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Novel compression rat model for developmental spinal stenosis

Developmental spinal stenosis (DSS) is characterized by pre‐existing circumferential narrowing of the bony spinal canal which predisposes neural tissue to compression. This study aims to create a reproducible animal model mimicking DSS for investigation of its pathoanatomy. Developmental spinal canal constriction was simulated using circumferential compression. Eighteen female Sprague–Dawley rats (13.0–14.5 weeks‐old) underwent circumferential compression at L4‐L5 using silicone sheets; or dorsal compression using overlapping silicone sheets; or as controls. A series of outcome scores were used for locomotor function assessment, together with electrophysiological and histological assessment. Assessment time‐points were at preoperative, postoperative 1‐week, 2‐weeks, 3‐weeks, 1‐month, and pre‐sacrifice. Statistical analyses were performed. At all postoperative time‐points, circumferential group had the worst mean Basso, Beattie and Bresnahan locomotor scores with significant difference from the control group (p < 0.05), as well as the lowest mean Louisville Swim Scale scores, as compared to the dorsal (p < 0.05) and to the control (p < 0.01) groups. Circumferential group had worse mean foot fault score for both hindlimbs (p < 0.01 to p < 0.05) and highest error rate in foot placement accuracy, especially higher than dorsal (p < 0.05) and control (p < 0.05) groups at pre‐sacrifice. Electrophysiological assessment revealed postoperative increase in P1 latency was higher in circumferential than dorsal compression. Highest postoperative mean P1 latency was observed for both paws at all postoperative time‐points for circumferential group (except at postoperative 1‐week). Circumferential group had lower myelin‐to‐axonal area ratio and higher g‐ratio than both the dorsal and control groups (p < 0.001). For each study group, hindlimb P1 latency and P1‐N1 amplitude were each correlated with g‐ratio (p < 0.05); and mean myelin‐to‐axonal area ratio correlated with P1 latency of both hindlimbs (p < 0.05). Based on these more severe axonal demyelination and neurological deficits, a valid DSS rat model is created with somatosensory evoked potential neuro‐monitoring technique. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res