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)

400 sleep-apnoeic patients with an intact autonomic nervous system underwent twenty-four-hour electrocardiography with simultaneous polygraphy recording at night. At onset of sleep apnoea all showed progressive bradycardia, followed by abrupt tachycardia on resumption of breathing. The electrocardiographic pattern, which is identifiable by computer analysis, can be used as a screening tool for sleep apnoea; it was not seen in controls without sleep apnoea syndrome. A subgroup of patients with sleep apnoea and impairment of autonomic nervous control of the heart (heart transplants, autonomic neuropathy, Shy-Drager syndrome) did not show the cyclical heart rate pattern. In obstructive sleep apnoeic patients with normal autonomic nervous function, atropine sulphate blocked the pattern by eliminating the bradycardia component, while 100% oxygen, even at high rates of administration, caused only moderate blunting of the heart rate variation. The electrocardiographic changes observed in sleep apnoea syndrome are therefore mediated by the autonomic nervous system; hypoxia is not the only factor involved.
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PMID:Cyclical variation of the heart rate in sleep apnoea syndrome. Mechanisms, and usefulness of 24 h electrocardiography as a screening technique. 614 Apr 42

Ten patients with autonomic nervous system dysfunction (familial dysautonomia, juvenile diabetes, or Shy-Drager syndrome) were studied to assess the impact of their impairment on breathing during sleep. Several types of breathing dysfunction during sleep were identified independent of the patients' primary complaints. Obstructive sleep apnea syndrome was the most common; central sleep apnea and disturbances of te respiratory oscillator also were seen. Esophageal reflux was found to be the cause of some sleep-related problems. The observed respiratory irregularities were not associated with the usual cardiac response; a "decoupling" of heart rate from the respiratory cycle was noted during sleep in these patients.
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PMID:The impact of autonomic nervous system dysfunction on breathing during sleep. 730 57

This is the first report on a case of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with Gerhardt syndrome (paralysis of bilateral vocal cords). A 67-year-old Japanese man suffering from progressive autonomic failure was diagnosed as having Shy-Drager syndrome (SDS) with hyponatremia due to SIADH and severe sleep apnea caused by a bilateral recurrent nerve palsy. Water load test showed alteration in diuresis which was corrected by phenytoin. Arginine vasopressin secretion was not suppressed by plasma osmolality below 280 mOsm/kgH2O. Impairment of the afferent pathways of baroreceptors, or impairment of the osmoreceptors could be speculated as the etiological factor of the SIADH observed in this case.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and Gerhardt syndrome associated with Shy-Drager syndrome. 771 59

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

Central autonomic dysfunctions can be due to primary (degenerative) or secondary disorders. Autonomic failure (AF) may be a major manifestation of multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD). In both MSA and IPD, AF is almost invariably associated with neuronal loss in the intermediolateral cell columns. Dysautonomia in MSA is early, severe, and progressive, including marked orthostatic hypotension and urinary incontinence and is complicated by respiratory disturbances, such as laryngeal stridor and sleep apnea. MSA/AF can be differentiated from primary (or pure) autonomic failure (PAF) without central nervous system involvement. PAF is mainly a disorder of the postganglionic neurons. In contrast to PAF, MSA/AF has preserved basal sympathetic activity, decreased cerebrospinal fluid (CSF) neurotransmitter markers, impaired vasopressin response to hypotension, and impaired adrenocorticotrophic hormone/beta endorphin response to hypoglycemia. AF in IPD is generally less severe than in MSA. Poor response to L-Dopa, abnormal urethral sphincter electromyography, and CSF markers may distinguish MSA from IPD. Secondary autonomic disorders may result from traumatic, vascular, inflammatory, demyelinating, or neoplastic lesions involving corticolimbic, hypothalamic, brainstem, or spinal autonomic network. These disorders can cause AF or autonomic hyperactivity, such as arrhythmia, hypertension, and hyperthermia. However, many disorders may only produce subclinical abnormalities.
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PMID:Central autonomic disorders. 845 95

Patients with Parkinson's disease (PD) and parkinsonian syndromes (eg, dementia with Lewy bodies, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. Sleepiness in PD is common (10% to 50% of patients) and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, viz, and narcolepsy with cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness, because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Men with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with Parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics may exacerbate sleepiness in a small subset of patients. The primary pathologies involved in Parkinsonism appear to be the greatest contributors to the development of daytime sleepiness. Sleepiness in Parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents, such as bupropion, modafinil, or traditional psychostimulants.
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PMID:Sleepiness and Unintended Sleep in Parkinson's Disease. 1267 Apr 12

A 72-year-old man was admitted to our hospital due to dysuria and frequent syncope. The patient had been well until the age of 70 years, when he began with these symptoms and neurogenic bladder was diagnosed in the other hospital. On admission, neurological examinations revealed no abnormal findings except blepharoptosis, anisocoria and orthostatic hypotension. Frequent apnea was evident during sleep. Autonomic function tests showed mainly sympathetic postganglionic dysfunction. Brain magnetic resonance imaging showed lacunar infarctions without cerebello-pontine atrophy or abnormal signals of the basal ganglia. We diagnosed pure autonomic failure (PAF) with sleep apnea syndrome (SAS). After starting nasal continuous positive airway pressure (CPAP) for SAS, his sneezing and sleep apnea drastically improved. Interestingly, CPAP also decreased the severity of orthostatic hypotension and syncope. Ambulatory blood pressure monitoring (ABPM) showed remarkable improvement in diurnal fluctuation of blood pressure after CPAP therapy. Although SAS is frequently associated with Shy-Drager syndrome but not with PAF, patients with PAF had been reported to have degenerative changes in the central nervous system overlapping with Shy-Drager syndrome or Lewy body disease. This case raised the possibility that nasal CPAP may be useful for orthostatic hypotension as well as SAS in neurodegenerative diseases.
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PMID:[A case of pure autonomic failure (PAF) with sleep apnea syndrome (SAS) and successful treatment of dysautonomia with nasal continuous positive airway pressure (CPAP)]. 1514 64

Patients with Parkinson's disease and parkinsonian syndromes (eg, dementia with Lewy body disease, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. This sleepiness is common and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, namely narcolepsy/cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Male patients with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics exacerbate sleepiness in a small subset of patients in a dose-dependent fashion. Nonetheless, the primary pathologies involved in parkinsonism appear to be the greatest contributors to daytime sleepiness. Sleepiness in parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents such as bupropion, modafinil, or traditional psychostimulants.
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PMID:Excessive daytime sleepiness and unintended sleep in Parkinson's disease. 1652 72


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