Home Subscription Services
 
   

 
Journal of Oral & Facial Pain and Headache
OFPH Home Page
About the Editor
Editorial Board
Accepted Manuscripts
Submit
Author Guidelines
Submission Form
Reprints / Articles
Permissions
Advertising
MEDLINE Search
 
 
 
 
 
FacebookTwitterYouTube
Quintessence Publishing: Journals: OFPH
Journal of Oral & Facial Pain and Headache

Edited by Barry J. Sessle, BDS, MDS, BSc, PhD, FRSC

Official Journal of the American Academy of Orofacial Pain,
the European, Asian, and Ibero-Latin Academies of Craniomandibular
Disorders, and the Australian Academy of Orofacial Pain

ISSN 2333-0384 (print) • ISSN 2333-0376 (online)

Publication:
Fall 2004
Volume 18 , Issue 4

Back
Share Abstract:

Future Basic Science Directions Into Mechanisms of Neuropathic Pain

James L. Henry, PhD

Pages: 306 - 310
PMID: 15636013

The aim of this article is to outline mechanisms underlying generation and maintenance of pain arising from trauma to peripheral nerve fibers and to present an overview of our recent studies of animal models of peripheral neuropathic pain and pain of temporomandibular disorders (TMD). The former model was induced by placing a polyethylene cuff around the sciatic nerve of the Sprague-Dawley rat and the TMD model was induced by injection of complete Freundís adjuvant into the ratís temporomandibular joint. In cuff-implanted rats, ongoing activity of dorsal horn neurons was greater than in controls, the cutaneous receptive field size of the neurons was greater, and both noxious and innocuous mechanical stimuli to the receptive field elicited an excitatory response during stimulation but also a marked afterdischarge that lasted up to 30 minutes; this afterdischarge was never observed in control rats in response to innocuous stimulation. The model of TMD was characterized by joint space narrowing, bone remodeling, infiltration of immune cells, loss in the range of jaw opening, and signs of nociception. Alterations in the neural substrate of nociception in animal models, and therefore also possibly in humans, appear to include changes in peripheral as well as central neurons. In the periphery, changes include alterations in the phenotype and central projections of large-diameter sensory nerve fibers. At the level of the trigeminal brainstem and spinal cord, there appear to be several types of change. One type is an increased efficacy of synaptic transmission onto second-order neurons. Another type of change is a reduction in inhibitory mechanisms, including a shift of gamma-amino butyric acid (GABAA) receptor activation to excitation. There is a need for further studies to focus on mechanisms for either the generation or the maintenance, or both, of neuropathic pain.

Full Text PDF File | Order Article

 

 
Get Adobe Reader
Adobe Acrobat Reader is required to view PDF files. This is a free program available from the Adobe web site.
Follow the download directions on the Adobe web site to get your copy of Adobe Acrobat Reader.
  © 2014 Quintessence Publishing Co Inc
 

Home | Subscription Services | Books | Journals | Multimedia | Events | Blog
Terms of Use | Privacy Policy | About Us | Contact Us | Advertising | Help | Sitemap | Catalog