AUTHOR=Macionis Valdas 

TITLE=Chronic pain and local pain in usually painless conditions including neuroma may be due to compressive proximal neural lesion

JOURNAL=Frontiers in Pain Research

VOLUME=Volume 4 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/pain-research/articles/10.3389/fpain.2023.1037376

DOI=10.3389/fpain.2023.1037376

ISSN=2673-561X

ABSTRACT=It has been unexplained why chronic pain does not invariably accompany chronic pain-prone disorders. This question-driven, hypothesis-based article suggests that the reason may be varying occurrence of concomitant peripheral compressive proximal neural lesion (cPNL), e.g., radiculopathy and entrapment plexopathies. Transition of acute to chronic pain may involve development (or aggravation) of cPNL. Nociceptive hypersensitivity induced and/or maintained by cPNL may be responsible for all types of general chronic pain as well as for pain in isolated tissue conditions that are usually painless, e.g., neuroma, scar, and Dupuytren's fibromatosis. Compressive PNL induces focal neuroinflammation, which can maintain dorsal root ganglion neuron (DRGn) hyperexcitability (i.e., peripheral sensitization) and thus fuel central sensitization (i.e., hyperexcitability of central nociceptive pathways) and a vicious cycle of chronic pain. DRGn hyperexcitability and cPNL-produced motor fiber damage may reciprocally maintain each other, because cPNL can result from reflexive myospasm-induced myofascial tension, muscle weakness, and consequent muscle imbalance- and/or pain-provoked compensatory overuse. Sensitization increases nerve vulnerability and thus catalyzes this cycle. Because of these mechanisms and relatively greater number of neurons involved, cPNL is more likely to maintain DRGn hyperexcitability in comparison to distal neural and non-neural lesions. Intermittent (dynamic) nature of cPNL may be essential, because healed (i.e., fibrotic) lesions are physiologically silent and, consequently, cannot provide nociceptive input to maintain chronic pain. Not all patients may be equally susceptible to develop cPNL, because this susceptibility may vary as vary patients’ predisposition to musculoskeletal impairment. Sensitization is accompanied by pressure pain threshold decrease and consequent mechanical allodynia and hyperalgesia, which can cause unusual local pain via natural pressure exerted by space occupying lesions or by their examination. Worsening of local pain is similarly explainable. Neuroma pain may be due to cPNL-induced axonal mechanical sensitivity and hypersensitivity of the nociceptive nervi nervorum of the nerve trunk and its stump. Intermittence and symptomatic complexity of cPNL may be the cause of frequent misdiagnosis of chronic pain.