Abstract
Objectives Raised intracranial pressure is proposed to be a mediator of acute mountain sickness. However, establishing this is difficult due to the invasive nature of intracranial pressure measurement. In this study we used a non-invasive estimate of intracranial pressure, ultrasound of the optic nerve sheath diameter (ONSD), during ascent to high altitude in both low-altitude residents and high-altitude natives.
Methods 42 (30 low-altitude, 12 high-altitude residents) participants ascended from 1300 to 5050m with ONSD, cerebral blood flow (CBF, duplex ultrasound), and arterial blood gas measurements at 1300, 2700, 3400, 4125 and 5050m. Lake Louise acute mountain sickness scores were collected at 5050m.
Results Ascent to high-altitude was associated with an increase in median [IQR] ONSD (4.61mm [4.39–5.26] at 1300m to 6.47mm [5.78–7.34] at 5050m). At 5050m, those with more symptoms of acute mountain sickness had larger optic nerve sheath diameters (r =0.47, p=0.015). The increase in ONSD was related to an increase in CBF with altitude (p=0.005). High-altitude residents ascending to altitude had higher baseline ONSD, however this did not increase with altitude as much as low-altitude residents (interaction p=0.0001).
Conclusions Increased optic nerve sheath diameter with ascent to altitude supports the theory that intracranial pressure rises during ascent to high altitude and that this may contribute to acute mountain sickness. The increases in ONSD are mediated in part by increased cerebral blood flow. The smaller increase in ONSD in Sherpa may protect against acute mountain sickness.