Clinical Case Example

A 60-year-old man presents with progressive back and leg pain that is worse with standing and walking. On further discussion the patient admits to decreasing ability to walk for longer than 10 minutes, and he feels relief with sitting. The patient answers positively when asked if he can walk longer if he leans forward on a grocery cart. The patient admits to prior physical therapy and epidural steroid injections without relief. On examination the patient has a normal gait, with positive distal pulses at 70 beats per minute and no cyanosis or edema in the lower extremities. His reflexes are rated 2/4; strength is rated 5/5; he exhibits negative straight leg raise, no radiculopathy, and no myelopathy with no focal neurological deficits. Review of his T2-weighted magnetic resonance imaging (MRI) axial images of the lumbar spine demonstrates significant stenosis at the L4-L5 level secondary to hypertrophied ligamentum flavum and facet hypertrophy (Figure 14-1).

FIGURE 14-1 Axial T2-weighted MRI of L4-L5 demonstrating significant lumbar stenosis secondary to hypertrophied ligamentum flavum, bulging annulus, and facet hypertrophy.

Basic Science

The pathogenesis of lumbar stenosis is an interesting degenerative cascade that eventually leads to the pathognomonic signs and symptoms. In brief, the degenerative cascade begins at the level of the intervertebral disc, which consists of an inner nuclear core called the nucleus pulposus and an outer supporting layer of the disc called the annulus fibrosus. Beginning early in life, the nucleus pulposus loses its vascular supply and depends on diffusion for its nutrient base, which slowly becomes insufficient. This change in vascular supply leads to dehydration and altered proteoglycan matrix, thus altering the mechanical properties of the disc and the pressure distribution within the disc and leading to a stressed and bulging annulus with loss of disc height.²

Vascular regression within the disc is thought to occur as the child moves from quadrupedal to bipedal motion, thus increasing the load on the disc space in the vertical position. The increasing intradisc pressure leads to involution of the blood supply. By 4 years of age the disc largely depends on cellular diffusion for survival.² With increasing age the metabolic strain to the intervertebral disc increases, yet the vascular supply is insufficient and diffusion cannot maintain the demands. The altered metabolism in the disc changes the overall electrolyte balance in the disc space, decreasing the net inward flow of fluid and decreasing water content from 90% to 70%; this change ultimately leads to loss of disc height and expandability.²

The aforementioned degeneration of the intervertebral disc leads to altered local and segmental mechanics, generating a cascade of compensatory changes within the facet complex, bones, and ligaments.² Along with degenerative changes occurring with the normal aging spine, the surrounding support structures are also aging and thus degenerating. The most important of the surrounding structures are the core muscles, which include the paraspinal musculature and the abdominal muscles.³ As these supporting muscles lose tone, the spinal column stability depends more on the facet joints, ligaments, and intervertebral discs leading to compensatory hypertrophy of the ligaments, hypertrophied facet joints, and calcified annular-vertebral osteophytes (Table 14-1).³

TABLE 14-1 The Basic Degenerative Cascade for Lumbar Stenosis