Developmental spinal stenosis : from bedside to bench

Abstract

Lumbar spinal stenosis is a common worldwide concern. Compression of the dural sac and nerve roots with spinal canal narrowing leads to symptoms of back or referred pain, radicular pain and claudication. Reoperation is not uncommon after decompression surgery for spinal stenosis. One possible reason for reoperation is pre-existing developmental narrowing of the spinal canal. Patients have generalized short pedicles and are likely at risk of multiple level compressions. Developmental spinal stenosis (DSS) has a predilection for early age symptomatology. With a pre-existing narrowed bony spinal canal, only a small degree of degeneration and increase in the size of structures within the spinal canal will already cause symptomatic neural compression. This condition has not been well-understood in the past and its impact and etiology is unknown. Our knowledge of this entity has been enhanced through the series of clinical and basic science studies. The imaging phenotype is better defined on both plain radiographs and magnetic resonance imaging (MRI). On MRI, critical stenosis has been defined as 14mm at L4, 14mm at L5 and 12mm at S1 with excellent sensitivity and specificity. On x-rays, a sagittal body width to pedicle width ratio of 3 is diagnostic of DSS. Its clinical implications as an independent risk factor for reoperation after decompression surgery and influence on ligamentum flavum pathology have been elucidated. Controlled for severity of disc degeneration and ligamentum flavum thickness, DSS has an adjusted odds ratio of 3.93 for reoperation at the adjacent level after an index decompression surgery. The degree of fibrosis in ligamentum flavum was negatively correlated with the severity of developmental narrowing. This is in contrast to degenerative spinal stenosis in which the fibrosis is much more severe despite similar thickness of ligamentum flavum. The structures within the spinal canal will likely have similar maldevelopment potential. As a natural next step to understanding etiology, breakthroughs in the genetic etiology of the disease have been made. Candidate gene analysis identified the lipoprotein receptor related protein 5 (LRP5) gene on chromosome 11 to reach Bonferroni threshold of significance. This is a key component of the Wnt signaling pathway which is important for bone development. Finally, a mechanistic rat model mimicking circumferential compression has been created for future testing. The model produced the most severe functional deficits in the hindlimb postoperatively that are monitored with electrophysiology. With these studies, we can translate our findings into a new clinical dogma for lumbar spinal stenosis. We now have a deeper understanding of the specific phenotype known as DSS which is not influenced by degenerative processes. It is an independent risk factor for multiple surgeries as only a mild degenerative change is adequate to give rise to symptoms. Routine screening of patients for developmental narrowing is important especially for patients requiring surgery to gauge the risk of further surgery. The results reported here are fuel for launching future clinical trials to determine the role of prophylactic decompression for at-risk spinal levels during the index operation.