[abstract] A MECHANISM FOR EXPLAINING THE PATHOPHYSIOLOGY OF PAIN ONLY (LIMB) BENDS.

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[abstract] A MECHANISM FOR EXPLAINING THE PATHOPHYSIOLOGY OF PAIN ONLY (LIMB) BENDS.

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dc.contributor.author Strauss, MB
dc.date.accessioned 2008-06-19T18:35:13Z
dc.date.available 2008-06-19T18:35:13Z
dc.date.issued 1990
dc.identifier.citation Undersea Biomedical Research, Vol. 16, No. 1 Supplement, March 1990 en
dc.identifier.uri http://archive.rubicon-foundation.org/7024
dc.description Abstract of the Undersea and Hyperbaric Medical Society, Inc. Joint Annual Scientific Meeting with the International Congress for Hyperbaric Medicine and the European Undersea Biomedical Society held 11-18 August 1990. Okura Hotel, Amsterdam, The Netherlands (http://www.uhms.org) en
dc.description.abstract Pain only, Type I Decompression Sickness (DCS), appears to be a distinct clinical entity from the more serious Type II DCS. Although invascular bubbles and secondary ischemic changes to vital tissues is the accepted mechanism for Type II DCS, there is no presently accepted mechanism for explaining the pathophysiology of limb bends. The diving profiles, clinical presentations, and dramatic responses to recompression therapy (with or without increased oxygen percentages) suggest Type I DCS is a mechanical problem and its pathophysiology is due entirely to the distention of pain sensitive structures. However, to date, such a structure or the presence of bubbles within tissues in Type I DCS has defied discovery. The orthopaedic literature (Halatha, et al. Ultra-structure of sensory nerve endings in monkey [Macaca fascicularis] knee joint capsule. J Ortho Res 2:169-176, 1984) discusses an organelle, the Ruffini Type II corpuscle, which is an ideal model for explaining the pathophysiology of Type II DCS. The organelle is embedded in joint capsules. It is pain sensitive, responding to stretch when its thick peripheral perineural capsule is distended. Its central fluid intracapsular space is a site for bubble formation when the inert gas pressure differential is great enough to precipitate bubble formation. Once bubbles form in the microscopic intracapsular space, the perineural capsule becomes distended and pain without other detectable signs occurs. The dramatic response to recompression in this proposed model is due to the physical reduction or collapse of the bubble and the immediate relaxation of the pain sensitive perineural cpasule. No contemporary model exists that better explains the pathophysiology of Type I DCS. This paper is presented to share this hypothesis with the individuals interested in undersea and hyperbaric medicine and promote studies to verify it. en
dc.format.extent 193 bytes
dc.format.mimetype text/plain
dc.language.iso en en
dc.publisher Undersea and Hyperbaric Medical Society, Inc. en
dc.subject DIVING en
dc.subject decompression sickness en
dc.subject pain en
dc.subject invascular bubbles en
dc.subject pathophysiology en
dc.subject Bubble en
dc.subject joint en
dc.subject intracapsular space en
dc.title [abstract] A MECHANISM FOR EXPLAINING THE PATHOPHYSIOLOGY OF PAIN ONLY (LIMB) BENDS. en
dc.type Article en

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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