What role does the blood brain barrier play in acute mountain sickness?

Summary 

As high altitude travel increases, acute mountain sickness (AMS) and life threatening high altitude cerebral oedema (HACE) are becoming more prevalent. Acute mountain sickness occurs in 45% of lowlanders above 4250 m. Predisposing factors are still unknown and its development is more complex than the original “tight fit” hypothesis. This review examines evidence relating to a possible role of the blood brain barrier in AMS as suggested by MRI studies. Underlying mechanisms may involve vascular endothelial growth factor and free radicals in addition to increases in hydrostatic pressure. An increased understanding is important in advising patients planning high altitude adventures.

Current studies have linked increased blood brain barrier permeability to high altitude cerebral oedema, but the role of the blood brain barrier in acute mountain sickness is less clear; varied symptoms include headache. MRI shows vasogenic oedema occurs in high altitude cerebral oedema, suggesting blood brain barrier permeability increases, and acute mountain sickness typically precedes high altitude cerebral oedema. Hypoxia leads to increased hydrostatic pressure, and blood brain barrier permeability has been shown to increase in stroke patients. Vascular endothelial growth factor is upregulated in hypoxia, and may increase blood brain barrier permeability.

Keywords: High altitude cerebral oedema (HACE), Vascular endothelial growth factor (VEGF), Hypoxia, Altitude