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Heat Insensitive Pain?

Emeline

Emeline

Messages
29
When I’ve over done it and have pain, often in my back, if I lay on a heat pad, I can’t feel the heat, and when I apply biofreeze I can only feel the cool menthol sensation in odd spots that aren’t painful. This lack of heat sensitivity moves with the pain, but it’s not numbness- I can still feel pressure and touch. A really over hot heating pad can also get through.

I thought this was a normal thing for pain, but I’ve now spoken with half a dozen non-CFS (but 2 fibromyalgia) people who disagree.

The idea it’s a nerve problem has been floated, but web searching hasn’t returned anything that matches since the insensitivity moves with the pain, and the pain does seem to respond to OTC painkillers.

Does anyone else experience this?

Any idea what/why is?
 
D

datadragon

Senior Member
Messages
407
Location
USA
When I was gathering together some initial general info on Pain, one piece below mentioned that a Shank3 deficiency impairs heat hyperalgesia as a starting point. It is interesting that Shank3 levels are also lowered via zinc deficiency that regulates Shank levels as well as NLRP3 over activation as that also leads to a lowering of shank3 and subsequently zinc uptake in the gut so this just means that it can be a downstream effect from inflammation/infection. More on that here if you want more detail/studies https://forums.phoenixrising.me/thr...acute-pain-nejm-08-03-2023.90696/post-2442397

SHANK3 Deficiency Impairs Heat Hyperalgesia and TRPV1 Signaling in Primary Sensory Neurons. Homozygous and heterozygous Shank3 complete knockout results in impaired heat hyperalgesia in inflammatory and neuropathic pain. TRPV1 modulates glutamate release from nociceptor afferents in the spinal cord, and the authors found that loss of SHANK3 impaired this function. loss of SHANK3 impairs TRPV1 signaling in human neurons. Biochemical experiments showed that SHANK3 and TRPV1 can physically interact and that SHANK3 regulates the surface expression and trafficking of TRPV1 in cell culture. Further analysis showed that the proline-rich domain of SHANK3 is responsible for mediating these interactions and regulating TRPV1 function. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5182147/ The mean score for affective pain sensitivity to heat stimulation was lower in the ASD (Autism) group than in the control group which relates to the shank3 deficency https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4779208/
 
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