Pain, hyperalgesia and activity in nociceptive C units in humans
Check out this great bit of work by LaMotte et al from 1992.
Here’s some simple reflections of the science:
– First they’re exploring activity of nociceptors in humans. That means someone volunteered for this!
– They use a crude way of ‘finding’ C-mechanoheat nociceptive units (CMHs) – scrape the skin or pinch it between the fingers
– It is only classified as a C-fibre if the conduction velocity is less than 2 m/s
– It is only classified as mechanoheat nociceptor if it selectively responds to technical or heat stimuli which typically cause pain
– They carefully map the receptive field
– Then they inject capsaicin i.e. the active component of chili peppers
– Interestingly, they tried to limit the numerical rating scale of pain to sensation only (is it possible to separate yourself from the unpleasantness or tolerability?)
What did they find?
– Heat and pain threshold reduced after injecting capsaicin. Now temperatures as low as 30C were felt as painful!
– Cooling the skin reduced pain and the spontaneous firing of the CMHs
– Warming increased this again!
– There was evidence of mechanical hyperalgesia i.e. increased pain to mechanical stimuli
– Some of this was outside of the skin zone affected by the injection i.e. ‘secondary hyperalgesia’
– There was evidence of analgesia around the injection site too
A simple summary:
– Ask a bunch of crazy people if it’s ok to inject some chili into them
– Scrape, pinch, electrically stimulate, heat and cool them whilst asking if it hurts
– Find that the injection makes these things simultaneously hurt more or less depending on where you do it
– Then discover something totally cool but keep in under wraps
Here’s the cool discovery – hang in there!
“A few presumably chemosensitive C units were discovered serendipitously during studies of CMH units….” In other words, it looks like these researchers were (?) the first to discover sleeping or silent nociceptors in humans. BOOM
It’s worth hearing their summary and considering some of the current proposed models to understand pain with.
“An interesting question is why pain from intradermal injection of [capsaicin] is so intense….One possible explanation might be that the discharge pattern in C polymodal nociceptors on capsaicin injection is irregular, with bursts of impulses …. It is conceivable that such high instantaneous firing rates during bursts of impulses could give rise to considerable pain due to temporal summation….It is also possible that several types of nociceptors are activated by capsaicin. Candidate nociceptors in addition to the CMHs could include purely chemosensitive units as well as the heat nociceptors that respond both to noxious heat and to capsaicin but not to mechanical or cold stimuli.”