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Effects of Phospholipase A2 on Lumbar Nerve Root Structure and Function

Chen, Chaoyang, MD; Cavanaugh, John M., MD; Ozaktay, Cuneyt A., MD; Kallakuri, Srinivasu, MS; King, Albert I., PhD

Basic Science

Study Design. To investigate the effects of phospholipase A2 on the neurophysiology and histology of rat lumbar spinal nerves and the corresponding behavioral changes.

Objectives. To study possible mechanisms of sciatica.

Summary of Background Data. The pathophysiology of sciatica is uncertain, although mechanical, chemical, and ischemic factors have been proposed.

Methods. Phospholipase A2 was injected into the rat L4-L5 epidural space, and the rats were observed for 3 or 21 days. Behavioral studies were conducted daily during the survival period. On the 3rd or 21st day, extracellular nerve recordings were made from dorsal roots, to determine discharge properties and mechanical sensitivity. The nerve roots were then sectioned for a light-microscopic examination.

Results. Motor weakness of hind limbs and altered sensation were observed. In the 3-day phospholipase A2 groups, squeezing the dorsal roots at the L4-L5 disc level (force = 0.8 g) evoked sustained ectopic discharge that lasted approximately 8 minutes. Squeezing the roots distal to the L4-L5 area did not result in sustained discharges. In sham, control, and 21-day phospholipase A2 groups, squeezing the dorsal roots elicited only a transient firing that lasted approximately 0.1 second. Loss of myelin was seen in the nerve root cross sections in the 3-day group, and remyelination was observed in the 21-day group. No abnormality was found in the control groups.

Conclusions. Based on these studies, it is hypothesized that phospholipase A2 causes demyelination that results in hypersensitive regions where ectopic discharge may be elicited by mechanical stimulation. These ectopic discharges may be a source of sciatica. We believe that, as long as these irritating factors are present, the hypersensitive nerve root nerve will continue to fire, and sciatic pain will persist.

From the Bioengineering Center, Wayne State University, Detroit, Michigan.

Supported by NIH Grant No AR41739 (JMC) and the Wayne State University Office of Research and Sponsored Programs.

Acknowledgment date: June 5, 1996.

First revision date: January 6, 1996.

Acceptance date: January 13, 1997.

Device status category: 1.

Address reprint requests to Chaoyang Chen, MD; Bioengineering Center; Wayne State University; 818 W. Hancock; Detroit, MI 48202

© 1997 by Lippincott Williams & Wilkins