header advert
Orthopaedic Proceedings Logo

Receive monthly Table of Contents alerts from Orthopaedic Proceedings

Comprehensive article alerts can be set up and managed through your account settings

View my account settings

Visit Orthopaedic Proceedings at:

Loading...

Loading...

Full Access

Spine

NOVEL FLEXION-RESTRICTING STABILIZATION SYSTEM RESTORES STABILITY IN FLEXION AND TRANSLATION AFTER SIMULATED INJURY

British Association of Spinal Surgeons (BASS)



Abstract

Statement of Purpose

The purpose of this experiment was to characterize the biomechanical properties of a minimally-invasive flexion-restricting stabilization system (FRSS) developed to address flexion instability.

Background

Lumbar flexion instability is associated with degenerative pathology such as degenerative spondylolisthesis (DS) as well as resection of posterior structures during neural decompression. Flexion instability may be measured by increased total flexion/extension range of motion (ROM), as well as reduced stiffness within the high flexibility zone (HFZ, the range in which most activities occur). Flexion and segmental translation are known to be coupled; therefore increased flexion may exacerbate translational instability, particularly in DS.

Method

Five cadaveric lumbar spines were tested intact; after L4-L5 destabilization including nucleotomy and midline decompression; and following restabilization with the FRSS secured to the spinous processes. Specimens were loaded in flexion (8Nm) and extension (6Nm) under 400N compressive follower preload. Flexion stiffness in the HFZ and segmental translation were also measured.

Results

Destabilization increased L4-L5 flexion by 69%±31% (p<.01); decreased HFZ flexion stiffness 56%±12% (p=.01) and increased segmental translation 70%±49% from 1.5±0.4mm to 2.4±0.4mm (p<.01). With the FRSS segmental flexion was reduced by 45%±15% (p<.01); average HFZ flexion stiffness was increased by 232%±104% (p<.01); and segmental translation was reduced by 25%±9% to 1.8±0.2mm (p<.01). These values were not significantly different from the intact condition (p=.54, p=.21, p=.19).

Discussion and Conclusion

The destabilization modeled here simulated degenerative and iatrogenic destabilizations often seen clinically. Implantation of the FRSS on the destabilized segments restored flexion, stiffness and translation to intact levels. The segmental coupling of translation and flexion seen in this experiment indicates that translation may be manipulated by altering flexion kinematics. The FRSS represents a novel system for treating flexion and translational instabilities.