Ectopic firing due to artificial venous stasis in rat lumbar spinal canal stenosis model: a possible pathogenesis of neurogenic intermittent claudication.

STUDY DESIGN: An electrophysiologic analysis was performed on a chronic lumbar spinal stenosis model of rats. The effects of venous stasis on ectopic firing originating in the nerve root were investigated.

OBJECTIVES: To elucidate the mechanisms of neurogenic intermittent claudication in lumbar spinal canal stenosis.

SUMMARY OF BACKGROUND DATA: Neurogenic intermittent claudication has been known as a characteristic symptom of lumbar spinal canal stenosis (LSCS), but the pathogenesis is poorly understood. Venous stasis of cauda equina has been speculated as a possible factor in the development of symptoms of the lower extremities while walking. On the other hand, ectopic firing originating in the dorsal root ganglia is thought to play an important role in the development of radicular pain or abnormal sensation. However, a direct association between venous stasis and ectopic firing has been never demonstrated.

METHODS: Using 10 Wistar rats, the LSCS group was prepared by inserting two silicone strips into the L3 and L5 dorsal epidural spaces. Another 10 animals were treated without silicone insertion as a sham group. Fourteen days later, the ectopic firing originating in the L5 nerve root was antidromically recorded from the distal stump of the severed sural nerve. After recording initial spontaneous firing, the posterior vena cava was clamped for 60 seconds to simulate a transient venous stasis and the changes in firing were analyzed.

RESULTS: None of the animals in the sham group showed a significant change in firing due to venous stasis. In contrast, most animals in the LSCS group showed a marked increase in firing during the venous stasis with some latency and then returned to the initial firing state after the release of the clamp. This phenomenon was repeated as long as the animals were maintained.

CONCLUSIONS: We demonstrated that ectopic firing was elicited by venous stasis only in the LSCS animals. Therefore, the venous stasis may be a major factor of neurogenic intermittent claudication.