Headaches caused by a lack of oxygen
Hypoxia is a condition in which the body is deprived of adequate oxygen supply at the tissue level. Hypoxia causes secondary headaches associated with low oxygen tensions, such as high-altitude headache (HAH) and headache due to acute mountain sickness (AMS). HAH is one of the neurological symptoms associated with ascent to high altitudes. Hypoxia may also play an important role in primary headaches such as migraine and cluster headache.
A study was done to estimate the prevalence and clinical impact of HAH and to identify the risk factors and headache characteristics which may provide new insights into better understanding of hypoxia being a trigger for high-altitude headache or even migraine attacks. Some people develop headache when they travel high altitudes. A study showed that 77 adults (43 males, 34 females) with simulated high altitude (4500 m) by controlled normobaric hypoxia (FiO2 = 12.6%) in an attempt to investigate acute mountain sickness (AMS) and headache characteristics.
According to Lake Louise Scoring system (LLS), acute mountain sickness symptoms were recorded before and after 6 and 12 hours in hypoxia. Using pulse oximetry, oxygen saturation was also measured at each time point respectively. Patients with a history of headache, especially episodic or chronic migraine were excluded.
As per results, 63 males (81.18%) and 40 females (71.4%) reported headache at 6 or 12 hours with height and SpO2 being significantly different between headache groups at 6 hours. According to International Classification of Headache Disorders, hypoxia triggered migraine-like headache in n=5 (8%) or n = 6 (15%), at 6 and 12 hours, respectively.
The results revealed that normobaric hypoxia is the potential trigger for the development of high-altitude headache also in healthy volunteers with no family history of migraine. Overall, the findings of the study confirm that hypoxia plays a crucial role in acute mountain sickness development and the researchers found that it may be associated with the pathophysiology of migraine.