Natural History of Lumbar Spinal Stenosis
Shrinkage and narrowing of disks as well as osteoarthritic changes can lead to both spinal stenosis and spinal instability (Jane, Jane, Helm et al., 1996; Mirkovic, Garfin, Rydevik et al., 1992; Mirkovic, Garfin, Rydevik et al., 1992; Postacchini and Perugia, 1991; Rowe, 1969). Therefore, disk degeneration and osteoarthritis of the spine are discussed in this Natural History section as underlying conditions that can lead to spinal stenosis, even though treatment for disk herniation and rupture and osteoarthritis is outside the scope of our analysis.
Disk Degeneration
Ordinary wear and tear, combined with age-associated changes in the tissue composition of the spinal disks, lead to disk degeneration (see Figure 2). Type II collagen, the more hydrated form, decreases in proportion to type I collagen (Jane, Jane, Helm et al., 1996). Proteoglycan content declines (Mirkovic, Garfin, Rydevik et al., 1992). In the absence of hydrostatic proteoglycans, the water content of the disk declines. As the overall hydration of the disk decreases, the disk becomes less elastic and thus less able to evenly distribute the constantly shifting loads placed upon it (Prescher, 1998). Unevenly distributed stresses may lead to the development of tears and weaknesses in the disk. To a certain extent, this degeneration is an inevitable result of aging (Jane, Jane, Helm et al., 1996). Degeneration begins as early as the second decade in men and the third in women (Mirkovic, Garfin, Rydevik et al., 1992). By the age of 40, 80 percent of males' and 65 percent of females' disks are moderately degenerated (Mirkovic, Garfin, Rydevik et al., 1992).
In susceptible individuals, disk degeneration can lead to pain and damage to the spinal nerves. Whether joint degeneration leads to pathologic consequences depends upon the characteristics of the individual patient (Jane, Jane, Helm et al., 1996).
Osteoarthritis in the Spine
Incremental microdamage in the lower disks of susceptible patients ultimately results in venting and loss of pressure in the disk nucleus (Rowe, 1969). As the disk degenerates, it narrows, decreasing the distance between vertebrae. The distribution of forces in the joint is altered. The ligaments connecting the vertebrae become lax, destabilizing the joint. Instability and altered force distribution lead to mechanical stress, which in turn can cause osteoarthritic changes in the articular processes (Fast and Greenbaum, 1995). Consequently, the vertebral facets become enlarged, the vertebral pedicles thicken, and the ligamentum flavum thickens. Type II collagen replaces elastic tissue (Jane, Jane, Helm et al., 1996; Schrader, Grob, Rahn et al., 1999), and calcium crystals are deposited (Schrader, Grob, Rahn et al., 1999). Hyalinization of the collagen fibers and proliferation of chondrocytes also contribute to the ossification of the ligament. Facet hypertrophy, thickening of the pedicles, and ossification of the ligamentum flavum lead to narrowing of the central spinal canal. Traction spurs may develop. These spurs can also impinge on the spinal canal or the nerve roots.
Eventually, vertebral stability may be regained as scarring occurs across the nuclear compartment (Rowe, 1969). Osteoarthritic changes may also lead to increased stability or even fusion between two vertebrae (Postacchini and Perugia, 1991; Rosenberg, 1975).
In susceptible individuals, the degenerative changes in the facet joints lead to two overlapping pathological and clinical entities: central and lateral stenosis. The two conditions may not be distinguished by their symptoms (Amundsen, Weber, Lilleas et al., 1995). The extent to which the degree and location of stenosis correlates with the nature, intensity, and location of symptoms is unclear. Individuals are frequently observed to have marked stenosis and no symptoms (LaRocca and Macnab, 1969; Nagler and Bodack, 1993; Postacchini and Perugia, 1991; Splithoff, 1953). Among patients with symptoms, long periods of remission are thought, at least by some, to be common (Rosenberg, 1976). However, the incidence and duration of these periods of remission are not well studied.
Degenerative Central Lumbar Stenosis
Lumbar spinal stenosis can be separated into three broad categories, specifically central stenosis, lateral stenosis, and spondylolisthesis. We have used these categories in our analysis to organize the literature and assist in combining evidence. Specific consideration of the etiology of the stenosis is important because different conservative and/or surgical treatments may be more or less effective depending on the nature of the stenosis.
Central stenosis refers to a narrowing of the spinal canal across the anteroposterior diameter, the transverse diameter, or both (Gunzburg and Szpalski, 1999; Postacchini, 1999; Woolsey, 1986). The central canal is enclosed anteriorly by the posterior portion of the vertebral body and the vertebral disk and posteriorly by the lamina and the base of the spinous process (see Figures 3, 5, and 6).
Degenerative Lateral Stenosis
Entrapment and compression of the nerve root in its pathway through the spine, referred to as the nerve root canal, is termed lateral stenosis (Gunzburg and Szpalski, 1999; Jenis and An, 2000; Postacchini, 1999; Woolsey, 1986). The nerve root canal begins where the nerve root exits the dura and ends where the nerve root leaves the intervertebral foramen. The nerve root canal is bordered by the pedicle of the vertebra above and the pedicle of the vertebra below. The anterior side of the canal is formed by the vertebral body and vertebral disk. The posterior side of the canal is formed by the facet joint structures of the vertebrae above and below (see Figures 3, 4, and 5). Lateral stenosis occurs when the spinal nerve is compressed within the nerve root canal and/or the vertebral foramina (Fritz, Delitto, Welch et al., 1998). As the disk narrows, the pedicle may move in an inferior direction, narrowing the lateral recess and pinching the spinal nerve (Jane, Jane, Helm et al., 1996; Mirkovic, Garfin, Rydevik et al., 1992). MacNab (1977) originally described this entrapment and compression of the nerve root between a diffuse lateral bulge of the disk and the pedicle above as pedicular kinking. Narrowing of the lateral recess can also be the result of facet hypertrophy or enlargement and ossification of the ligamentum flavum. Radiculopathy, or decreased function of a nerve root, is commonly observed with lateral stenosis. Impingement of the disk into the lateral recess is considered a separate condition (Amundsen, Weber, Lilleas et al., 1995) and is beyond the scope of this evidence report.
Degenerative Spondylolisthesis
Degenerative spondylolisthesis is a slippage of one lumbar (L) vertebra over an adjacent vertebra and commonly occurs between L4-L5 (Woolsey, 1986). When L4 slips forward, the central canal and the nerve roots become entrapped between the posterior body of L5 and the inferior articular facets of lamina of L4 (see Figure 7).
Disk degeneration may lead to spinal instability. Decreased disk height and degenerative changes in the angles of the facet joints contribute to this instability (Mirkovic, Garfin, Rydevik et al., 1992; Postacchini and Perugia, 1991; Rowe, 1969). This can lead to spondylolisthesis, or displacement of the vertebrae. Lumbar vertebrae have a tendency to be displaced forward due to their normal anterior curve and the action of gravity, muscular force, and other forces (Kim and Lee, 1995). As the vertebra slips forward, the medial edge of the superior facet may encroach on the central canal (Postacchini and Perugia, 1991). Distal to the slipping vertebra, the dural sac becomes trapped between the intervertebral disk and the posterosuperior angle of the underlying vertebral body on one side and the advancing neural arch of the slipping vertebra on the other. This is most commonly observed at the L4-5 level (Herkowitz, 1995; Newman, 1976). The anatomical reasons for the greater likelihood of degeneration at L4-5 have been described by MacGibbon and Farfan (MacGibbon and Farfan, 1979). Lateral stenosis may also result from spondylolisthesis when the nerve root becomes compressed between the inferior facet of the superior vertebra and the vertebral body of the inferior vertebra (Newman, 1976).
Further remodeling of the articular processes may eventually limit the vertebral slippage (Postacchini and Perugia, 1991). The degree of slippage usually does not exceed 20 percent to 30 percent of the width of the inferior vertebra (Herkowitz, 1995; Postacchini and Perugia, 1991; Rosenberg, 1975).
Spinal Stenosis and Spondylolisthesis in the Asymptomatic Population
As mentioned above, not all patients with spinal stenosis are symptomatic. Five studies (Boden, Davis, Dina et al., 1990; Healy, Healy, Wong et al., 1996; Jensen, Brant-Zawadzki, Obuchowski et al., 1994; Parkkola, Rytokoski, and Kormano, 1993; Wiesel, Tsourmas, Feffer et al., 1984) have looked at the proportion of the asymptomatic adult population that has spinal stenosis upon imaging (see Table 4). Their results suggest that 3.3 percent to 5 percent of the adult population have central stenosis but is asymptomatic; 7 percent to 16 percent have neural foramen stenosis or narrowing. The proportion of stenotic, asymptomatic individuals was larger in older age groups (Boden, Davis, Dina et al., 1990), 21 percent (3/14) of adults age 60 and over, versus <1 percent (1/53) of adults below age 60.
Although the presence of apparent stenosis in the asymptomatic population raises a question about whether stenosis per se causes symptoms, those with more severe symptoms are more likely to have stenosis. In one study, stenosis was observed by imaging in 50 percent (5/10) of patients with severe low back pain, 11 percent (4/38) of patients with less severe low back pain, and 3.3 percent (2/60) of asymptomatic controls matched to the back pain patients by sex, age, employment, and profession (Parkkola, Rytokoski, and Kormano, 1993).
There is also evidence that not all individuals with vertebral displacement are symptomatic. Based on lateral radiographs taken for the longitudinal Framingham Heart Study (Kauppila, Eustace, Kiel et al., 1998), at the mean age of 79, 19 percent (90/483) of patients without vertebral slippage had back pain or stiffness on most days compared to 32 percent (39/123) of patients with slippage (χ2 = 10.5, p = 0.001). This latter proportion implies that 68 percent of patients with slippage did not have chronic back pain. From this, we were able to calculate that 17.6 percent (84/477) of patients without chronic back pain had degenerative spondylolisthesis (see Table 5).
The presence of stenosis and slippage in spinal images of asymptomatic people indicates that treatment must be based on the convergence of symptoms and image evidence rather than on either type of evidence alone. And in spite of the relationship between image evidence and more severe symptoms, the possibility exists that, even in more severe cases, treatment based on the image and symptoms may actually address a coincidental condition without eradicating the actual cause of symptoms.
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