While extensive in vitro and in vivo work has been performed in the area of spinal biomechanics1, correlation of biomechanical data with the symptoms reported by patients is difficult. The authors of this study attempted to combine clinical and biomechanical information by measuring spinal range of motion during functional activities in patients with a history of symptomatic degenerative disc disease.
The study improves on previous work as it was limited to the assessment of patients with pain thought to be primarily discogenic. While degenerative disc disease as a cause of back pain, discography as a diagnostic tool, and spinal surgery as a treatment are all controversial, the authors attempted to streamline patient selection and to correlate symptoms with the limited disc-assessment tools available today: MRI, radiography/fluoroscopy, and discography. Patients with degeneration within the intervertebral disc were characterized according to the Modic and Pfirrmann grading scales. Those with associated facet pathology, neural entrapment, or instability as confounding variables were excluded. Motion was then evaluated in flexion-extension, lateral bending, and axial rotation from L2 through S1. The authors recognized small coupled motions in all three directions associated with movement in any one primary direction. The methodology that was employed for the assessment of range of motion was accurate to within 0.4 mm of translation.
While reasonable attempts were made to correlate laboratory data and clinical information in this study, one must remain cautious in relating clinical relevance to these findings. It remains unclear to what degree adjacent-segment degeneration is a de facto process that is part of the natural history of a degenerative spine or a phenomenon representing the acceleration of disease through modification of biomechanical forces after surgery. "Motion-preserving technologies" such as intervertebral disc replacement and posterior flexible instrumentation "stabilization" without fusion have gained attention in recent years as intuitive strategies to avoid adjacent-segment degeneration. However, the long-term implications of these non-fusion procedures are unclear, and convincing data showing a decrease in clinically symptomatic degeneration, not only radiographic degeneration, remain lacking2-4. The manner in which surgical interventions alter spinal biomechanics is variable as well5.
This study shows that hypermobility develops adjacent to a segment with degenerative disc disease even before spinal surgery is performed. Surgeons who believe that adjacent-segment degeneration is a natural process will find credence in the argument of these authors. However, those who believe that adjacent-segment degeneration is accelerated after a fusion will point out that hypermobility occurred adjacent to a stiff segment. The truth is likely in a gray zone between both arguments. A follow-up analysis of these patients to evaluate adjacent-segment motion and degeneration several years after surgery may provide further perspective, although the sample size in this study is small.
The authors noted hypermobility at L3-L4 and attributed it to caudad degenerative disc disease at L4-L5 and L5-S1. However, L4-L5 was also noted to be hypermobile in flexion-extension movements, even with a similar degree of degeneration as the L5-S1 level. Is hypomobility at L5-S1 responsible for hypermobility at two cephalad levels? The evaluation of patients with a transitional lumbosacral junction may be of interest in order to assess if the L4-L5 level assumes the hypermobility seen in this study when adjacent to a stiff L5-S1 segment or if the mobility pattern shifts one level up. Finally, patients with isolated L4-L5 disease could be evaluated as well. While many questions in this area remain to be answered, the authors have contributed valuable information in a well-done study that can be used as a base for future studies.