Hi all,
I apologize if this is a repeat topic, but I couldn't find a similar post.
Does anyone know why physiologically some people have constant pain and others have "triggered" pain? Is there an understood difference between damage to the nerve in terms of location and type? Any feedback would be appreciated, as well as references to published literature.
Thank you!
"Classic" facial or glossopharyngeal neuralgia normally presents as volleys of electric-shock stabs, while "atypical" facial neuralgia has a more constant, burning, throbbing quality. The pain mechanisms in both types of pain are still not fully understood. But there is informed speculation by professionals that classic neuralgia involves damage to the myelin layer surrounding the nerve, with pulsed stimulus from a compressing blood vessel. Atypical neuralgia or neuropathy, on the other hand, appear to involve deeper damage to one or more types of nerve fiber that are woven through the nerve. As either type of pain develops over time, there is evidence that permanent changes can occur in multiple nerve fibers within the nerve, causing what is called "Central Nervous System" pain or "deafferentiation" pain.
Some of these mechanisms are discussed peripherally in a paper written by Dr. Jeff Brown on Balloon Compression, a type of rhizotomy used in some cases of trigeminal neuralgia. The technique itself may not apply to GPN, but the damage mechanisms discussed there appear to be in common. Please don't pass on the paper further, as it is still under copyright.
Regards,
Red Lawhern, Ph.D.
Adjunct Moderator, Glossopharyngeal Neuralgia Community
Thanks for the info.
In the classical case where there may be damage to the myelin, it makes sense that something like MVD would have a relatively high success rate. An offending artery would be compressing the nerve but it shouldn't be causing deep damage without a lot of pressure. Wouldn't this suggest that for the atypical case - there is damage that is more distal from the brain?
Damage could conceivably be closer to the nerve endings. But it could equally well be more distributed on the nerve, or even concentrated in the spinal column itself (central nervous system pain). So far I've seen nothing in medical literature that addresses an end-to-end explanation of the several processes that may be involved.
Regards, Red
Good info Red
Hi Stephen,
I found the quote below in the article linked below that was listed on the "useful links" thread:
It is from the introduction section of this article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322380/
"It is important to make a “clinical” differential diagnosis between idiopathic GN and secondary forms due to inflammation and tumors. In the first case, the neuralgic pain is severe, episodic, lancinating, and of short duration, whereas inflammatory or neoplastic pain is more constant, long-lasting, and of deep-seated quality. The “mapping” of the distribution of the pain has to be performed in order to evaluate if other cranial nerves are involved."
I haven't seen that article, Rachel. Thanks!
I recently had a chat with my own neuro on the difference. His take on it, in layman's terms was with the typical its hardware (nerve); atypical is more complex and usually involves software (brain chemistry) and possible hardware issues.
Smiley, I've heard similar characterizations from other practitioners too. There is a lot in ATN and Atypical GN that we probably don't know with precision as yet.
Regards,