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)

A 34-year-old female was admitted on June 25, 1990, for the evaluation of alveolar hypoventilation which worsened after her second delivery. She showed impairment of both hypercapnic and hypoxic ventilatory responses, and marked desaturation due to hypopnea and apnea during sleep. Although administration of methylxanthine and medroxyprogesterone was not very effective, after treatment with low flow oxygen, there was a marked decrease in the frequency and duration of desaturation during sleep and improvement of arterial daytime blood gases, which suggested the existence of hypoxic ventilatory depression in the pathophysiology of her nocturnal desaturation. Furthermore, the use of a negative pressure ventilator for 3 hours in the daytime for 10 days resulted in marked improvement of symptoms, arterial blood gases, respiratory muscle strength, and the frequency and duration of sleep desaturation. These findings suggest that both low flow oxygen therapy during sleep, and daytime negative pressure ventilation may be beneficial in patients with primary alveolar hypoventilation and central sleep apnea syndrome.
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PMID:[A case of primary alveolar hypoventilation syndrome with a good response to nocturnal low-flow oxygen inhalation and negative pressure ventilation]. 128 38

We investigated diurnal sleep apnea in myotonic dystrophy with respiratory inductive plethysmography. Five of eight patients met criteria for sleep apnea syndrome and had central apnea mainly. In a case showing periodic breathing with apnea like Cheyne-Stokes type breathing, the duration of apnea and breath was even and the tidal volume went waxing and waning regularly. In the other four cases, central apneas were observed in sequence, but the duration of apnea and the tidal volume changed variously. Large breaths between apneas elevated arterial oxygen saturation rather than stable breaths without apnea. We suspected that hypoxemia, which exacerbated by involvement of respiratory muscles, supine position and sleep, initiated the hyperventilation between apneas. And then the saturation of oxygen raised by hyperventilation would cause central sleep apnea.
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PMID:[Diurnal sleep apnea in myotonic dystrophy]. 129 Nov 58

Myotonic dystrophy (MyD) involves a variety of systems. Respiratory disorders are common, namely elevation of diaphragm, alveolar hypoventilation, aspiration pneumonia and sleep apnea. We evaluated respiratory involvement. The subjects were 11 patients with MyD. Also 6 patients with limb girdle muscular dystrophy (LG) were examined to be compared with MyD. Both groups had the similar activities of daily living. All of them never complained of dyspnea. Arterial blood gas studies were performed in supine position and standing position. A new evidence was found that hypoxemia was aggravated and alveolar-arterial oxygen pressure difference was increased in supine position in MyD. Next, pulmonary function tests were done in supine position and sitting position. Functional residual capacity (FRC) were more reduced in supine position in MyD compared with LG. The value to subtract closing capacity from FRC was negative in supine position in MyD, showing closing phenomenon. We propose the mechanism of the aggravation of hypoxemia may be the following. The reduction of FRC caused by respiratory muscle involvement brings out the closing phenomenon. Abnormal uneven distribution of ventilation-perfusion ratio happens and then hypoxemia is worsened in supine position in MyD.
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PMID:[Aggravation of hypoxemia in supine position in myotonic dystrophy]. 129 47

Disordered nocturnal breathing with significant arterial oxygen desaturation and sleep apnoea is a feature of extreme obesity which is often difficult to manage in the short term. We have evaluated the effect of fluoxetine, a centrally acting 5-HT re-uptake inhibitor, on sleep-breathing patterns in asymptomatic extremely obese subjects. A double-blind cross-over study was used to compare fluoxetine (60 mg for three days) to placebo. Eleven obese subjects (ten males, one female, mean weight +/- s.d. 131 +/- 2 kg) slept overnight in a sleep laboratory with the polysomnographic study recorded after an initial acclimatization night. The obese subjects had normal respiratory function and normal fully awake arterial oxygen saturation (%SaO2 97 +/- 1). Marked O2 desaturation was seen in all the subjects during sleep but the average asleep %SaO2 did not differ between the two treatment phases (placebo 90 +/- 5; fluoxetine 92 + 2%). However, fluoxetine significantly increased the minimum %SaO2 recorded during the study night either by abolishing or reducing REM sleep (placebo 73 +/- 2%; fluoxetine 81 +/- 8%; P < 0.05, 95% CI -12.3 to -2.03). Frequent hypopnoea was observed in all subjects in both REM and non-REM sleep whereas apnoea was uncommon. The total apnoea/hypopnoea index fell in six subjects during the fluoxetine night, the largest reduction being seen in the most severely affected. In five of the six the improvement was associated with the abolition of REM sleep. Total sleep time did not differ between the placebo and fluoxetine nights nor did a qualitative assessment of sleep using a visual analogue score.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Short-term use of fluoxetine in asymptomatic obese subjects with sleep-related hypoventilation. 133 Sep 62

Nasal continuous positive airway pressure (CPAP) is an effective therapy for sleep apnea. Little is known about long-term patient compliance and side effects with this therapeutic modality in the Chinese. In order to evaluate this, we collected 8 obstructive sleep apnea patients who received home nasal CPAP therapy between January 1990 and July 1991. Each received two sets of nap polysomnographic studies. The initial set was performed to diagnose and evaluate patient response to CPAP as well as defining the CPAP pressure the patient would be using at home. The second set of studies were conducted for follow up and re-evaluation. Seven of these patients reported using nasal CPAP during sleep at night, and one did not use it all. Nasal CPAP improved clinical symptoms, particularly daytime sleepiness, and 7 patients were generally satisfied with nasal CPAP. Initially the side effects were a dry throat and nose. After 5 to 15 months of CPAP treatment, the follow-up nap sleep studies showed no significant change in the apnea/hypopnea index, duration of apnea, or oxygen desaturation between the diagnostic and follow-up (without CPAP) studies. However the amount of nasal CPAP pressure setting declined in 4 of 7 patients. Our own experience indicates that long-term nasal CPAP is an important new means of treatment for sleep apnea and allows a normal daytime life. It was well-tolerated by most sleep apnea patients. However, it is necessary to further evaluate of morbidity and the amount of pressure setting relative to long-term home nasal CPAP.
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PMID:An evaluation of long-term nasal CPAP therapy for sleep apnea. 133 87

To evaluate the incidence of sleep apnea syndrome (SAS), oxygen desaturation during sleep and sleep quality in patients with chronic obstructive pulmonary disease (COPD), 30 COPD patients and 20 healthy snorers (without SAS) were studied. Each subject received a pulmonary function test (PFT) (simple spirometry), arterial blood gas determination and an overnight sleep study. COPD patients were divided into two groups: those with SAS (group I) and those without (group II). Group II patients were further subdivided into: group IIa [delta SaO2 < 15% (delta SaO2 = baseline SaO2-lowest SaO2) and group IIb (delta SaO2 > or = 15%); group IIc (baseline SaO2 > 90%) and group IId (baseline SaO2 < or = 90%). Our results showed that only six of 30 (20%) COPD patients had an associated SAS. Among group II patients, the lowest SaO2 and delta SaO2 were correlated with baseline SaO2, PaO2 and PaCO2 but were not correlated with age, % of ideal body weight, FVC, FEVl, FEVl/FVC. Group IIb patients (n = 10) had a lower SaO2 during sleep, a lower baseline PaO2, and a lower hematocrit level than group IIa patients (n = 14). Group IId patients (n = 9) had a lower PaO2 and a higher delta SaO2 during sleep than group IIc patients (n = 15). However, there were no significant differences in age, percent of ideal body weight (IBW), FVC, FEVl or FEVl/FVC values between groups IIa and IIb, or between groups IIc and IId. Group II patients had a lower percentage of sleep efficiency, higher arousal and movement indices and a longer period of stage 1 sleep, compared to the control group. In conclusion, the incidence of COPD patients with SAS is 20%. Age, percentage of IBW, FEVl, and FEVl/FVC values are not reliable predictors of the risk of nocturnal hypoxemia among COPD patients. However, a possible correlation between baseline SaO2, PaO2 and PaCO2 values and the incidence of nocturnal hypoxemia exists. Finally, COPD patients experienced a poorer quality of sleep in comparison with the control group.
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PMID:[Sleep quality and nocturnal hypoxemia in patients with chronic obstructive pulmonary disease]. 136 10

Nocturnal oxygen desaturation (NOD) is commonly seen not only in sleep apnea syndrome (SAS) but also in chronic lung disease (CLD) including chronic obstructive lung disease even without sleep apnea. However, the relationship of NOD to clinical symptoms such as morning headache, sleep deprivation due to breathlessness, and daytime sleepiness is not known. In this study, we examined by polysomnography the relationship between several NOD indexes, parameters of apnea, and subjective symptoms in 25 patients with SAS and 22 patients with CLD. In addition, the relation between daytime arterial blood gas data and NOD indexes, parameters of apnea, was examined. In the SAS group, there were no differences in any parameters of NOD and apnea between patients with subjective symptoms and those without symptoms. However, in the CLD group, symptomatic patients had significantly lower lowest SaO2, higher mean SaO2, and longer total desaturation time. In both groups, daytime PaCO2 had a significant correlation with several NOD parameters such as mean SaO2, lowest SaO2, and total desaturation time. In the SAS group, daytime PaCO2 was also correlated with the parameters of apnea. On the other hand, daytime PaO2 was significantly correlated with mean SaO2 only in the CLD group. From these data, we conclude that in patients with SAS, daytime PaCO2 is a variable that is related to the degree of NOD, and that in patients with CLD, subjective symptoms and daytime PaO2 in addition to daytime PaCO2 are associated with NOD.
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PMID:[Relationship between clinical symptoms and nocturnal oxygen desaturation in sleep apnea syndrome and chronic lung disease]. 140 71

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

Although central nervous system (CNS) involvement, such as intellectual impairment simulating dementia, in myotonic dystrophy (MyD) has been well documented, the cause of this condition remains unclear. In has been reported that the progressive cases of MyD are often accompanied with respiratory disturbance and sleep apnea syndrome (SAS). We studied the relation between CNS involvement and respiratory disorders in 15 MyD patients. They consisted of 10 males and 5 females with ages ranging from 21 to 58 years (average 46 +/- 8.4 years old). Arterial blood gas (ABG) analysis, respiratory function test, and monitoring of arterial oxygen saturation (SaO2) during sleep were carried out. In some cases abnormal respiration during sleep was analyzed with polysomnography. For an assessment of CNS involvement the following examinations were performed; intelligence quotient (WAIS-IQ); electroencephalography (EEG); brain computed tomography (CT); and cerebrospinal fluid (CSF) levels of neuron-specific enolase (NSE), S-100b and creatine kinase BB isoenzyme (CK-BB) which were estimated by using enzyme immunoassay. ABG analysis demonstrated the presence of hypercapnia (PaCO2 > 45 torr) during wakefulness in MyD patients. During sleep 14 of the 15 patients showed frequent desaturation phenomenon (SaO2 < 90%), indicating the episodic hypoxemia. Polysomnographic study revealed the occurrence of SAS of both obstructive and central types in all the cases examined. IQ test disclosed intellectual impairment in 80% of the 15 patients, and EEG showed slowing of basic rhythm in the majority of the cases. On brain CT both enlarged ventricles and dilated sulci were commonly observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central nervous system disorders in patients with myotonic dystrophy--in relation to respiratory dysfunction]. 142 35

Muscle biopsies from the palatopharyngeal muscle of eight patients with obstructive sleep apnoea were performed during uvulopalatopharyngoplasty. Control biopsies were performed during tonsillectomy in seven control patients with no history of symptoms suggesting obstructive sleep apnoea. The diagnosis was based on the patient's history and a whole night recording of arterial oxygen saturation and respiration movements. The mean number of oxygen desaturations > or = 4% per sleeping hour was 39 (range 7-80) in patients with obstructive sleep apnoea. In the control patients the occurrence of muscle fibre type and size relation between type I and type II fibres were comparable to what is found in the quadriceps femoris muscle, but the mean size of the fibres was < 25% of what is found in limb muscles. All biopsies from patients with obstructive sleep apnoea showed abnormalities. Atrophy with a fascicular distribution, increased number of angulated atrophic fibres, a twin or multiple peak distribution of the fibre size spectra, and an abnormal distribution of fibre types in many muscle fascicles corresponding to "type grouping" all points to a neurogenic alteration. This neurogenic lesion may be a primary phenomenon or secondary to the trauma of repetitive and prolonged stretching of the pharyngeal structures during apnoeas. A disturbance of the function of the dilating muscles of the upper airway may be important in causing the abnormal airway collapse seen in obstructive sleep apnoea.
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PMID:Neurogenic effects on the palatopharyngeal muscle in patients with obstructive sleep apnoea: a muscle biopsy study. 143 55


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