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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Much has been written about snoring and its affects on health, in particular its possible influence on cardiovascular disease. However, there are many assumptions made when linking the report of snoring to any consequences such as hypertension, heart disease or stroke. In particular it is not clear how snoring might influence the cardiovascular system, whether subjective reports of snoring are accurate, and snoring might only be acting as a marker for some common risk factor such as upper body obesity; a particular risk factor for cardiovascular disease, and through neck circumference, snoring. There is much better evidence that snoring is an important cause of sleepiness, even in the absence of conventional sleep apnoea.
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PMID:Epidemiology of snoring and its consequences. 761 44

Patients with mitochondrial disease may present to the Intensive Care Unit (ICU) with a variety of neurological and general medical disorders. Eleven patients were admitted to a neurological ICU between 1970 and 1992 because of respiratory insufficiency, status epilepticus and/or metabolic encephalopathy associated with mitochondrial disease. Respiratory impairment occurred in eight patients and was associated with nocturnal hypoventilation due to respiratory muscle weakness, aspiration due to bulbar weakness and abnormalities of central control leading to a reduced CO2 drive, irregular respiratory patterns and sleep apnoea. Seven patients received continuous respiratory support during the acute illness; three were subsequently weaned to domiciliary ventilation, and four died. Five patients had stroke-like episodes, which in two were recurrent. Four patients developed tonic-clonic grand mal epilepsy associated with myoclonic fits (2 patients), absences (2), focal fits (1) and status epilepticus (2). Encephalopathy was associated with recurrent lactic acidosis (2 patients), cardiac failure (2), hyponatraemia (2), renal abnormalities (3) and complete heart block (1). Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.
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PMID:Management of mitochondrial disease on an intensive care unit. 776 70

Sleep pattern and breathing in humans are altered following cerebrovascular accidents involving the brainstem. Sleep apnea is a well-established complication of stroke involving the brainstem. On the other hand, the effect of cerebral stroke on sleep and breathing has not been well defined. The diffuse cerebral symptoms such as cognitive deficits, depression or fatigue, after hemispheric stroke mimic those present in patients with sleep apnea. To define the breathing pattern in patients with stroke involving cerebral hemispheres without brainstem lesion and without the prior history of sleep-disordered breathing, we studied 10 patients within 1 year of their stroke. The data collected during polysomnography from the stroke patients were compared with a group of subjects matched for age, body mass index, presence of hypertension, and smoking history without stroke. Patients with stroke had an abnormal sleep architecture with significantly lower slow wave sleep and rapid eye movement (REM) sleep when compared with controls. Sleep was fragmented because of the presence of increased respiratory disturbances. Stroke patients had a respiratory disturbance index of 52 +/- 10 events per hour when compared with 3 +/- 1 in controls (p < .05). Majorities of respiratory events were obstructive apneas and were associated with arterial oxygen desaturations and arousals. The pathogenic mechanism of sleep-disordered breathing in patients with hemispheric stroke seems to be related to the physiological effect of sleep on already compromised upper airway muscle control. Patients with stroke and diffuse cerebral symptoms should be investigated for the possibility of sleep-disordered breathing.
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PMID:Sleep apnea in patients with hemispheric stroke. 781 Nov 79

This article provides an in-depth overview of the relationship between primary hypertension and adult obstructive sleep apnea syndrome. The background data and research are taken from the English-language literature through 1993. Primary hypertension is a common cause of major medical illnesses, including stroke, heart disease, and renal failure, in middle-aged males. Its prevalence in the United States is around 20%, with the rate of newly diagnosed hypertensive patients being about 3% per year. Sleep apnea syndrome is common in the same population. It is estimated that up to 2% of women and 4% of men in the working population meet criteria for sleep apnea syndrome. The prevalence may be much higher in older, non-working men. Many of the factors predisposing to hypertension in middle age, such as obesity and the male sex, are also associated with sleep apnea. Recent publications describe a 30% prevalence of occult sleep apnea among middle-aged males with so called "primary hypertension." Is this association fortuitous, related to a high prevalence of both diseases in the same population, or is it caused by a factor common to both diseases, such as obesity? Should the diagnosis of apnea be actively sought with sleep studies in hypertensive populations? If a diagnosis of "asymptomatic" sleep apnea is made in a hypertensive person, should the apnea be treated? Current research data provide only partial answers to these and other questions regarding the association of apnea and hypertension. Logic dictates that clinically symptomatic patients in hypertensive clinics should receive appropriate evaluation for apnea, but broad populations of hypertensive individuals should not be referred for sleep studies.
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PMID:The relationship between systemic hypertension and obstructive sleep apnea: facts and theory. 784 28

We have investigated cerebral blood flow velocity (CBVF) in 14 patients with marked obstructive sleep apnea syndrome using transcranial Doppler ultrasonography during sleep. The CBFV increased during apnea, with a mean acceleration of 0.9 cm/s2, followed by a rapid decrease during snoring. The same effect was obtained by voluntary apnea in healthy subjects, showing a smaller acceleration rate (0.6 cm/s2). These results provide evidence for a normal CO2 regulation of cerebral vessels during sleep apnea and do not support the notion of cerebral hypoperfusion during sleep being a risk factor for stroke.
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PMID:Cerebral hemodynamics in obstructive sleep apnea. 790 37

Forty-five patients with homozygous sickle cell disease who had tonsillectomy for recurrent tonsillitis, when compared with 45 matched controls with haemoglobin genotype AA, showed significant differences in the clinical manifestations and complications of recurrent tonsillitis between the two groups. Although throat swabs in the sickle cell group were mostly negative because they were on prophylactic penicillin, all tonsils harboured Streptococcus pneumoniae when cultured. This study suggests the tonsils to be the more specific source of pneumococcal infection that causes systemic complications which increase morbidity and mortality in sickle cell disease. Although the sickle cell patients may be less clinically symptomatic with tonsillitis, the incidence of serious complications caused by pneumococcal infections, now shown to arise from the tonsils, is significant. Adenotonsillar hypertrophy is linked with an increased risk of a sleep apnoea which causes serious neurological complications such as cerebral infarction and stroke. Tonsillectomy has greatly reduced the incidence of complications from pneumococcal infections in the sickle cell group and should therefore be recommended for sickle cell patients taking prophylactic penicillin and still developing pneumococcal infections.
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PMID:The significance of recurrent tonsillitis in sickle cell disease. 792 45

A cross-sectional study of 1385 Saudi females attending 15 health centres in urban and rural areas in the Riyadh region was conducted during September and October 1992 to determine the prevalence of obesity and its associated factors. The mean age was 32.2 +/- 11.7 years and body mass index (BMI) 29.2 +/- 7.0 kg m-2. Only 26.1% of subjects were their ideal weight (BMI < 25 kg m-2), while 26.8% were overweight (BMI 25-29.9 kg m-2), 41.9% were moderately obese (BMI 30-40 kg m-2) and 5.1% were morbidly obese (BMI > 40 kg m-2). High-risk groups for obesity were mostly middle aged, multiparous housewives. Patients living in rural areas had greater BMIs than those living in urban areas (P < 0.01). Thirty per cent of overweight participants did not think they were overweight. The study emphasizes the need for community based programmes for preventing and reducing obesity since weight control is effective in ameliorating most of the disorders associated with obesity such as Type 2 non-insulin dependent diabetes mellitus, hypertension, stroke, heart disease, sleep apnoea syndrome and osteoarthritis of the knees. The focus of efforts should be directed towards young mothers who are at risk of developing obesity and who play a central role in perpetuating it in their offspring.
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PMID:High prevalence of clinical obesity among Saudi females: a prospective, cross-sectional study in the Riyadh region. 800 60

Patients with sleep apnea may experience two types of apnea, central and obstructive. We compared cardiovascular effects of these two types of apnea matched for changes in arterial blood gas tensions and periodicity. In 12 anesthetized, closed chest dogs, obstructive apneas were induced by completely occluding the endotracheal tube at end-expiration for 1 min and allowing 1 min of spontaneous ventilation. Central apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on with the same periodicity as obstructive apneas. During both types of apnea, changes in arterial PO2 and PCO2 were approximately the same. During obstructive apneas, mean blood pressure (BP) and cardiac output (CO) did not change significantly, heart rate (HR) decreased by 27% (p < 0.001), and stroke volume increased by 7.8 ml (p < 0.005). During central apnea, BP did not change, but HR and CO decreased by far more than with obstructive apneas: 44% (p < 0.001) and 27% (p < 0.05) respectively, and stroke volume increased by 5.0 ml (p < 0.05). During obstructive apneas, right atrial pressure increased, as did right heart blood volume. During central apneas, both right atrial pressure and left atrial pressure increased, as did pulmonary blood volume. We conclude that: (1) HR decreases are more severe during central apnea, most likely due to lack of respiratory mechanoreceptor input; (2) CO decreases more with central compared with obstructive apnea due to the heart rate response; (3) HR-induced cardiac dysfunction with central apnea could lead to pulmonary vascular congestion.
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PMID:Cardiovascular effects of periodic obstructive and central apneas in dogs. 802 78

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66


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