Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central sleep apnea is a disorder characterized by apneic episodes during sleep with no associated ventilatory effort. More commonly than not these apneas are seen in patients who also have obstructive and mixed events. Although patients with this disorder frequently complain of insomnia and depression, frank hypersomnolence is rarely encountered. As these complaints are common ones seen in numerous clinical situations, and since sleep studies are rarely conducted to investigate their etiology, the true incidence of central sleep apnea has not been determined. The etiology of central apnea remains unknown, although the association between these breathing events and a number of other disease processes has increased our understanding of the disorder. Central apneas during sleep commonly occur after hyperventilation with the associated hypocapnic alkalosis. This occurs at high altitude when hyperventilation is induced by hypoxia and at sea level when spontaneous nocturnal hyperventilation occurs. This suggests that PCO2 is the primary stimulus to ventilation during sleep and that loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine's curse (central alveolar hypoventilation) or the obesity-hypoventilation syndrome may also have central apneas. For reasons that remain unexplained, central sleep apnea is commonly seen in patients with congestive heart failure, nasal obstruction, and certain neurologic disorders. However, in most patients with central sleep apnea no obvious cause or association can be found. The treatment of this disorder is not entirely satisfactory. If it is severe, mechanical ventilation during sleep can be provided by any one of a number of techniques. However, for the patient who simply complains of insomnia and is found to have a moderate number of central apneas, the treatment choices are limited. Acetazolamide has been shown to decrease central apneas during short-term use, but results have been variable with prolonged administration. Other ventilatory stimulants seem to have little efficacy. Interestingly, oxygen administration has been shown to reduce central apneas considerably in a number of studies, although the explanation for its success is unknown. Central sleep apnea therefore remains a relatively rare disorder whose etiology is not fully understood and whose treatment is not completely satisfactory.
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PMID:Central sleep apnea. 393 82

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

Headache is known to be the predominant symptom in acute mountain sickness which is also frequently accompanied by nausea, vomiting and insomnia. Nowadays, every year millions of skiers and mountaineers are attracted to mountains all over the world. At altitudes between 2500 m and 5000 m about 20% to 90% of those who are not adapted to high altitude will experience high altitude headache (HAH). It is well documented that HAH can be best prevented by observance of the golden rule: not to go too high too fast. Although many mountaineers are aware of this rule, its observance is complicated by unknown individual susceptibility, the location of mountain huts, the use of cable cars, limited holiday time, unfavorable weather or avalanche conditions. Therefore, there is a widespread use of drugs for the treatment and prevention of HAH. In the past, the increase in cerebral blood flow during acute hypoxia was thought to be the main cause of HAH. More recent findings, however, have caused this hypothesis to be reduced in importance and have supported the pathogenetic consequence of sensitization of intracranial pain-sensitive structures. The effectiveness of cyclooxygenase inhibition for the treatment and prevention of HAH suggests that especially prostaglandins may be an important mediator between hypoxia and HAH. Besides oxygen, acetazolamide, dexamethasone and especially inhibitors of prostaglandin synthesis such as ibuprofen and naproxen are approved for the treatment of HAH. Acetazolamide, dexamethasone, and aspirin were also found to prevent HAH. The most beneficial effects however, may be achieved by the combined application of acetazolamide and aspirin. This combination increases oxygenation and reduces prostaglandin synthesis.
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PMID:[High altitude headache: epidemiology, pathophysiology, therapy and prophylaxis]. 1058 87