Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article gives the probable location within 65 km of the Big Headache Mountain where mountain sickness was first reported by Too Kin, a Chinese official, in 37-32 B.C. We believe that traveling over the western edge of the Himalayan Karakoram Range or in the Pamirs caused the major difficulties, probably when travelers crossed the Kilik Pass at an altitude of 4827 m or 15837 ft or within 60 km of this pass and at an altitude of at least 4500 m or 14750 ft. We theorize that the route Too Kin described is from Kashi, an important center in Sinkiang or Chinese Turkestan, to Kabul in Afghanistan. This particular route has two other altitude maxima; one at the Ulagh Rabat Pass in Sinkiang about 15 km west of the Muztagata peak where the elevation is 4250 m or 14000 ft, and the other at the Shandur Pass over the Hindu Kush in Pakistan where the elevation is 3734 m or 12250 ft.
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PMID:The first documented report of mountain sickness: the China or Headache Mountain story. 635 Dec 9

Phenytoin sodium was evaluated for its effect on the development and intensity of acute mountain sickness (AMS) because of its ability to reduce intracellular Na+ concentrations in brain and thereby minimize any tendency to increase cellular volume, a hypothetical cause of AMS. Six men aged 19-35 were exposed to approximately 4600 m altitude in a hypobaric chamber for 52 h on two occasions separated by 10 d at sea level. Subjects received wither phenytoin or placebo for 18 h before (700 mg, divided dose) and throughout (100 mg t.i.d.) each altitude exposure in a double-blind, repeated-measures (crossover) design. Phenytoin serum concentrations ranged from 4.4-13.9 micrograms/ml during altitude exposure. Twice daily questionnaires and clinical evaluations showed no marked benefit from phenytoin on the occurrence, severity, or duration of AMS symptoms: headache, nausea, insomnia, and general malaise. Overall, 1 subject felt better, 2 felt worse, 1 felt the same; 2 were not suitably comparable. There was no observed relationship between serum levels and symptoms of AMS. Moderate degrees of weakness and dizziness were each reported by 3 subjects with phenytoin but not with placebo, however. Resting pulmonary ventilation, end-tidal PO2 and PCO2, map reading abilities and respiratory mask donning times were not affected by phenytoin. Under the conditions of this trial, phenytoin did not appear to be useful in managing AMS.
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PMID:Phenytoin: ineffective against acute mountain sickness. 676 69

Sixty-four climbers participated in a randomized clinical trial of acetazolamide prophylaxis for acute mountain sickness (AMS) during rapid, active ascent of MT Rainier. Twenty-nine (93.6%) of 31 climbers receiving acetazolamide and 25 (75.8%) of 33 receiving placebo attained the summit. Time spent ascending from sea level to the summit (4,394 m) averaged 33.5 hours (range, 23 to 48 hours). On the summit AMS was less common in climbers receiving acetazolamide, and they experienced less headache, nausea, drowsiness, shortness of breath, and dizziness and a greater sense of satisfaction and psychological well-being. Minute ventilation on the summit was significantly greater in subjects taking acetazolamide (24.9 +/- 2.0 L/min compared with 16.9 +/- 3.8 L/min). Expired vital capacity was also greater on the summit in the acetazolamide group (6.9 +/- 0.4 L compared with 5.8 +/- 0.4 L). We conclude that acetazolamide is effective in the prophylaxis of AMS for climbers attempting rapid, active ascent. Increased ventilation at altitude, producing an increased alveolar oxygen tension, may be related to the observed amelioration of symptoms.
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PMID:Acute mountain sickness and acetazolamide. Clinical efficacy and effect on ventilation. 704 33

The symptoms and signs of acute mountain sickness are present in about half of the tourists trekking in Nepal to an altitude of 42000 m. The most common symptoms are headache and nausea. Pulmonary rales are found in more than 10% of trekkers, while high altitude pulmonary edema is rare. Retinal hemorrhages occur almost exclusively above 5000 m. A careful history and physical examination are generally sufficient for medical evaluation of fitness for high altitude. There are no specific tests to predict performance at altitude. The most effective prophylaxis of acute mountain sickness is "slow" ascent, which is arbitrarily defined as an increase in sleeping altitude of 300-400 m per 24 hours. Sufficient fluid intake is also very important. Prophylactic administration of acetazolamide reduces the incidence and severity of acute mountain sickness. Mild forms of acute mountain sickness are treated by a rest day, whereas patients with severe disease should descend as soon as possible.
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PMID:[Incidence, prevention and therapy of acute mountain sickness]. 707 85

The effect of previous physical conditioning on young well-conditioned mountaineers in relationship to acquiring acute mountain sickness is controversial. Data show both increased and decreased effects on the incidence of altitude illness. How general tourists at moderate altitudes are affected is unknown. To determine the influence of sea-level habitual physical activity on the incidence of mountain sickness, we surveyed 205 participants in a scientific conference at 3,000 m (9,840 ft). A 36-item questionnaire was distributed to the subjects 48 hours after arrival at altitude. Their sea-level physical activity (SLPA) was measured by a published and validated instrument that included questions about patterns of work, sporting, and leisure-time activities. Acute mountain sickness was defined as the presence of 3 or more of the following symptoms: headache, dyspnea, anorexia, fatigue, insomnia, dizziness, or vomiting. Most of the respondents were male (62%) from sea level (89%) with a mean age of 36 +/- 8.7 (standard deviation) years (range, 22 to 65). Nearly all (94%) were nonsmokers, and 28% had acute mountain sickness. The mean SLPA score was 8.0 +/- 1.3 (range, 5.1 to 12.0). No statistically significant difference in mean SLPA scores was found between those with and without acute mountain sickness (8.1 versus 7.8), nor in the individual indices (work, 2.5 versus 2.4; sport, 2.9 versus 2.7; leisure, 2.8 versus 2.7). We conclude that habitual physical activity performed at sea level does not play a role in the development of altitude illness at moderate altitude in a general tourist group.
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PMID:Sea-level physical activity and acute mountain sickness at moderate altitude. 757 57

In the epidemiological study among 379 adult men with permanent residence at 4300 meters (14,200 feet), we found 32.2% with migraine (mostly migraine with aura), 15.2% with tension-type headache (episodic more than chronic), and 7.2% with other headaches. The frequency of migraine increased with age from 30.1% in the 20-29 year age group to 36.8% in the 50-59 year group. Episodic tension-type headaches also showed this trend. We found an age-specific increase in the frequency of high hemoglobin (Hb > 213 milligrams), low oxygen saturation (O2 saturation < 81.5%) and high chronic mountain sickness scores. Male migraineurs and those with more than two headaches per month had the highest hemoglobin levels and chronic mountain sickness scores when compared with high altitude men without headaches.
Cephalalgia 1994 Oct
PMID:Migraine, polycythemia and chronic mountain sickness. 782 85

A massive expansion of mountain tourism and the practice of sports at altitude (mountaineering, skiing, cycling, hang-gliding, parapente, etc) has been observed in the last decades. This emphasis on new forms of sports and recreation represented as a social phenomenon is accompanied by an increase in the mountain associated-disorders and related-accidents. These include headache, lassitude, pain, difficulty in breathing, rapid heartbeat, and in the worst of the cases loss of consciousness, always possible, manifest by poor judgement, fatigue, etc, and death. However, medical studies are rare, mainly because the molecular mechanisms of tissue damage induced by oxygen free radicals are still poorly understood. Therefore, the goals of the present report are: 1) to summarize the main adaptations of the body at high altitude, introducing the concepts of altitude sickness and oxygen free radicals and their relation; 2) to propose a mechanism of action of oxygen free radicals in the development of this pathology, with special attention in hypoxia and related mechanisms; 3) to suggest a role for antioxidants in the therapy of altitude-related disorders.
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PMID:Role of oxygen free radicals in altitude-related disorders. 802 27

Up to half of those who ascend rapidly to altitudes of over 3,000 m may experience symptoms of acute mountain sickness (AMS) and of these some 95% may suffer from high altitude headache. We report the first controlled trial specifically to assess an oral drug therapy for this common symptom. Subjects were 21 members of mountaineering expeditions to similar altitudes in the Bolivian Andes and the Himalayas in Nepal. The study was of a randomized, placebo-controlled, double-blind, within-patient crossover design. Ibuprofen was significantly superior to placebo both in reducing headache severity and in speed of relief (a mean difference of 94 min in time to no/minimal headache). Only 14% of subjects who initially took ibuprofen felt the need for further medication compared to 83% of those who took placebo first (p = 0.02). Of the 11 subjects completing both phases of the crossover, 8 (73%) favored ibuprofen while the remainder had no preference (p = 0.004). No attributable adverse effects occurred. The results suggest that ibuprofen is a safe and effective treatment for high altitude headache.
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PMID:High altitude headache: treatment with ibuprofen. 811 20

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Headache, nausea, vomiting, insomnia and peripheral edema are the most important symptoms of acute mountain sickness (AMS), which occur within 6 to 12 h. after exposure to altitudes of more than 2500 m a. s. l. Usually, these symptoms resolve spontaneously; however, they may progress to life-threatening cerebral edema in some cases. High-altitude pulmonary edema (HAPE) is a noncardiogenic edema, which is often preceded by acute mountain sickness. Frequency and severity of these illnesses depend on the altitude, the rate of ascent and the degree of individual susceptibility. A low hypoxic ventilatory drive, sodium and water retention as well as increased capillary permeability are the most important pathophysiological factors which contribute to hypoxemia and edema formation in AMS. They are also important in the pathophysiology of HAPE. In addition, excessive hypoxic pulmonary artery hypertension is most likely crucial in the pathogenesis of HAPE. Constitutional factors which regulate ventilation and pulmonary artery pressure under hypoxia are considered the most important determinants of susceptibility to AMS and HAPE.
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PMID:[Clinical aspects and pathophysiology of altitude sickness]. 837 71


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