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.