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)

Rare upper airway lesions may be mistaken for asthma. A 16-year-old Hispanic male athlete presented to our allergy clinic with a 4-month history of wheezing and snoring with hoarseness and progressive fatigue on exertion or during sleep. His mother taped periods of harsh stridor and sleep apnea. There was no family history of vocal cord abnormalities. A year before the onset of symptoms, he suffered injury to his oral cavity with a loss of consciousness during a wrestling match. He denied dysphagia or dysphonia. He failed to respond to bronchodilators, cromolyn, or prednisone therapy during 4 weeks. On referral to our clinic, his physical examination and tape recording were characterized by harsh inspiratory stridor. His pulmonary function tests were significant for peak flow depressed out of proportion to FEV1 with reduced FVC, no response to bronchodilator, and flattened inspiratory loop unresponsive to cough or panting. Fluoroscopy and endoscopy of the upper airway was consistent with "marked bilateral limitation of vocal cord abduction." Sleep study demonstrated desaturation with CO2s in the 60s during sleep. He was started on continuous positive airway pressure, 10 cm at night, with no desaturation or sleep disturbance on follow-up.
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PMID:Bilateral abductor paresis masquerading as asthma. 337 24

Although the relationship between breathing and sleep has only recently been "discovered" by the medical community, excellent literary descriptions of what we know to be the sleep apnea syndrome were made long ago. Although ancient Greek writings described probable sleep apnea, the most important literary contributions in this area are by Charles Dickens. His description of Joe the fat boy in the Pickwick Papers is an example of his brilliant skills of observation and description. It was not until about 140 years after Pickwick Papers was published that we understood what he was describing.
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PMID:Fat, sleep, and Charles Dickens: literary and medical contributions to the understanding of sleep apnea. 391 Mar 33

We present a case of severe breathing abnormality during sleep in a young man who had had poliomyelitis 20 yr before. His sleep disorder led to respiratory failure and cor pulmonale, which were greatly improved by oxygen therapy. A study of this case and those previously described supports the notion that brainstem damage during acute poliomyelitis is important in the later appearance of sleep-disordered breathing. In addition, such patients usually have mechanical abnormalities involving the thoracic cage and respiratory muscles. These ventilatory restrictions amplify the pathophysiologic effects of abnormal central nervous system control of breathing during sleep, and we suggest that their presence has a key role in the development of sleep apnea syndrome in these patients.
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PMID:Sleep apnea syndrome after poliomyelitis. 684 37

A 17-year-old man presented with daytime sleepiness, episodic attacks of sleep and probable cataplexy. His EEG showed rapid eye movements and central sawtooth waves at sleep onset, and supported the clinical impression of narcolepsy. He improved with methylphenidate but died suddenly, and had cardiomegaly, right ventricular enlargement, and pulmonary hypertension at autopsy. These findings suggested concomitant features of sleep apnea which were not evident by history or examination.Central apneas have been frequently described in the sleep of narcoleptic patients. Few patients have had indications of obstructive or mixed apneas. This patient's course suggests that ventilation during sleep should be included in the polygraphic assessment of patients with suspected narcolepsy, as the agents used for treatment of narcolepsy may aggravate the cardiac complications of sleep apnea.
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PMID:Narcolepsy with concomitant features of obstructive sleep apnea. 712 May 1

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.
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PMID:[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords]. 795 87

A 47 year old man with a long history of chronic loud snoring and daytime sleepiness presented with hypercapnic respiratory failure and right ventricular failure. The diagnosis of obstructive sleep apnoea (OSA) leading to the 'obesity-hypoventilation syndrome', was supported by the findings of an overnight cardio-respiratory monitoring during sleep. His symptoms and arterial blood gases improved following treatment with nocturnal nasal continuous positive airway pressure (CPAP).
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PMID:Cor pulmonale due to obstructive sleep apnoea. 818 51

A 22-year-old man was admitted to the department of plastic surgery in our university with diagnosis of ankylosis and microgeniea. His complaints were snoring and somnolence in the daytime, so we performed a Respigraph (Chest) that showed obstructive apnea during sleep. We diagnosed obstructive sleep apnea syndrome. So we observed pulmonary circulation and measured lung water using the double indicator dilution method (Nihon Koden, MTV-1100) during sleep. During the period of apnea, arterial oxygen pressure and mixed venous saturation decreased, reversely, mean pulmonary arterial pressure rose, lung water (ETV) and central blood volume increased. We considered that the increase of lung water during sleep apnea is caused by hemodynamic change due to hypoxia and increase of venous return. After operation, the value of blood gas assay and apnea index were improved.
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PMID:[A case of obstructive sleep apnea syndrome with increased lung water during sleep]. 828 44

Progressive day-time sleepiness developed in a 73-year-old man for 3 years known to have kappa-light-chain myeloma, treated with radio- and chemotherapy. His powers of concentration and intellectual performance were diminished. Neither clinical nor biochemically was there any indication of abnormal water and electrolyte metabolism or hyperviscosity syndrome. The neurological examination was unremarkable. His wife's observation of nocturnal breathing pauses suggested sleep-related abnormal breathing. Polysomnography showed severe central sleep apnoea: an apnoea index of 60/h and blood oxygen saturations as low as 78%. On biphasic positive airway pressure (BIPAP) ventilation by nasal mask at night the apnoea index fell to 6/h and the symptoms improved. During a break in treatment the day-time sleepiness again increased and regressed once again with BIPAP ventilation. There is a 1-5% prevalence of sleep-related impaired breathing among adults. This condition should thus be considered in the differential diagnosis of characteristic day-time sleepiness.
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PMID:[Central sleep apnea syndrome as a cause of impaired wakefulness in multiple myeloma]. 828 78

A 55-year-old obese man was admitted to our hospital because of a severe morning headache. He snored and had recurrent episodes of sleep apnea that began 10 years earlier and had since become much worse. An overnight polysomnographic recording confirmed that he had sleep apnea syndrome, predominantly of the central type. The apneas were more frequent when he lay on his back (apnea index 54.5) than on his side (apnea index 1.2). He was treated with sleep position adjustment and nasal bi-level positive airway pressure, inspiratory positive airway pressure at 5 cmH2O and expiratory positive airway pressure at 2 cmH2O. His snoring, headache, and oxygen desaturation resolved. This case suggests that airway collapse may cause central apnea, and that nasal continuous positive airway pressure, and nasal bi-level positive airway pressure and adjustment of sleep position can be effective in some patients with central-type sleep apnea syndrome.
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PMID:[Central sleep apnea syndrome successfully treated with nasal bi-level positive airway pressure and sleep position adjustment]. 916 57

Shakespeare was a consummate dramatist and profound observer of human behavior. He vividly described many clinical disorders, including those of sleep. His characters suffered from somnambulism, sleep apnea, insomnia, and nightmares. Sleep, to Shakespeare, was a blessing denied to many of his protagonists.
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PMID:Shakespeare and sleep disorders. 933 14


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