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J Appl Physiol 68: 1368-1375, 1990;
8750-7587/90 $5.00
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Journal of Applied Physiology, Vol 68, Issue 4 1368-1375, Copyright © 1990 by American Physiological Society

ARTICLES

Bubble-induced dysfunction in acute spinal cord decompression sickness

T. J. Francis, J. L. Griffin, L. D. Homer, G. H. Pezeshkpour, A. J. Dutka and E. T. Flynn
Diving Medicine Department, Naval Medical Research Institute, Bethesda, Maryland 20814-5055.

Five anesthetized dogs undertook a chamber dive, on air, to 300 feet of seawater for 15 min. After the dive, spinal cord decompression sickness was detected by recording a reduced amplitude of the somatosensory evoked potential compared with predive base-line values. After the diagnosis of decompression sickness and rapid perfusion fixation of the animal, the spinal cord was removed and examined histologically. Numerous space-occupying lesions (SOL) that disrupted the tissue architecture were found in each cord, mainly in the white matter. The size and distribution of the SOL were determined using computerized morphometry. Although SOL occupied less than 0.5% of the white matter volume, we tested a number of algorithms to assess whether the SOL may have been directly involved in the loss of spinal cord function that followed the dive. We determined that the loss of somatosensory evoked potential amplitude may be attributed to the SOL if 30-100% of the spinal cord fibers that they displaced were rendered nonconducting. A number of possible mechanisms by which SOL may interfere with spinal nerve conduction are discussed.


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T. S. Neuman
Arterial Gas Embolism and Decompression Sickness
Physiology, April 1, 2002; 17(2): 77 - 81.
[Abstract] [Full Text] [PDF]


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