Transient cervical nerve root compression in the rat induces bilateral forepaw allodynia and spinal glial activation: mechanical factors in painful neck injuries.
METHODS
An in vivo rat model of transient cervical nerve root compression.


OBJECTIVE
To investigate the potential for cervical nerve root compression to produce behavioral hypersensitivity and examine its dependence on compression.


BACKGROUND
Clinically, nerve root injury has been hypothesized as a potential source of neck pain, particularly because cervical nerve roots are at mechanical risk for injury during neck loading. Lumbar radiculopathy models of nerve root ligation show that mechanical allodynia and spinal glial changes depend on nerve root deformation magnitude. However, no investigation has been performed to examine cervical nerve root compression as a cause of pain.


METHODS
Two compressive forces (10 and 60 grams force [gf]) were transiently applied to the C7 nerve roots unilaterally using microvascular clips in separate groups (n = 12 each). Sham procedures were also performed in a separate group of rats (n = 12). Bilateral forepaw mechanical allodynia was monitored after surgery for 7 days. On day 7, spinal glial activation was assessed using immunohistochemistry to investigate its dependence on nerve root compressive force, in the context of behavioral hypersensitivity.


RESULTS
Bilateral allodynia was observed following injury, which was significantly (P < 0.042) increased over sham and baseline responses. No difference in allodynia was found between the 10 and 60 gf injuries. Astrocytic and microglial activation were observed in the ipsilateral dorsal horn following compression, with only astrocytic activation paralleling allodynia patterns.


CONCLUSIONS
Results imply a force threshold exists less than 10 gf for persistent pain symptoms following transient cervical nerve root compression. Findings also suggest that spinal glial activation may be related to behavioral sensitivity and may modulate cervical nerve root mediated pain.
Hubbard
Raymond D
RD
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104-6392, USA.
Winkelstein
Beth A
BA
D000818:Animals; D000911:Antibodies, Monoclonal; D001253:Astrocytes / Q000378:metabolism; D005552:Forelimb; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006930:Hyperalgesia / Q000209:etiology* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D017628:Microglia / Q000378:metabolism; D019838:Neck Injuries / Q000150:complications* / Q000503:physiopathology; D009408:Nerve Compression Syndromes / Q000150:complications* / Q000503:physiopathology; D009457:Neuroglia / Q000378:metabolism; D010812:Physical Stimulation / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology*; D013126:Spinal Nerve Roots; D013997:Time Factors
D000911:Antibodies, Monoclonal; D005904:Glial Fibrillary Acidic Protein