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Resolution of inflammation-induced axonal mechanical sensitivity and conduction slowing in C-fiber nociceptors.
J Pain. 2008 Feb; 9(2):185-92.JP

Abstract

The present study is an in vivo investigation into the time course of inflammation-induced axonal mechanical sensitivity (AMS) in intact C-fiber axons. After induction of a localized neuritis in the rat sciatic nerve, AMS developed in C-fiber axons at 1 (18.2%) and 4 weeks (11.6%). By 8 weeks, AMS was virtually absent (2.1%). AMS was also tested in intact L5 neurons after L4 spinal nerve transection, which induces a diffuse inflammation within the sciatic nerve. At 1 week, AMS developed in 10% of neurons. No AMS was observed in unoperated animals. The localized neuritis also caused changes in L5 dorsal root conduction velocities (CVs). CVs decreased at 1 week (-7.7%) and 4 weeks (-17.6%) and returned to normal by 8 weeks. L4 transection similarly reduced CVs (-13.7%) of L5 dorsal root axons. There were no significant changes among any groups in the proportion or rate of ongoing activity. These results demonstrate that the axonal changes due to neuritis are not permanent. Therefore, in patients with persistent movement-induced radiating limb pain with few clinically apparent signs of nerve damage, there may be a persisting inflammatory lesion affecting the nerve.

PERSPECTIVE

Nerve inflammation, or neuritis, causes axonal mechanical sensitivity, which is the neural substrate for radiating limb pain induced by movement. This study examined the time course of induced axonal mechanical sensitivity and conduction velocity changes in intact C-fiber axons after nerve inflammation. The results suggest that treatment to reduce nerve inflammation may be beneficial to patients with radiating pain.

Authors+Show Affiliations

Dilley A
Department of Anesthesia, Critical Care and Pain Management, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. a.dilley@bsms.ac.uk
Bove GM
No affiliation info available

MeSH

AnimalsAxonsAxotomyElectrophysiologyHyperalgesiaInflammationMaleNerve Fibers, UnmyelinatedNeural ConductionNeuritisNociceptorsPainPhysical StimulationRatsRats, WistarSpinal Nerves

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18309534

Citation

Dilley, Andrew, and Geoffrey M. Bove. "Resolution of Inflammation-induced Axonal Mechanical Sensitivity and Conduction Slowing in C-fiber Nociceptors." The Journal of Pain : Official Journal of the American Pain Society, vol. 9, no. 2, 2008, pp. 185-92.
Dilley A, Bove GM. Resolution of inflammation-induced axonal mechanical sensitivity and conduction slowing in C-fiber nociceptors. J Pain. 2008;9(2):185-92.
Dilley, A., & Bove, G. M. (2008). Resolution of inflammation-induced axonal mechanical sensitivity and conduction slowing in C-fiber nociceptors. The Journal of Pain : Official Journal of the American Pain Society, 9(2), 185-92.
Dilley A, Bove GM. Resolution of Inflammation-induced Axonal Mechanical Sensitivity and Conduction Slowing in C-fiber Nociceptors. J Pain. 2008;9(2):185-92. PubMed PMID: 18309534.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Resolution of inflammation-induced axonal mechanical sensitivity and conduction slowing in C-fiber nociceptors. AU - Dilley,Andrew, AU - Bove,Geoffrey M, PY - 2008/3/1/pubmed PY - 2008/3/19/medline PY - 2008/3/1/entrez SP - 185 EP - 92 JF - The journal of pain : official journal of the American Pain Society JO - J Pain VL - 9 IS - 2 N2 - UNLABELLED: The present study is an in vivo investigation into the time course of inflammation-induced axonal mechanical sensitivity (AMS) in intact C-fiber axons. After induction of a localized neuritis in the rat sciatic nerve, AMS developed in C-fiber axons at 1 (18.2%) and 4 weeks (11.6%). By 8 weeks, AMS was virtually absent (2.1%). AMS was also tested in intact L5 neurons after L4 spinal nerve transection, which induces a diffuse inflammation within the sciatic nerve. At 1 week, AMS developed in 10% of neurons. No AMS was observed in unoperated animals. The localized neuritis also caused changes in L5 dorsal root conduction velocities (CVs). CVs decreased at 1 week (-7.7%) and 4 weeks (-17.6%) and returned to normal by 8 weeks. L4 transection similarly reduced CVs (-13.7%) of L5 dorsal root axons. There were no significant changes among any groups in the proportion or rate of ongoing activity. These results demonstrate that the axonal changes due to neuritis are not permanent. Therefore, in patients with persistent movement-induced radiating limb pain with few clinically apparent signs of nerve damage, there may be a persisting inflammatory lesion affecting the nerve. PERSPECTIVE: Nerve inflammation, or neuritis, causes axonal mechanical sensitivity, which is the neural substrate for radiating limb pain induced by movement. This study examined the time course of induced axonal mechanical sensitivity and conduction velocity changes in intact C-fiber axons after nerve inflammation. The results suggest that treatment to reduce nerve inflammation may be beneficial to patients with radiating pain. SN - 1526-5900 UR - https://www.unboundmedicine.com/medline/citation/18309534/Resolution_of_inflammation_induced_axonal_mechanical_sensitivity_and_conduction_slowing_in_C_fiber_nociceptors_ L2 - https://medlineplus.gov/pain.html DB - PRIME DP - Unbound Medicine ER -