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

Narcolepsy may affect as many as 200,000 Americans. The illness involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. A characteristic history of cataplexy establishes the diagnosis. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, blackouts (or automatic behavior), and disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Symptoms may also appear in young children who may be misdiagnosed as hyperactive or psychotic. No completely satisfactory treatment is available at the present time. The current treatments of choice are methylphenidate (for sleepiness and sleep episodes) and imipramine (for cataplexy). Medication dosages must be adjusted for individual patients. A careful history of the illness can rule out hypothyroidism, hypoglycemia, and epilepsy. Sleep apnea is a serious complication of narcolepsy and may be life threatening.
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PMID:Narcolepsy. Diagnosis and treatment. 105 17

We present the case of a 63 years old man (177 cm height, 111 kg weight) with autoimmune thyroiditis. He had a long term history of hypersomnolence and heavy snoring. Two years ago, because of a bifascicular block and sinus pauses, a cardiac pace-maker was placed. Polysomnography recording showed a systematic periodic breathing characterized by profound desaturation waves (often 92% Sa O2 to 60% Sa O2) every 60 seconds, secondary to prolonged mixed apneas. Hormone replacement therapy and a 17 kg weight loss completely suppressed the sleep apnea syndrome within five months. We conclude that SAS is a major component of the respiratory depression in hypothyroidism and that normalisation of thyroid function can definitely cure the patient.
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PMID:[Sleep apnea syndrome and hypothyroidism: apropos of a new case and a review of the literature]. 265 40

The symptoms of hypothyroidism are protean and include apathy, somnolence, lethargy, personality change, and intellectual deterioration. Many of these symptoms may be related to hypothyroid-induced sleep disorders. Hypothyroidism is associated with abnormal ventilatory drive, abnormal sleep architecture, and sleep apnea. Central, obstructive, and mixed patterns of sleep apnea are commonly observed in hypothyroidism. A case of severe sleep apnea in a grossly myxedematous patient who improved dramatically following thyroid replacement alone is presented. Myxedema is a reversible cause of sleep apnea, and thyroid function testing should be considered in its diagnostic work-up.
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PMID:Sleep apnea, sleep disorders, and hypothyroidism. 276 18

After irradiation of the neck for a squamous cell carcinoma of the tonsillar pillar and vocal cord, a 71-year-old man presented with a rapidly progressive sleep apnea syndrome. Previous reports describe the condition of patients with obstructive sleep apnea that developed after neck irradiation and secondary to supraglottic edema. Our patient had an obstructive component to his apnea similar to that described in previous cases, but, in addition, he had hypothyroidism. Myxedema is a well-described cause of both obstructive and central apnea. We believe both contributed to his condition. He was successfully treated by placement of a tracheostomy and by thyroid supplementation. In patients who present with sleep apnea after neck irradiation, especially with acute or severe symptoms, the differential diagnosis should include both a central cause from hypothyroidism as well as a peripheral obstructive cause from laryngeal edema.
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PMID:Sleep apnea syndrome after irradiation of the neck. 281

Thyroid deficiency states are now a well recognized cause of the sleep apnea syndrome. The spectrum of disease ranges from mild, asymptomatic hypothyroidism to severe myxedema, and the disorder is associated with both obstructive and central types of sleep apnea. A variety of factors may be involved, including upper airway obstruction with or without obesity, and alterations in ventilatory drive. The definitive therapy is thyroid hormone replacement, which has been shown to diminish or completely eliminate apneic episodes and arterial oxygen desaturation, as well as to effect many improvements in sleep patterns and overall sleep efficiency. The incidence of thyroid deficiency states in patients with sleep apnea syndrome is not known, but it seems reasonable to evaluate thyroid function in all patients. Thyroid replacement therapy seems logical for the treatment of sleep apnea in patients with previously unrecognized subclinical hypothyroidism. Much remains to be learned about the diagnosis and treatment of sleep apnea syndromes associated with thyroid hormone deficiency, and further studies are needed.
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PMID:Sleep apnea and hypothyroidism. 305 27

Two patients are described who presented with depression and were later found to have both obstructive sleep apnea and hypothyroidism. Both patients had normal thyroxine (T4) levels but elevated thyroid-stimulating hormone (TSH) levels. Thyroid replacement led to resolution of both apnea and depression. The possibility of hypothyroidism as a cause of sleep apnea and depression is discussed.
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PMID:Sleep apnea and hypothyroidism presenting as depression in two patients. 355 30

To determine the incidence and frequency of sleep apnea in persons with hypothyroidism, 11 consecutive patients with newly diagnosed disease were studied before and during thyroid hormone replacement therapy. Nine patients had episodes of apnea, with the number of episodes per hour of sleep ranging from 17 to 176 (mean, 71.8). Six of the nine patients were obese and had 99.5 episodes per hour compared with 16.3 episodes per hour in the 3 nonobese patients (p less than 0.02). After 3 to 12 months of thyroxine replacement therapy, mean apnea frequency decreased from 71.8 +/- 18.0 (SE) to 12.7 +/- 6.1 episodes per hour, without reduction in body weight. There were fewer changes in sleep stage per hour during treatment (22.1 +/- 4.9) than pretreatment (57.6 +/- 14.5). Carbon dioxide response tests done under non-loaded and flow-resistive loaded conditions before and during thyroxine replacement therapy showed increases in the loaded respiratory effort and ventilation during thyroxine treatment. Sleep apnea episodes are common in persons with untreated hypothyroidism, even with normal lung function. Thyroxine replacement therapy decreases apnea frequency, even without change in body weight.
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PMID:Obstructive sleep apnea in hypothyroidism. 647 35

A 58-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 microIU/ml (normal, less than 12 microIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (VE/VCO2), and the ventilatory response to exercise (delta VE/delta VCO2) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38 to 33 mm Hg), and an increase in VE/VCO2 (17%), mouth occlusion pressure (50%), and AVE/VCO2 (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and VE/VCO2 despite a 23% increase in VE. Mouth occlusion pressure increased 37% but delta VE/delta VCO2 was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted completed relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.
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PMID:Disordered breathing during sleep in hypothyroidism. 679 57

This is a report of a 45-yr-old male patient who developed central sleep apnea syndrome because of hypothyroidism. In response to L-thyroxine therapy, the patient became euthyroid, and the apneic phenomenon disappeared. Previous reports have suggested that hypothyroidism can produce obstructive sleep apnea from either narrowing of the upper airway secondary to deposition of mucopolysaccharides and protein extravasation into the tissues or from abnormalities in ventilatory control. The present patient did demonstrate evidence of profound dysfunction of his respiratory control center: before therapy, the patient manifested blunted ventilatory and occlusion pressure responses to hypoxia and normal responsiveness to hypercapnia; after therapy, hypoxic responsiveness was restored and the ventilatory response to hypercapnia doubled. Hypothyroidism should be included in the differential diagnosis of central sleep apnea.
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PMID:Central sleep apnea in hypothyroidism. 683 58

While hypothyroidism is considered to predispose to obstructive sleep apnoea (OSA), the presence of a goitre itself is not a recognized cause of OSA. We present the cases of two euthyroid patients with large goitres and clinical evidence of OSA, whose OSA symptoms significantly improved following partial thyroidectomy. This finding suggests that the goitre contributed to their symptoms.
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PMID:Goitre: a cause of obstructive sleep apnoea in euthyroid patients. 904 57


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