Literature DB >> 16284585

Spinal neuropeptide responses in persistent and transient pain following cervical nerve root injury.

Sarah M Rothman1, Rob A Kreider, Beth A Winkelstein.   

Abstract

STUDY
DESIGN: Behavioral and immunohistochemical analysis in rat models of persistent and transient allodynia.
OBJECTIVES: To examine separate cervical nerve root injuries (compression, transection) for producing behavioral hypersensitivity and investigate spinal neuropeptides to understand relationships to pain symptoms. SUMMARY OF BACKGROUND DATA: Mechanical cervical nerve root injury can be a source of neck pain. Painful lumbar radiculopathy models show that different nerve root ligation intensities produce differential allodynia responses. Spinal neuropeptides can mediate pain responses. Yet, little is known about their contributions to pain in the cervical spine.
METHODS: Rats underwent separate procedures on the right C7 nerve roots: transection (n = 12), 10-gf compression for 15 minutes (n = 11), or sham (n = 5). Ipsilateral forepaw mechanical allodynia was measured after surgery for 7 days. C7 spinal cord tissue was analyzed by immunohistochemistry for substance P and calcitonin gene-related peptide (CGRP) expression on days 1 and 7 for each injury; densitometry quantified immunoreactivity in lamina I of the ipsilateral dorsal horn.
RESULTS: Both injuries immediately produced significant increases in allodynia. Sensitivity was sustained following root compression, and at day 7, was not different from day 1. By day 7 after transection, allodynia had returned to baseline and sham levels, significantly decreasing from day 1 (P = 0.0012). Spinal substance P and CGRP were increased over normal at day 1 for both injuries and decreased with time for CGRP after transection, which paralleled behaviors. For individual rats, substance P was significantly (P < 0.001) correlated with CGRP expression for both injuries.
CONCLUSIONS: Compression and transection of the cervical nerve root produce different forepaw allodynia responses, with persistent and transient sensitivity, respectively. Spinal neuropeptide expression in these models parallels this sensitivity, suggesting their potential role in pain symptoms.

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Year:  2005        PMID: 16284585     DOI: 10.1097/01.brs.0000186316.38111.4b

Source DB:  PubMed          Journal:  Spine (Phila Pa 1976)        ISSN: 0362-2436            Impact factor:   3.468


  14 in total

1.  The potential for salmon fibrin and thrombin to mitigate pain subsequent to cervical nerve root injury.

Authors:  Christine L Weisshaar; Jessamine P Winer; Benjamin B Guarino; Paul A Janmey; Beth A Winkelstein
Journal:  Biomaterials       Date:  2011-09-22       Impact factor: 12.479

2.  Activating transcription factor 4, a mediator of the integrated stress response, is increased in the dorsal root ganglia following painful facet joint distraction.

Authors:  L Dong; B B Guarino; K L Jordan-Sciutto; B A Winkelstein
Journal:  Neuroscience       Date:  2011-07-28       Impact factor: 3.590

3.  Chemical and mechanical nerve root insults induce differential behavioral sensitivity and glial activation that are enhanced in combination.

Authors:  Sarah M Rothman; Beth A Winkelstein
Journal:  Brain Res       Date:  2007-09-06       Impact factor: 3.252

4.  Dorsal root compression produces myelinated axonal degeneration near the biomechanical thresholds for mechanical behavioral hypersensitivity.

Authors:  Raymond D Hubbard; Beth A Winkelstein
Journal:  Exp Neurol       Date:  2008-05-17       Impact factor: 5.330

5.  Cytokine mRNA expression in painful radiculopathy.

Authors:  Sarah M Rothman; Zhong Huang; Kathryn E Lee; Christine L Weisshaar; Beth A Winkelstein
Journal:  J Pain       Date:  2008-10-10       Impact factor: 5.820

6.  Ketorolac reduces spinal astrocytic activation and PAR1 expression associated with attenuation of pain after facet joint injury.

Authors:  Ling Dong; Jenell R Smith; Beth A Winkelstein
Journal:  J Neurotrauma       Date:  2013-05-06       Impact factor: 5.269

7.  High force reaching task induces widespread inflammation, increased spinal cord neurochemicals and neuropathic pain.

Authors:  M B Elliott; A E Barr; B D Clark; M Amin; S Amin; M F Barbe
Journal:  Neuroscience       Date:  2008-11-07       Impact factor: 3.590

8.  Transient cervical nerve root compression modulates pain: load thresholds for allodynia and sustained changes in spinal neuropeptide expression.

Authors:  Raymond D Hubbard; Zhen Chen; Beth A Winkelstein
Journal:  J Biomech       Date:  2007-10-31       Impact factor: 2.712

9.  Peripheral neuritis and increased spinal cord neurochemicals are induced in a model of repetitive motion injury with low force and repetition exposure.

Authors:  Melanie B Elliott; Ann E Barr; David M Kietrys; Talal Al-Shatti; Mamta Amin; Mary F Barbe
Journal:  Brain Res       Date:  2008-04-23       Impact factor: 3.252

10.  Controlled release of GDNF reduces nerve root-mediated behavioral hypersensitivity.

Authors:  Raymond D Hubbard; Joan J Martínez; Jason A Burdick; Beth A Winkelstein
Journal:  J Orthop Res       Date:  2009-01       Impact factor: 3.494

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