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INTRODUCTION: The pathophysiological basis of neurological decompression sickness and the association between cerebral subcortical white matter (WM) change and nonhypoxic hypobaria remain poorly understood. Recent study of altitude decompression sickness risk evaluated acute WM responses to intensive hypobaric exposure using brain magnetic resonance imaging.

METHODS: Six healthy men (20 to 50 yr) completed 6 h of hyperoxic hypobaria during three same-day altitude chamber decompressions to pressure altitudes ≥ 22,000 ft (6706 m). Research magnetic resonance imaging sequences, conducted on the days preceding and following decompression, evaluated subcortical WM integrity, cerebral blood flow, neuronal integrity (fractional anisotropy), and neurometabolite concentrations.

RESULTS: No subcortical lesions were evident on diffusion weighted imaging and WM fractional anisotropy was unaffected. Mean WM blood flow was upregulated by 20% to over 25 mL · 100 g−1 · min−1. Gray matter flow was unchanged. There were no changes in gray matter or cerebellar neurometabolites. In parietal subcortical WM, levels of γ-aminobutyric acid (GABA) fell from (mean ± SD) 1.68 ± 0.2 to 1.35 ± 0.3 institutional units while glutathione (GSH) fell from 1.71 ± 0.4 to 1.25 ± 0.3 institutional units. Lactate increased postexposure in five subjects.

CONCLUSIONS: Postexposure decrements in GABA and GSH imply WM insult with loss of neuroprotection and oxidative stress. An association between decrements in GABA and GSH support a common origin, while GSH decrements also correlate with WM blood flow responses. WM lactate increments are prone to error but suggest dysregulation of subcortical microvascular flow. WM neurometabolite and blood flow indices did not normalize by 24 h postexposure.

Connolly D, Davagnanam I, Wylezinska-Arridge M, Mallon D, Wastling S, Lee VM. Brain magnetic resonance imaging responses to nonhypoxic hypobaric decompression. Aerosp Med Hum Perform. 2024; 95(10):733–740.

Keywords: non-hypoxic hypobaria; decompression stress; hyperoxia; subcortical white matter; neurometabolite; cerebral blood flow
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Copyright: Reprint and copyright © by the Aerospace Medical Association, Alexandria, VA.
Fig. 1.
Fig. 1.

A) Pre- (blue) and postexposure (red) whole brain fractional anisotropy (FA) showing six sets of individual data and group means. B) Corresponding data for white matter FA.


Fig. 2.
Fig. 2.

Pre- and postexposure global white matter (left) and gray matter (right) cerebral blood flow from arterial spin labeling MRI, represented as interquartile boxplots (upper graphs) showing median (horizontal bar) and mean (X), and individual subject responses (lower graphs).


Fig. 3.
Fig. 3.

Pre- and postexposure parietal white matter neurometabolite concentrations for: A) γ-aminobutyric acid (GABA); B) glutathione (GSH); and C) lactate. Data expressed in institutional units (iu) showing cohort means (± SE) and individual responses (dashed lines).


Fig. 4.
Fig. 4.

Linear regression analyses indicating: A) an association between the magnitudes of the postexposure decrements in GABA and GSH, supporting a common origin; and B) an association between altered postexposure WM blood flow and the GSH decrement.


Contributor Notes

Address correspondence to: Dr. Desmond M. Connolly, QinetiQ, Cody Technology Park, Old Ively Road, Farnborough, Hampshire GU14 0LX, United Kingdom; dmconnolly@qinetiq.com.
Received: Feb 01, 2024
Accepted: May 01, 2024