Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Migraine prevalence is increased in high-altitude populations and symptoms of acute mountain sickness mimic migraine symptoms. Here we tested whether normobaric hypoxia may trigger migraine attacks. As positive control we used nitrolgycerin (NTG), which has been shown to induce migraine attacks in up to 80% of migraineurs. Sixteen patients (12 females, mean age 28.9 +/- 7.2 years) suffering from migraine with (n = 8) and without aura (n = 8) underwent three different provocations (normobaric hypoxia, NTG and placebo) in a randomized, cross-over, double dummy design. Each provocation was performed on a separate day. The primary outcome measure was the proportion of patients developing a migraine attack according to the criteria of the International Headache Society within 8 h after provocation onset. Fourteen patients completed all three provocations. Migraine was provoked in six (42%) patients by hypoxia, in three (21%) by NTG and in two (14%) by placebo. The differences among groups were not significant (P = 0.197). The median time to attacks was 5 h. In conclusion, the (remarkably) low response rate to NTG is surprising in view of previous data. Further studies are required to establish fully the potency of hypoxia in triggering migraine attacks.
Cephalalgia 2006 Jul
PMID:Normobaric hypoxia and nitroglycerin as trigger factors for migraine. 1677 96

The present study applied T2- and diffusion-weighted magnetic resonance imaging to examine if mild cerebral edema and subsequent brain swelling are implicated in the pathophysiology of acute mountain sickness (AMS). Twenty-two subjects were examined in normoxia (21% O2), after 16 hours passive exposure to normobaric hypoxia (12% O2) corresponding to a simulated altitude of 4,500 m and after 6 hours recovery in normoxia. Clinical AMS was diagnosed in 50% of subjects during hypoxia and corresponding headache scores were markedly elevated (P<0.05 versus non-AMS). Hypoxia was associated with a mild increase in brain volume (+7.0+/-4.8 ml, P<0.05 versus pre-exposure baseline) that resolved during normoxic recovery. Hypoxia was also associated with an increased T2 relaxation time (T2rt) and a general trend toward an increased apparent diffusion coefficient (ADC). During the normoxic recovery, brain volume and T2rt recovered to pre-exposure baseline values, whereas a more marked reduction in ADC in the splenium of the corpus callosum (SCC) was observed (P<0.05). While changes in brain volume and T2rt were not selectively different in AMS, ADC values were consistently lower (P<0.05 versus non-AMS) and associated with the severity of neurologic symptoms. Acute mountain sickness was also characterized by an increased brain to intracranial volume ratio (P<0.05 versus non-AMS). These findings indicate that mild extracellular vasogenic edema contributes to the generalized brain swelling observed at high altitude, independent of AMS. In contrast, intracellular cytotoxic edema combined with an anatomic predisposition to a 'tight-fit' brain may prove of pathophysiologic significance, although the increase in brain volume in hypoxia was only about 0.5% of total brain volume.
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PMID:Magnetic resonance imaging evidence of cytotoxic cerebral edema in acute mountain sickness. 1702 10

Droma, Yunden, Masayuki Hanaoka, Buddha Basnyat, Amit Arjyal, Pritam Neupane, Anil Pandit, Dependra Sharma, and Keishi Kubo. Symptoms of acute mountain sickness in Sherpas exposed to extremely high altitude. High Alt. Med. Biol. 7:312-314, 2006.--The aim of this field interview was to investigate the current state of affairs concerning acute mountain sickness (AMS) in high-altitude residents, specifically the Sherpas at 3440 m above sea level, when they are exposed rapidly to altitudes significantly higher than their residing altitudes. Out of 105 Sherpas (44 men and 61 women, 31.2 +/- 0.8 yr), 104 had mountain-climbing experiences to 5701.4 +/- 119.1-m altitude in average 3.5 times each year. On the other hand, only 68 out of 111 non-Sherpas (29.9 +/- 0.8 yr) had experience of 1.4 +/- 1.5 climbs to an average 2688.6 +/- 150.4-m altitude in their mountaineering histories (p < 0.0001). Among the 104 Sherpas, 45 (43.3%) complained of at least one AMS symptom (headache, gastrointestinal symptoms, weakness, dizziness, and difficulty sleeping) in their experiences of mountaineering at an average 5518.9 +/- 195.9-m altitude. And 16 out of the 68 non-Sherpas (23.5%) reported the AMS symptoms at a mean altitude of 2750.0 +/- 288.8 m. Moreover, we also noticed that the Sherpa women showed a significantly higher Sa(O(2) ) (93.9 +/- 0.2%) than did Sherpa men (92.4 +/- 0.3%, p = 0.0001) at an altitude of 3440 m. The brief field interview evidenced that Sherpas might suffer from AMS when exposed to altitudes significantly higher than their residing altitude.
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PMID:Symptoms of acute mountain sickness in Sherpas exposed to extremely high altitude. 1717 17

A human being's exposure to altitude, and the consequent hypobarism, entails a complex series of adaptive mechanisms that depend on the rate of ascent and the altitude reached. When these mechanisms fail, so-called acute mountain sickness (AMS) results, with headache as its predominant symptom. It has been observed, nonetheless, that well-acclimated mountaineers may have headache without symptoms of AMS. We consider that high altitude and ensuing hypobarism bring about three possibilities of cephalalgia: the first is covered by the set of AMS clinical manifestations and is undoubtedly the most frequent; the second occurs independently of acute mountain sickness and is probably due exclusively to hypoxia; and the third includes altitude-triggered migraine or migraine-like episodes. These are neurogenic problems secondary to hypoxia caused by hypobarism and, in all events, have a common denominator: hypoxia and a fundamental white organ, the brain.
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PMID:High-altitude headache. 1734 Nov 72

Headache is the cardinal symptom of acute mountain sickness (AMS). The headache normally worsens, with increased cerebral affection and the development of high-altitude cerebral edema (HACE). A Norwegian expedition aimed to climb Baruntse (7129 m) in Nepal in 2003. At 5400 m a 35-year-old man felt exhausted. The next day he aborted his attempt at further climbing as a result of extreme fatigue. Over the next 24 hours he developed cough, dyspnea, and severe hypoxia before progressing to ataxia and blurred vision. At no point did he experience headache or nausea. The patient was evacuated by helicopter. He improved immediately after descent and recovered completely within a week. The speed of progression from AMS to HACE varies. Abrupt onset of HACE is occasionally reported. High-altitude pulmonary edema (HAPE) may induce severe hypoxia that can lead to rapid development of HACE. High-altitude cerebral edema in the setting of HAPE was the most likely diagnosis despite the unusual lack of headache. Rapid onset of HAPE with subsequent severe desaturation should raise awareness of the development of HACE, even in the absence of headache.
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PMID:High-altitude cerebral edema with absence of headache. 1744 14

Symptoms of high altitude sickness including headache and neuropsychological dysfunction are thought to result from prolonged exposure to hypoxia. In order to explain how the brain adapts to lower oxygen pressure at high altitude, CD1 mice were exposed to 3 weeks of hypobaric hypoxic conditions. Analyses of the neuronal morphology of striatal medium spiny neurons (MSNs) revealed a significant decrease in dendritic length, yet no change in dendritic volume, in hypoxic mice relative to normoxic mice. Vascular data indicated an increase in blood vessel area in the striatum of mice exposed to prolonged hypoxia. A mouse model of high altitude exposure may assist in elucidating the mechanisms of cerebral adaptation to high altitudes in humans, and therefore aid in developing successful prevention techniques and treatment of problems associated with high altitude disease.
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PMID:Effect of hypoxia on the morphology of mouse striatal neurons. 1751 72

The Lake Louise Scoring System (LLSS) was designed to evaluate adults for symptoms of acute mountain sickness (AMS). The language used in the LLSS may be too complex for young children to comprehend. This study evaluates if age-appropriate language alters the results of AMS diagnostic scores in 4- to 11-yr-old children. With parental help, subjects completed the LLSS and an equivalent Lake Louise Age-Adjusted Symptom Score (LLAASS) daily for 3 days. Measurements were made at 1605 m, in the subjects' homes, without any altitude change. Equivalent questions between the two surveys were assessed for agreement on the day when the most symptoms were recorded for each question. Thirty-seven children (19 girls), ages 4 to 11 yr (mean age 7.4 +/- 2.3 yr) completed the study. Kappa values: headache (kappa = 0.22), gastrointestinal (kappa = 0.34), fatigue (kappa = 0.88), dizziness (kappa = 0.65), and sleep (kappa = 0.88) ranged from fair to very good. The LLAASS resulted in higher mean symptom scores (1.14 +/- 0.98) compared to LLSS questions (0.61 +/- 0.82) (p < 0.01). The AMS diagnostic threshold was reached in 9% (95% CI, 4-16) of measurements using the LLAASS and 4.5% (95% CI, 1.5-10) with the LLSS. The LLSS results in reporting of fewer AMS symptoms in this population when compared with a diagnostic tool using age-appropriate language and/or visual representations. Age-appropriate communication must be used to assess AMS, particularly for headache (the key symptom of AMS) and gastrointestinal symptoms. Young children report symptoms of AMS at baseline without altitude gain; therefore, the AMS diagnostic threshold in this population may require modification.
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PMID:Language used in Lake Louise Scoring System underestimates symptoms of acute mountain sickness in 4- to 11-year-old children. 1758 6

Previous research has demonstrated that blood and urine concentrations of various leukotrienes are elevated with acute hypoxic exposure. Some of these studies have suggested that leukotrienes may be mediators in the pathogenesis of acute mountain sickness (AMS). We conducted a randomized, double-blind study to determine if AMS symptoms correlated with the increase in leukotriene synthesis and if prophylactic leukotriene receptor blockade would prevent the development of AMS in a simulated high altitude exposure. Three male and five female subjects completed two normobaric hypoxia chamber exposures (average F(IO2) 12.4 +/- 0.09%), receiving montelukast 10 mg daily for 4 days prior to one session and placebo for 4 days prior to the other session. There were no differences in Lake Louise AMS scores, time spent in the chamber, average oxygen saturation, and average heart rate during the montelukast and placebo sessions. Headache scores were higher during treatment with montelukast than during treatment with placebo. Compared to preexposure values, urinary leukotriene E4 concentrations were unchanged during the hypoxic chamber exposure following treatment with placebo or montelukast. Urinary leukotriene E4 excretion during the hypoxic exposure did not differ between the two sessions. A 4-day course of leukotriene receptor blockade does not prevent symptoms of AMS. These results suggest that leukotrienes do not play a causal role in the pathophysiology of AMS.
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PMID:Leukotriene receptor blockade does not prevent acute mountain sickness induced by normobaric hypoxia. 1758 7

No evidence is available to show that nasal congestion is a manifestation of exposing an individual to high altitude and hypoxia. Since both nasal congestion and high-altitude headache are vasogenic, we explored whether there is a coincidence between these two symptoms. A prospective observational study was carried out on a cohort of 118 adults (>18 years old) in a mountain clinic at 3450 m. After 24 h of ascent, an interview was held to ask if each individual experienced acute mountain sickness symptoms (headache, etc.) and nasal congestion. Sixty-six (55.9%) individuals mentioned headache within 24 h after ascent and nasal congestion was reported by 34 (28.8%) individuals. There was a reverse association between headache and nasal congestion (P < 0.001). In conclusion, there is a reverse association between altitude headache and nasal congestion, probably as result of contradictory autoregulation effects or exaggerated sympathetic activity.
Cephalalgia 2007 Aug
PMID:Reverse association between high-altitude headache and nasal congestion. 1759 98

A 32-year-old Japanese woman with headache, anorexia and malaise, just after travelling cities of the altitude of over 4,000 m by a long-distance coach is described. Her magnetic resonance imaging (MRI) demonstrated strikingly increased T2 signal in the corpus callosum, particularly in the splenium, and MR angiography (MRA) revealed widespread vasospasm. These abnormalities resolved on subsequent MRI studies. We diagnosed her as high altitude cerebral edema (HACE), considered to be the end stage of acute mountain sickness (AMS).
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PMID:Acute mountain sickness with reversible vasospasm. 1761 24


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