Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain.
METHODS
An analysis of pathologic changes after different degrees of cauda equina compression.


OBJECTIVE
To explore the association between the degree of the cauda equina compression and the extent of pathologic change, expression of tumor necrosis factor (TNF-alpha), and neuropathic pain. To compare with distal nerve compression injury.


BACKGROUND
Compression of the cauda equina reduces blood flow in compressed nerve roots and causes TNF-alpha expression and neuropathological change. In peripheral nerve, expression of TNF-alpha in Schwann cells is associated with primary demyelination without pain while TNF-alpha expression by macrophages is associated with axonal (Wallerian) degeneration and pain.


METHODS
Two square-shaped pieces of silicon were placed into the fourth and sixth epidural space in rats. Various sized silicon was used in each group (mild, moderate, and strong compression groups), while no silicon was used in the sham-operated group. Mechanical allodynia was determined by the von Frey test. Comparisons of the number of TNF-alpha- and apoptosis-positive cells were made using immunohistochemistry.


RESULTS
There was no significant mechanical allodynia observed in any group. Some nerve roots showed demyelination following mild cauda equina compression. Axonal degeneration was observed in the moderate and strong cauda equina compression groups. TNF-alpha-immunoreactive cells were increased in all compression groups. Apoptosis of dorsal root ganglion cells was less than apoptosis in the spinal cord.


CONCLUSIONS
Mild cauda equina compression induces TNF-alpha expression and demyelination. Moderate and strong cauda equina compression induces TNF-alpha expression and degeneration associated with macrophage invasion. Neither demyelination nor degeneration in the cauda equina induced mechanical allodynia. Nerve lesions proximal to the dorsal root ganglion do not produce significant mechanical allodynia. Dorsal root ganglion apoptosis may be important for pain.
Sekiguchi
Miho
M
Department of Orthopaedic Surgery, Fukushima Medical University, School of Medicine, Fukushima City, Japan. miho-s@fmu.ac.jp
Kikuchi
Shinichi
S
Myers
Robert R
RR
D000818:Animals; D017209:Apoptosis; D002420:Cauda Equina / Q000737:chemistry / Q000473:pathology; D003711:Demyelinating Diseases / Q000209:etiology / Q000473:pathology; D005260:Female; D005528:Foot / Q000294:innervation; D005727:Ganglia, Spinal / Q000737:chemistry / Q000503:physiopathology / Q000648:ultrastructure; D006941:Hyperesthesia / Q000209:etiology / Q000503:physiopathology; D018613:Microscopy, Confocal; D023421:Models, Animal; D009186:Myelin Sheath / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000032:analysis; D009437:Neuralgia / Q000209:etiology* / Q000503:physiopathology; D011128:Polyradiculopathy / Q000209:etiology* / Q000503:physiopathology; D011312:Pressure; D019736:Prostheses and Implants; D051381:Rats; D017207:Rats, Sprague-Dawley; D012583:Schwann Cells / Q000473:pathology; D013130:Spinal Stenosis / Q000150:complications*; D013314:Stress, Mechanical; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D009419:Nerve Tissue Proteins; D014409:Tumor Necrosis Factor-alpha