Risk factors for high-altitude headache upon acute high-altitude exposure at 3700 m in young Chinese men: a cohort study

Abstract

BackgroundThis prospective and observational study aimed to identify demographic, physiological and psychological risk factors associated with high-altitude headache (HAH) upon acute high-altitude exposure.MethodsEight hundred fifty subjects ascended by plane to 3700 m above Chengdu (500 m) over a period of two hours. Structured Case Report Form (CRF) questionnaires were used to record demographic information, physiological examinations, psychological scale, and symptoms including headache and insomnia a week before ascending and within 24 hours after arrival at 3700 m. Binary logistic regression models were used to analyze the risk factors for HAH.ResultsThe incidence of HAH was 73.3%. Age (p =0.011), physical labor intensity (PLI) (p =0.044), primary headache history (p <0.001), insomnia (p <0.001), arterial oxygen saturation (SaO2) (p =0.001), heart rate (HR) (p =0.002), the Self-Rating Anxiety Scale (SAS) (p <0.001), and the Epworth Sleepiness Scale (ESS) (p <0.001) were significantly different between HAH and non-HAH groups. Logistic regression models identified primary headache history, insomnia, low SaO2, high HR and SAS as independent risk factors for HAH.ConclusionsInsomnia, primary headache history, low SaO2, high HR, and high SAS score are the risk factors for HAH. Our findings will provide novel avenues for the study, prevention and treatment of HAH.

Is Smoking a Predictor for Acute Mountain Sickness? Findings From a Meta-Analysis

“…The publication dates for the studies ranged from 1991 to 2015, with 16 of the 21 appearing in 2006 or thereafter. The top three studies with the greatest contributory weight, Li et al, 29 Bian et al, 32 and MacInnis et al 33 (together accounting for 46.9% of weight), comprised only 4411 subjects (26.6% of the entire study population). One of these studies showed smoking-associated increased AMS risk, while the other two manifested a protective effect; all, however, were close to an OR = 1.0.…”

Variants of the Low Oxygen Sensors EGLN1 and HIF-1AN Associated with Acute Mountain Sickness

“…The subjects included 190 patients with AMS and 190 healthy Han Chinese controls randomly chosen from 850 volunteers who ascended from 500 m (Chengdu in Sichuan province) to 3700 m (Lhasa) in 2 h by plane. All included subjects were unrelated males who had lived at low altitudes prior to being recruited during the period from 21 June to 25 June 2012, as previously described [ 27 ]. Subjects who were exposed to altitudes ≥2500 m in the past 6 months, subjects who were taking acetazolamide or steroids for AMS prophylaxis and subjects who were diagnosed with psychological or neurological disorders were excluded.…”

Association of EPAS1 and PPARA Gene Polymorphisms with High-Altitude Headache in Chinese Han Population

“…HAH was diagnosed based on the criteria of International Classification of Headache Disorders: second edition, and the characteristics of headache need to meet at least two out of the five criteria: (1) bilateral, (2) frontal or frontotemporal, (3) dull or pressing pain, (4) mild to moderate intensity, and (5) aggravated by exertion, movement, straining, coughing, or bending down [4,6]. Due to the difficult condition of field trial and clinical research, HAH scores were classified as follows: 0 for no headache, 1 for mild headache, 2 for moderate headache, and 3 for severe headache [16][17][18]. Individuals with HAH score ≥1 were assigned to the HAH group, while those with HAH score � 0 were classified into the non-HAH group.…”

“…Yet another explanation emphasized that hypoxia caused cerebral edema and HAH by inducing damage of blood-brain barrier or by stimulating neurohumoral and hemodynamic responses, leading to cerebral vasodilation and overperfusion of microvascular beds via the release of inflammatory mediators [11,15]. From previous studies of our group, Bian SZ and Guo WY reported that HAH patients featured higher vertebral artery diastolic velocity, higher heart rate (HR), higher self-rating anxiety scale score, and lower arterial oxygen saturation (SaO 2 ) according to cohort study [16][17][18]. However, the exact pathophysiological mechanisms of HAH are multifactorial and far from specific elucidation.…”