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High-altitude headache: Insights into pathophysiology and potential treatment implications
Marika Falla1,2,3, Florian Frank4, Giacomo Strapazzon1,3,5
1Institute of Mountain Emergency Medicine, Eurac Research, Bolzano, Italy.
The Journal of Physiology
|June 3, 2026
Summary
High-altitude headache (HAH) is a common neurological issue caused by hypoxia. Research suggests the trigeminovascular system and specific molecules like CGRP are key, offering new therapeutic targets.
Area of Science:
- Neurology
- Altitude Medicine
- Hypoxia Research
Background:
- High-altitude headache (HAH) is the most frequent neurological symptom of rapid ascent above 2500m.
- It can occur alone or with acute mountain sickness (AMS), mimicking primary headaches like migraine.
- Prevalence is influenced by ascent speed, altitude, and mode of transport.
Purpose of the Study:
- To explore the pathophysiology of HAH.
- To identify molecular mediators involved in HAH.
- To suggest potential therapeutic strategies for HAH.
Main Methods:
- Analysis of clinical features and prevalence data.
- Controlled normobaric hypoxic chamber studies to confirm hypoxia as a trigger.
- Review of proposed pathophysiological mechanisms involving the trigeminovascular system.
Main Results:
- Hypoxia is a potent trigger for HAH, often developing within hours of ascent.
- The trigeminovascular system, nitric oxide, adenosine, CGRP, and PACAP are implicated in HAH pathophysiology.
- Hypoxia-inducible factor-1α (HIF-1α) stabilization by hypoxia influences pathways related to head pain.
Conclusions:
- HAH pathophysiology involves trigeminovascular system activation and sensitization.
- Targeted therapies against CGRP and PACAP may benefit HAH patients due to similarities with migraine.
- Further research is needed to understand the HAH-AMS continuum and evaluate multi-target therapies.
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