14(3.9) during NA; p less than 0.01 by ANOVA]. Movement arousals terminating periods of abnormal respiration also differed significantly [21(6.1) during OPA as compared to 12(3.6) during C and 14(4.6) during NA; p less than 0.05 by ANOVA]. No subject, however, developed clinically significant sleep apnea or significant oxygen desaturation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia. 359 5

Neurophysiological repercussions of sleep respiratory disorders (SRDs) are still unclear. It has been shown that SRDs induce disturbance on auditory event-related potentials with a delayed latency of the cognitive P300 potentials. Since the Auditory Brainstem Responses (ABRs) explore the auditory brainstem structures and are independent on cognition, we evaluated the neurological impact of SDRs on central nervous system by ABRs in these patients. Four groups of patients were studied: snorers (S, 17 subjects), sleep apnoea syndrome (SAS, 48 subjects), apnoeic patients with respiratory insufficiency (SAI, 17 patients) and patients with respiratory insufficiency alone (RI, 12 subjects). A standard polysomnographic study was done in each patient with further quantitative analysis of sleep, respiratory events, and oxygen arterial saturation. ABRs were recorded before the study night and interpeak latencies (IPLs) between waves I, III and V were measured. Results were expressed as the mean of each group for all the different parameters. ABR IPL latencies (IPLI-III, IPLIII-V, IPLI-V) of the four groups were within the normal range. However, comparing groups between themselves, there were significant differences (ANOVA) between groups. Longer IPLIII-V and IPLI-V (which explored the central conduction time) were observed in group SAI compared to group SAS. No evidence on the origin of this elongation was found; the level of hypoxia, in particular, was not related to IPL values. These results show that SAS alone do not affect lower brainstem auditory function, in contrast to the association of SAS and RI.
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PMID:Auditory brain-stem responses (ABRs) in sleep respiratory disorders. 803 48

It is well established that nocturnal hypoxemia in sleep apnea causes an inversion of the circadian arterial pressure rhythm and triggers nocturnal hypertension. Since sleep apnea is very frequent in dialysis patients, we hypothesized that nocturnal hypoxemia may be a factor that contributes to alter the 24-hour arterial pressure profile in these patients. To test the hypothesis 32 dialysis patients underwent 24-hour blood pressure (BP) monitoring and continuous monitoring of arterial O2 saturation during the night-time. Hemodialysis patients were studied during the non-dialysis day. All patients underwent an echocardiographic study. Thirteen patients had no episode of nocturnal hypoxemia (group I), 7 had at least one episode overnight but less than 2 episodes/hr (group II) and 12 had > or = 2 episodes/hr (group III). The average daytime systolic pressure was similar in the three groups. However, the average nocturnal systolic pressure fell in the first group (-2.5 +/- 4.2%) and rose in the second (+2.0 +/- 3.6%) and in the third (+3.9 +/- 2.2%) group (one way ANOVA, P < 0.005). The relative wall thickness of the left ventricle (RWT) was significantly (P < 0.05) higher in group III than in group I, and in the aggregate (N = 32) there was an inverse relationship between average nocturnal SaO2 and RWT (r = -0.43, P = 0.015). The proportion of patients with concentric remodeling or concentric hypertrophy was higher (P = 0.05) in the group with a more severe degree of nocturnal hypoxemia (group III, 8 of 12) than in the other two groups (group I, 3 of 13; group II, 2 of 7). Nocturnal hypoxemia is associated with the "non-dipping" arterial pressure profile in dialysis patients. Disturbed respiratory control during the night may represent an important cardiovascular risk factor in dialysis patients.
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PMID:Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients. 955 20

The nocturnal secretion profile of the newly identified natriuretic peptide (NP), brain natriuretic peptide (BNP), was studied in 14 patients with obstructive sleep apnoea syndrome (OSAS) (apnoea hypopnoea index: 60.5 +/- 3.4, mean +/- SE) during two separate nights before and during nasal continuous positive airway pressure (NCPAP) therapy. Plasma levels of NPs (atrial natriuretic peptides; ANP and BNP) were measured at 2-h intervals during sleep. Simultaneously, blood pressure was measured by a non-invasive method (Finapres, Ohmeda, Englewood, CO, USA) and urine was collected for determining volume and catecholamine levels. Urinary and serum sodium concentration were determined before and after the study. Eight non-snoring subjects were also studied for the investigation of normal nocturnal profiles of BNP levels. To understand the discrete secretion profiles of the two NPs during sleep, blood was sampled from an additional seven patients every 5 min over a 30-min period around 00.00 and 04.00 hours before NCPAP. In patients with OSAS, plasma BNP levels increased from the beginning of sleep (22:00 h) to the morning (06:00 h) before NCPAP therapy (P < 0.01, ANOVA). Baseline BNP levels were not significantly correlated with patient's clinical and polysomnographic parameters. However, in the latter half of the sleep period (02:00-06:00 h), increases in BNP levels during the night before NCPAP therapy were significantly correlated with blood pressure elevations (systolic: r = 0.784 P < 0.01, diastolic: r = 0.587 P < 0.01) and with apnoea duration (r = 0.582 P < 0.01). In normal subjects BP and BNP levels were not changed significantly during sleep. Plasma BNP levels were well correlated with concomitant ANP levels (P < 0.001). NCPAP therapy reduced ANP and BNP levels during sleep and in the morning (P < 0.01). Plasma levels of BNP at 5 min intervals before NCPAP therapy revealed few variations. On the other hand, ANP levels fluctuated over the 30-min period. Changes in BNP levels during sleep in the patients with OSAS may be related to blood pressure variations, but may be too small to play a significant physiological role in regulating diuresis in OSAS. Further work is required to determine the precise role of dual natriuretic system in cardiovascular load and natriuresis in OSAS.
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PMID:The nocturnal secretion of cardiac natriuretic peptides during obstructive sleep apnoea and its response to therapy with nasal continuous positive airway pressure. 978 75

The number of K-complexes recorded at the central-temporal EEG derivation (C3-T3) during 5 min periods for both the ascending and descending phase of Stage 2 of NREM sleep for cycles 1, 2. etc. were counted in 10 subjects for each of the following five groups: normal persons, patients with a primary generalized form of epilepsy, narcolepsy, insomnia and obstructive sleep apnoea. The differences in time spent in different stages of sleep were as expected for these types of patients. A 2-within, 1-between factors, repeated measure ANOVA was applied to the data on K-complexes. Overall, there was no significant difference between the number of K-complexes observed during the ascending and descending phases of the different sleep cycles. Patients with a sleep disorder had significantly less well-defined K-complexes than the normals and the patients with a primary form of generalized epilepsy: for insomnia (P = 0.035), for apnoea (P = 0.011) and for narcolepsy (P = 0.001). There was a significant, but very low correlation coefficient between the number of K-complexes observed during Stage 2 of NREM sleep and the time spent during that stage for all groups combined (Rho 0.27, P = 0.002) and for the narcoleptic patients (Rho 0.44, P = 0.017). In all, the findings lend support to the hypothesis that a K-complex can be seen as a 'defensive response', or has a sleep protective function.
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PMID:K-complexes: are they signs of arousal or sleep protective? 1060 52

Sleep apnoeas are accompanied by large variations in heart rate (HR) and blood pressure (BP). This nocturnal variability in BP may be involved in the increased cardiovascular morbidity of these patients. Due to the complex interaction between asphyxia, intrathoracic pressure, cardiac function and autonomic activation, the exact haemodynamic mechanisms are unclear. To evaluate the components of the BP surges at resumption of breathing (RB) a non-invasive beat-to-beat measurement was taken of cardiac output (CO) by the pulse contour analysis of the Finapres signal. Six male normotensive patients, free of medication (37-60 y, BMI 26.5-43.0 kg m-2) were studied during polysomnography (apnoea index: 22-69 h-1). Systolic blood pressure rose from 126.5 +/- 1.3 mmHg at beginning apnoea (P1) to 140.4 +/- 1.3 at RB (P < 0.01, ANOVA). During sleep Stages 2 and 3, stroke volume decreased during RB to 96% of P1 value (NS). Due to an opposite change in HR, CO tended to rise at RB to 106% of P1. Computed total peripheral resistance rose during RB to 105% of P1 value (P < 0.011. Therefore, it is concluded that the surge in BP at RB after apnoea is due to concomitant increases in CO and in TPR. Both rises are presumably a consequence of sympathetic nervous activation by the arterial chemoreceptors.
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PMID:Non-invasive measurement of haemodynamics during sleep apnoea. 1060 79

Diurnal variations in daytime sleepiness were studied in 26 men with sleep apnea syndrome (SAS) [age, 41.7 +/- 9.9 years (mean +/- SD); body mass index, 30.0 +/- 6.2 kg/m2; Epworth Sleepiness Score, 8.7 +/- 4.1; apnea-hypopnea index, 50.2 +/- 22.0]. Sleep latencies measured at 09.00 h, 11.00 h, 13.00 h, 15.00 h, and 17.00 h were 3.4 +/- 3.6 min, 4.7 +/- 5.5 min, 5.2 +/- 4.4 min, 5.3 +/- 5.4 min, and 9.3 +/- 7.2 min, respectively (ANOVA, P < 0.05). Daytime sleepiness in patients with SAS was more pronounced in the morning than in the afternoon and evening.
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PMID:Diurnal variation in daytime sleepiness of patients with sleep apnea syndrome. 1204 14

OSA (obstructive sleep apnoea) stimulates sympathetic nervous activity and elevates resting HR (heart rate) and BP (blood pressure). In the present study in a cohort of 309 untreated OSA patients, the resting HR and BP during the daytime were correlated with AHI (apnoea/hypopnea index) and compared with patients with R389R (n = 162), R389G (n = 125) and G389G (n = 22) genotypes of the beta1-adrenoreceptor R389G polymorphism. We analysed the impact of the genotype on the decline of HR and BP in a subgroup of 148 patients (R389R, n = 86; R389G, n = 54; G389G, n = 8) during a 6-month follow-up period under CPAP (continuous positive airway pressure) therapy during which cardiovascular medication remained unchanged. In untreated OSA patients, we found an independent relationship between AHI and resting HR (beta = 0.096, P < 0.001), systolic BP (beta = 0.09, P = 0.021) and diastolic BP (beta = 0.059, P = 0.016). The resting HR/BP, however, did not differ among carriers with the R389R, R389G and G389G genotypes. CPAP therapy significantly reduced HR [-2.5 (-1.1 to -4.0) beats/min; values are mean difference (95% confidence intervals)] and diastolic BP [-3.2 (-1.5 to -5.0) mmHg]. The decline in HR was more significantly pronounced in the R389R group compared with the Gly(389) carriers [-4.1 (-2.3 to -5.9) beats/min (P < 0.001) compared with -0.2 (2.1 to -2.6) beats/min (P = 0.854) respectively; Student's t test between groups, P = 0.008]. Diastolic BP was decreased significantly (P < 0.001) only in Gly389 carriers (R389G or G389G) compared with R389R carriers [-5.0 (-2.3 to -7.6) mmHg compared with -2.0 (0.4 to -4.3) mmHg respectively]. ANOVA revealed a significant difference (P = 0.023) in HR reduction between the three genotypes [-4.1 (+/-8.4) beats/min for R389R, -0.5 (+/-9.3) beats/min for R389G and +1.9 (+/-7.2) beats/min for G389G]. In conclusion, although the R389G polymorphism of the beta1-adrenoceptor gene did not influence resting HR or BP in untreated OSA patients, it may modify the beneficial effects of CPAP therapy on these parameters.
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PMID:Modifying effects of the R389G beta1-adrenoceptor polymorphism on resting heart rate and blood pressure in patients with obstructive sleep apnoea. 1628 27


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