Abstract Information


Vasomotor and Sudomotor Activity during Heat Stress in Persons with Spinal Cord Injury

Trbovich M, Kellogg D
UT Health Science Center at San Antonio, San Antonio, Texas, USA

Background:It is well accepted that persons with spinal cord injury (SCI) have impaired ability to regulate core temperature due to compromised thermoregulatory vasomotor and sudomotor activity. In the setting of heat stress, impaired cutaneous vasodilation obviates skin blood flow (SkBF) increases and prevents convective cooling while impaired sweating responses (SR) prevents evaporative cooling. As a result, persons with SCI have difficulty maintaining thermal homeostasis, especially under heat stress. While multiple body cooling intervention trials have been performed, these have all proven minimally successful likely due to lack of complete mechanistic understanding of changes in the peripheral autonomic nervous system post SCI. In the non-SCI person, it is commonly thought that sympathetic cholinergic mechanisms mediate efferent control of both SkBF and SR through one and the same set of nerves; however, definitive proof is lacking. Indeed, cholinergic vasodilator nerves and cholinergic sudomotor nerves could actually be anatomically separate. Interestingly, in the 1970s, it was reported that during heat stress, persons with complete SCI have skin regions where SkBF increases without concomitant SR increases and other regions where SR increases without concomitant SkBF increases. These results suggest that efferent cholinergic sympathetic vasomotor nerves and efferent cholinergic sympathetic sudomotor nerves are separate. We sought to re-examine this phenomena with more advanced techniques using laser doppler imaging (LDI) and the starch iodine test.

Methods: Three persons (C4 AIS B, T8 AIS A and able-bodied) underwent indirect heat stress via electrical heating blankets until core temperature (Tcore) rose 0.8deg C. Areas 10cm above and 20cm below neurological level of injury (NLOI) of persons with SCI were left uncovered so as to not stimulate vasodilation from local heating: After Tcore elevation, SkBF response were measured by LDI while SR were assessed via the starch iodine test.

Results: The person with C4 AIS B SCI demonstrated increases in SkBF as indexed by LDI flux both above and below the NLOI down to T2 dermatomal level but demonstrated no areas of intact SR. Meanwhile the person with T8 AIS A SCI demonstrated increased SR down to T9 and increases in SkBF down to T12. Finally, the AB person LDI scan from the T6 to T12 dermatomal level demonstrated intact SkBF and SR throughout the entire area.

Discussion: In both persons with SCI, the skin surface areas of preserved SkBF responses exceeded that of SR during indirect heat stress. Meanwhile the AB person demonstrated no discordant responses as SkBF and SR responses were concordant throughout the surface area examined. This pilot data confirms discordant SkBF and SR responses in persons with tetraplegia and paraplegia, consistent previous findings in the 1970s, and demonstrates that persons with SCI can serve as a model to further investigate the neurological controls of SkBF and SR during indirect heat stress which are not understood. This preliminary data is part of a larger study that will later utilize topical pharmacological agents to elucidate theneurological mechanisms underlying such areas, thereby providing rationale for therapy development.


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