Excitotoxic model of post-traumatic syringomyelia in the rat.
METHODS
A rat model was developed to elucidate the role of excitatory amino acids and spinal subarachnoid block in the genesis of post-traumatic syringomyelia. This excitotoxic model produces intramedullary cavities rather than the dilation of the central canal (canalicular syringomyelia) created by previous animal models.


OBJECTIVE
To produce extracanalicular cysts in the rat spinal cord with quisqualic acid, a potent agonist of multiple excitatory amino acid receptors, and to compare the effects of excitotoxic injury only with that of excitotoxic injury and subarachnoid block with kaolin.


BACKGROUND
In post-traumatic syringomyelia, primary injury and excitotoxic cell death secondary to elevated levels of excitatory amino acids may initiate a pathologic process leading to the formation of spinal cavities. Subarachnoid block by arachnoiditis may promote enlargement of the cavities.


METHODS
Three control rats received a unilateral injection of normal saline into the spinal cord, and another five rats received an injection of kaolin into the spinal subarachnoid space. Quisqualic acid was injected unilaterally into the spinal cord of 20 rats, and 13 additional rats received a unilateral injection of quisqualic acid into the spinal cord after injection of kaolin into the subarachnoid space. Histologic and immunocytochemical assessments were undertaken.


RESULTS
In the control groups, no parenchymal cyst developed in any of the animals. Spinal cord cyst formation was observed in 16 of 19 animals in the quisqualic acid groups, but no cysts exceeding two segments in the length of the spinal cord developed in any of the rats. Much larger cavities were seen in 9 of 11 animals in the group with quisqualic acid and kaolin, and cysts exceeding two segments developed in all 9 of these (9/11; 82%).


CONCLUSIONS
In post-traumatic syringomyelia, excitotoxic cell death occurring secondarily to elevated levels of excitatory amino acids may contribute to the pathologic process leading to the formation of spinal cord cysts. Subarachnoid block by arachnoiditis is likely to cause enlargement of the cavity.
Yang
L
L
Department of Surgery (Neurosurgery), University of Adelaide, Australia.
Jones
N R
NR
Stoodley
M A
MA
Blumbergs
P C
PC
Brown
C J
CJ
D000818:Animals; D001100:Arachnoiditis / Q000139:chemically induced / Q000150:complications / Q000473:pathology; D001253:Astrocytes / Q000737:chemistry / Q000473:pathology; D003560:Cysts / Q000139:chemically induced / Q000209:etiology / Q000473:pathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D018846:Excitatory Amino Acids / Q000502:physiology*; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D007150:Immunohistochemistry; D007616:Kaolin / Q000633:toxicity; D008136:Longevity / Q000187:drug effects; D008297:Male; D008845:Microinjections; D016318:Quisqualic Acid / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000737:chemistry / Q000473:pathology; D013119:Spinal Cord Injuries / Q000139:chemically induced / Q000150:complications / Q000473:pathology*; D013346:Subarachnoid Space / Q000473:pathology; D013595:Syringomyelia / Q000139:chemically induced / Q000473:pathology*
D018690:Excitatory Amino Acid Agonists; D018846:Excitatory Amino Acids; D005904:Glial Fibrillary Acidic Protein; D007616:Kaolin; D016318:Quisqualic Acid