Effects of diclofenac and ketoprofen on nerve conduction velocity in experimental nerve root compression.
METHODS
The effects of diclofenac and ketoprofen on nerve conduction velocity in experimental nerve root compression were evaluated in a setup using an established pig model.


OBJECTIVE
To assess the effects of two potent nonsteroidal antiinflammatory drugs, diclofenac and ketoprofen, in experimental nerve root compression.


BACKGROUND
Compression of spinal nerve roots is recognized to be of major etiologic importance for several common spinal pain syndromes. Secondary inflammatory changes, induced by microvascular permeability changes and leakage of inflammatory mediators into the endoneural tissue, have been proposed as important for the induction of spinal nerve root injury by chronic compression.


METHODS
This study involved 21 pigs. An ameroid constrictor was used to induce compression. Seven pigs were treated with daily intramuscular injections of diclofenac 3 mg/kg for 7 days. Seven other pigs were treated with daily intramuscular injections of ketoprofen 4 mg/kg. For a control, seven pigs did not receive any drug treatment. After 7 days, the pigs were reanesthetized, and the nerve conduction velocity in the compressed nerve root segments was determined.


RESULTS
The nerve conduction velocity was significantly higher (P < 0.05, Student's t test) in the pigs treated with diclofenac (50 +/- 16 m/second) than in the untreated pigs (32 +/- 15 m/second). The nerve conduction velocity also was significantly higher (P < 0.05) in the pigs treated with ketoprofen (59 +/- 16 m/second) than in the untreated pigs. There were no significant differences in nerve conduction velocity between pigs treated with ketoprofen and those treated with diclofenac.


CONCLUSIONS
The findings indicate that intramuscular administration of diclofenac or ketoprofen, both potent antiinflammatory drugs, may reduce nerve root dysfunction induced by compression of spinal nerve roots in an experimental pig model.
Cornefjord
M
M
Department of Orthopaedics, Göteborg University, Gothenburg, Sweden. michael.cornefjord@ortopedi.uu.SE
Olmarker
K
K
Otani
K
K
Rydevik
B
B
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000494:pharmacology*; D004008:Diclofenac / Q000008:administration & dosage / Q000494:pharmacology*; D004195:Disease Models, Animal; D007273:Injections, Intramuscular; D007660:Ketoprofen / Q000008:administration & dosage / Q000494:pharmacology*; D009408:Nerve Compression Syndromes / Q000209:etiology / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects*; D011843:Radiculopathy / Q000503:physiopathology*; D013126:Spinal Nerve Roots / Q000187:drug effects* / Q000293:injuries / Q000503:physiopathology; D013552:Swine
D000894:Anti-Inflammatory Agents, Non-Steroidal; D004008:Diclofenac; D007660:Ketoprofen