An investigation of the neurophysiologic mechanisms of tourniquet-related pain: changes in spontaneous activity and receptive field size in spinal dorsal horn neurons.
OBJECTIVE
Several theories have been proposed for the pain resulting from the nerve compression and ischemia associated with maintaining the inflation of a pneumatic tourniquet on an extremity. This investigation observes changes in the spontaneous activity and receptive field (RF) size of spinal dorsal horn neurons during tourniquet-related nerve compression and ischemia.


METHODS
Forty-eight pentobarbital-anesthetized rats were prepared for single-unit spinal dorsal horn cell recording utilizing an in vivo extracellular technique. Cells were characterized as either low threshold mechanoreceptor (LTM) neurons, wide dynamic range (WDR) neurons, or high threshold nociresponsive (NR) neurons based on their response to light touch (brush), non-noxious pressure, or noxious pinch. Receptive fields were carefully mapped. A 1 x 9 cm pneumatic tourniquet (Hokanson, Inc., Seattle, WA) was then applied to the animals' hind limb thigh and inflated to 300 mm Hg for 60 minutes. Throughout the 60-minute tourniquet inflation period, spontaneous activity, cell firing rate response characteristics, and RF size were carefully monitored.


RESULTS
Twenty-three cells in 20 animals were characterized and monitored: 8 LTM, 6 WDR, and 9 NR neurons. Receptive fields were distal to the tourniquet cuff for 16 cells and proximal for 7 cells. Low threshold mechanoreceptor neurons demonstrated little spontaneous activity prior to tourniquet inflation in the absence of RF stimulation. The RF size for all LTM neurons decreased or became silent during the tourniquet inflation period. The RF size increased in two of six WDR neurons with two cells demonstrating a progressive increase in intermittent spontaneous firing during the tourniquet inflation period. Receptive field size increased in five of five NR neurons with RF located proximal to the tourniquet cuff from 29 +/- 10 mm2 to 54 +/- 30 mm2 (RF area 1.9 +/- 0.7; t = 2.7, P = .03). All five of these NR neurons also demonstrated an increase in spontaneous activity at 37 +/- 14 minutes of tourniquet inflation which continued throughout the remainder of the tourniquet inflation period (P < .05).


CONCLUSIONS
The results of this study indicate that nerve compression and ischemia results in block of input to LTM neurons having RFs distal to the tourniquet cuff and an increase in spontaneous activity and expansion of the RFs of NRs, especially those with RFs located proximal to the tourniquet. Increases in spontaneous firing activity and expansion of the RFs of nociresponsive dorsal horn neurons receiving input from primary afferent nociceptors proximal to the tourniquet may explain, in part, the neurophysiologic mechanism of tourniquet-related pain.
Crews
J C
JC
Department of Anesthesiology, University of Cincinnati College of Medicine, Ohio, USA.
Cahall
M A
MA
D000818:Animals; D006614:Hindlimb / Q000098:blood supply; D007511:Ischemia / Q000209:etiology; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology; D008991:Monitoring, Physiologic; D009408:Nerve Compression Syndromes / Q000209:etiology / Q000503:physiopathology; D009475:Neurons, Afferent / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000209:etiology* / Q000503:physiopathology*; D010147:Pain Measurement / Q000379:methods; D017288:Pain Threshold / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000166:cytology / Q000502:physiology* / Q000503:physiopathology; D014111:Tourniquets / Q000009:adverse effects*