Study design: In vitro biomechanical testing was performed in human cadaveric lumbar spines, using pressure needle transducers to analyze the effects of spinal destabilization and instrumentation on lumbar intradiscal pressures.
Objectives: To quantify changes in lumbar intradiscal pressures at three adjacent disc levels under conditions of spinal reconstruction, and to evaluate the possibility of pressure-induced disc pathology secondary to spinal instrumentation.
Summary of background data: Lumbar intradiscal pressures under in vivo and in vitro conditions and the use and development of spinal instrumentation have been investigated comprehensively. However, the effects of spinal destabilization and instrumentation on lumbar intradiscal pressure have not been delineated clearly.
Methods: In 11 human cadaveric lumbosacral specimens, specially designed pressure needle transducers quantified intradiscal pressure changes at three adjacent disc levels (L2-L3, proximal; L3-L4, operative; and L4-L5, distal) under four conditions of spinal stability: intact, destabilized, laminar hook and pedicle screw reconstructions. Biomechanical testing was performed under axial compression (0-600 N), anterior flexion (+12.5 degrees) and extension (-12.5 degrees), after which the level of degeneration and disc area (cm2) were quantified.
Results: In response to destabilization and instrumentation, proximal disc pressures increased as much as 45%, and operative pressure levels decreased 41-55% (P < 0.05), depending on the instrumentation technique. Linear regression and correlation analyses comparing intradiscal pressure to the grade of disc degeneration were not significant (r = 0.24).
Conclusions: Changes in segmental intradiscal pressure levels occur in response to spinal destabilization and instrumentation (P < 0.05). Intradiscal cyclic pressure differentials drive the metabolic production and exchange of disc substances. Conditions of high or low disc pressure secondary to spinal instrumentation may serve as the impetus for altered metabolic exchange and predispose operative and adjacent levels to disc pathology.