Direct-trauma model of posttraumatic syringomyelia with a computer-controlled motorized spinal cord impactor

Abstract

OBJECTIVE The pathogenesis of posttraumatic syringomyelia remains enigmatic and is not adequately explained by current theories. Experimental investigations require a reproducible animal model that replicates the human condition. Current animal models are imperfect because of their low reliability, severe neurological deficits, or dissimilar mechanism of injury. The objective of this study was to develop a reproducible rodent model of posttraumatic syringomyelia using a spinal cord impactor that produces an injury that more closely mimics the human condition and does not produce severe neurological deficits. METHODS The study consisted of 2 parts. Seventy animals were studied overall: 20 in Experiment 1 and 48 in Experiment 2 after two rats with severe deficits were killed early. Experiment 1 aimed to determine the optimal force setting for inducing a cystic cavity without neurological deficits using a computer-controlled motorized spinal cord impactor. Twenty animals received an impact that ranged from 50 to 150 kDyn. Using the optimal force for producing an initial cyst determined from Experiment 1, Experiment 2 aimed to compare the progression of cavities in animals with and those without arachnoiditis induced by kaolin. Forty-eight animals were killed at 1, 3, 6, or 12 weeks after syrinx induction. Measurements of cavity size and maximum anteroposterior and lateral diameters were evaluated using light microscopy. RESULTS In Experiment 1, cavities were present in 95% of the animals. The duration of limb weakness and spinal cord cavity size correlated with the delivered force. The optimal force chosen for Experiment 2 was 75 kDyn. In Experiment 2, cavities occurred in 92% of the animals. Animals in the kaolin groups developed larger cavities and more vacuolations and enlarged perivascular spaces than those in the nonkaolin groups. CONCLUSIONS This impact model reliably produces cavities that resemble human posttraumatic syringomyelia and is suitable for further study of posttraumatic syringomyelia pathophysiology.