LUMBAR SPINAL STENOSIS - DIAGNOSIS, MANAGEMENT, AND TREATMENT

Spinal stenosis and the symptomatology from it are caused by a combination of congenital, developmental, and vascular factors.(11,12,18,19,21) Predisposition to spinal stenosis is affected by the congenital size of the spinal canal and the patient's rate of degenerative spinal disease with aging. As the skeleton ages, degenerative disc disease occurs. The majority of patients over the age of 30 will have some element of disc degeneration. As discs degenerate further, the facet joints and ligamentum flavum posteriorly hypertrophy to stabilize the spinal segments. As the facet joints and ligaments hypertrophy posteriorly, the dimension of the spinal canal is reduced. As the spinal canal dimensions are reduced, the ability of the nerve roots to receive their needed nutrition and blood supply is reduced. To some extent, vertebral osteophytes anteriorly can play a role, but in most cases, facet joint hypertrophy and hypertrophy of the posterior ligamentum flavum are what squeeze the nerve roots and their blood supply. This process is slow and gradual, taking many years to occur. It is uncommon for patients to present with acute neurologic deficits from spinal stenosis. In rare, long-standing severe cases, patients may present with wasting of their legs and difficulty with bowel and bladder control, but this is the exception. Although the underlying problem is mechanical, i.e., reduction of canal space for the nerve roots, the symptomatology and pain are caused by vascular compromise to the nerve roots, which is the reason that the claudication symptomatology associated with peripheral vascular disease and spinal disease presents in such a similar fashion.