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

Eight out of 12 unselected patients with Shy-Drager syndrome were found to have severe bilateral paresis of vocal cord abduction by fibre-optic laryngoscopy. This commonly presented as increased snoring followed by episodes of inspiratory and expiratory stridor and sometimes by sleep apnoea. Respiratory failure eventually developed in four cases and was reversed by tracheostomy. In another patient tracheostomy relieved severe attacks of sleep apnoea. This complication was not necessarily associated with advanced disease, and it should be considered in all patients with Shy-Drager syndrome as appropriate treatment can lead to a useful extension of life.
 ...
PMID:Vocal cord paralysis in the Shy-Drager syndrome. 42 62

Digoxin-like immunoreactive factor (DLIF) is an endogenous substance with natriuretic and diuretic activity. Elevated plasma levels of DLIF are found in various clinical states characterized by water and sodium retention. Chronic respiratory failure, particularly of an advanced stage, also is frequently associated with water and sodium retention. In order to determine whether elevated plasma levels of DLIF are present in chronic respiratory failure, we measured plasma DLIF levels in seven patients (four with COPD [two of whom had associated sleep apnea disturbance] and three with kyphoscoliosis) suffering from advanced chronic respiratory failure with severe hypoxemia and hypercapnia. We found that in these patients plasma levels of DLIF were significantly higher than in healthy control subjects. We conclude that patients with advanced chronic respiratory failure respond with increased levels of DLIF. This may represent an attempt at homeostasis of water and sodium metabolism which is frequently deranged in this clinical condition.
 ...
PMID:Endogenous digoxin-like immunoreactive factor is elevated in advanced chronic respiratory failure. 130 96

The clinico-pathological and polysomnographical findings of an adult male patient with severe type of Hunter's syndrome are presented. He died of respiratory failure aged 19, which was much older than the average in this disease. Mucopolysaccharidosis was suspected at the age of one year, and diagnosed by leucocyte enzyme assay at 4 years of age. Mental and physical activity gradually deteriorated until his death. He often showed central type sleep apnea during the sleep stage 2, in addition to common obstructive apnea in Hunter's syndrome. The autopsy showed marked fibrous thickening of the endocardium and valves, enlargement of the liver and spleen, dilatation of the lateral ventricles and diffuse atrophy of the brain. Histologically, diffuse cytoplasmic vacuolations were found in fibroblast-like cells in the thickened endocardium and vascular walls, in Kupffer cells, and in many neurons of the central and peripheral nervous systems. Most neuronal inclusions were considered to be a ganglioside, and in other cells to be a mucopolysaccharide, by their ultrastructure. Massive accumulation of ganglioside in the neurons in the respiratory center might be reflected on central type sleep apnea.
 ...
PMID:Severe type Hunter's syndrome. Polysomnographic and neuropathological study. 145 44

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.
 ...
PMID:Chronic lung disease in the sleep apnea syndrome. 211 88

Post-polio patients may develop additional neuromuscular and respiratory symptoms decades after the acute attack, the post-polio syndrome. We hypothesize some post-polio symptoms may be due to breathing disorders occurring during sleep. We performed polysomnography on 13 post-polio patients: group 1 (five patients) were those already on ventilatory assistance (rocking beds) and group 2 (eight patients), those without any assistance. Patients requiring new treatment were then evaluated on nasal CPAP or nasal mask ventilation. Group 1 patients, on rocking beds, demonstrated consistently poor sleep quality with decreased total sleep time, sleep efficiency, percentage stage 2, slow wave sleep, rapid eye movement sleep and an increase in the number of arousals and percentage stage 1 sleep. Respiratory abnormalities were also present and in all cases caused significant O2 desaturation. These patients did not respond to CPAP with the rocking bed. Repeat night-time polysomnography on nasal mask ventilation demonstrated an improvement in sleep structure and gas exchange. Three group 2 patients, (group 2a) had sleep within normal limits. The five remaining (group 2b) had poor sleep quality that was similar to but not as disrupted as group 1 patients. All but one patient demonstrated obstructive or mixed apnea and were treated effectively with nasal CPAP. One patient required nasal mask ventilation (due to mixed apnea and marked hypoventilation) to which there was a dramatic response. These patients demonstrated improved sleep quality and an improvement in daytime symptomatology. Sleep studies should be performed on post-polio patients with excessive daytime sleepiness and respiratory complaints. Those with obstructive and mixed apnea can often be treated with nasal CPAP. Those with hypoventilation syndrome and sleep apnea attributable to sleepiness and respiratory complaints. Those with obstructive and mixed apnea can often be treated with nasal CPAP. Those with hypoventilation syndrome and sleep apnea attributable to respiratory muscle weakness can be treated with nasal mask ventilation. Individuals already on respiratory assistance such as rocking beds who have features of respiratory failure can also be treated effectively with long-term nasal mechanical ventilation.
 ...
PMID:Sleep in postpolio syndrome. 236 79

This article reviews the pharmacology and respiratory actions of depressants and stimulants, and the use of these drugs in the management of dyspnea, respiratory failure, and sleep apnea syndrome.
 ...
PMID:The pharmacology of respiratory depressants and stimulants. 287 1

The occurrence of episodes of desaturation during sleep in patients suffering from chronic airflow obstruction is well known. The severity of nocturnal hypoxaemia depends, in part, on the level of the diurnal PaO2. Hypoventilation linked to sleep is the principle mechanism responsible for the decrease in PaO2 and the desaturation which results and depends on the level of oxyhaemoglobin saturation (SaO2) during wakefulness. However, it is not possible to predict the severity of nocturnal desaturation solely on the basis of diurnal oxyhaemoglobin saturation. Numerous factors may contribute to a worsening of nocturnal desaturation. In some patients it may be associated with hypoventilation and a worsening of the ventilation perfusion inequalities. A fall in the ventilatory response to hypoxaemia and hypercapnea contributes equally to the severity of desaturation. The awake response to hypoxia is variable according to the stage of their respiratory failure but may play a role in worsening nocturnal hypoxia. Snoring and obstructive apnoea are responsible for severe desaturation in chronic airflow obstruction presenting as hypoxaemia which may be moderated during the day. At present the value of systematic nocturnal polygraphic recordings in the "work-up" of chronic airflow obstruction has not been demonstrated. Its principle practical interest is in research into the associated sleep apnoea syndrome. It should be recognised in a patient with chronic airflow obstruction who snores and is somnolent with hypoxaemia and/or poorly explained hypercapnea. The therapeutic approach in respiratory failure should take account of nocturnal desaturation and the oxygen flow at night should be superior to the one to two litres which are required to correct the diurnal hypoxaemia.
 ...
PMID:[Frequency and severity of hypoxemia during sleep in COPD. Clinical and therapeutic impact]. 317 63

We examined the clinical and respiratory physiologic characteristics of 18 patients in whom a diagnosis of central sleep apnea syndrome was established by overnight polysomnographic studies. The patients could be readily divided into 2 groups on the basis of physiologic and clinical criteria. Five patients had an awake arterial PCO2 (PaCO2) of 53 +/- 4 (SEM) mmHg in the absence of intrinsic bronchopulmonary disease, a ventilatory response to CO2 of 0.6 +/- 0.2 L/min/mmHg, and a hemoglobin concentration of 180 +/- 6 g/L. Their clinical course was dominated by recurrent episodes of respiratory failure. In contrast, the other 13 patients had an awake PaCO2 of 35 +/- 1 mmHg (p less than 0.001), a CO2 response of 2.9 +/- 0.4 L/min/mmHg (p less than 0.005), and a hemoglobin concentration of 150 +/- 5 g/L (p less than 0.005). Clinically, they presented with features typical of sleep apnea; none had a history of respiratory failure. Despite the clinical and physiologic differences between the 2 groups, there were no differences between them in the frequency or duration of nocturnal apneic events or in sleep architecture. The findings indicate that the central sleep apnea syndrome is not a homogeneous disease entity. Rather, it includes 2 groups of patients that are clinically and physiologically distinct, with 1 group chronically hypoventilating and the other group either chronically hyperventilating or ventilating normally.
 ...
PMID:Clinical and physiologic heterogeneity of the central sleep apnea syndrome. 374 Jun 46

Seven patients with the severe obstructive sleep apnoea syndrome were treated with nasal continuous positive airway pressure for from three to 22 months. This treatment reversed all symptoms due to the syndrome in every patient and continued to be used in five patients. One patient stopped treatment after eight months and subsequently remained incapacitated and another underwent tracheostomy at the time of transphenoidal hypophysectomy. Nasal continuous positive airway pressure is a safe, non-invasive treatment, which may be used in the presence of cardiac and respiratory failure. It is able fully to reverse upper airway obstruction and can be used at home on a long term basis.
 ...
PMID:Severe obstructive sleep apnoea treated with long term nasal continuous positive airway pressure. 388 41

A 55-year-old man is presented who developed severe multifocal myoclonus and tonic clonic seizures in his early thirties, and progressive limb weakness in his mid forties, when a ragged red fibre myopathy was diagnosed. He went on to develop a distal motor neuropathy and respiratory failure. Respiratory function tests indicated respiratory failure secondary to respiratory muscle weakness and a central hypoventilation syndrome. CT scan revealed brain stem atrophy and brain stem evoked responses were abnormal. A sural nerve biopsy showed severe axonal degeneration. Cytochrome difference spectra and polarographic studies on isolated intact muscle mitochondria were normal. This study reports the association of respiratory failure and sleep apnoea with Fukuhara's syndrome and presents biochemical data suggesting that the mitochondrial respiratory chain may be intact in some patients with this syndrome.
 ...
PMID:Mitochondrial myoneuropathy with respiratory failure and myoclonic epilepsy. A case report with biochemical studies. 393 3


1 2 3 4 5 6 7 8 9 10 Next >>