Disc Degeneration with Root Irritation: Spinal Canal Stenosis

“The loss of youth is melancholy enough: but to enter into old age through the gate of infirmity, most disheartening.”

–Horace Walpole, 1765

Stenosis is defined as a narrowing or constriction of a passage or canal. When the term is applied to those changes that occur within the spinal canal, the additional connotations of irreversible and progressive narrowing of the canal are implied. Such irreversible narrowing is in contrast to the often waxing and waning symptoms of encroachment occurring with a herniated nucleus pulposus (HNP). Although both conditions are mechanical in nature, that is, aggravation with activity, relief with rest, there are often gaps of days to months in the history of patients with an HNP, during which time they function reasonably well. There are no gaps in the history of patients with spinal canal stenosis (SCS) except early in the disease.

The term claudication means “limp.” Often, patients with spinal stenosis experience claudication or “limping,” after walking. The lameness is thought to be caused by an upset in neurologic function, thus, the term neurogenic claudication. Infrequently, patients with spinal stenosis have more radicular symptoms than the typical picture of neurogenic claudication. However, claudication is prevalent enough that it forms the foundation of the definition of SCS: (a) claudicant limitation of leg(s) function, (b) clinical evidence of chronic nerve root compression with the presence of, (c) a stenotic spinal canal lesion on imaging and, (d) in the absence of vascular impairment to the lower extremities.

Neurogenic claudication is generally defined as calf discomfort (pain, numbness, paresthesia, weakness, tiredness, heaviness), that is aggravated by both walking and standing and is relieved only after many minutes of resting in the flexed (sitting) lumbar spine position. The posterior and occasionally anterior thigh can also be involved.

Classification and Description

The standard classification of SCS is outlined in Table 12-1 (1). This classification and the term spinal stenosis are used by most authors to describe narrowing of the central spinal canal as well as “lateral recess” narrowing in the subarticular and foraminal area. Although the central and lateral recess division helps in understanding the pathoanatomy of the two conditions, it is an artificial separation that often does not stand the test of clinical medicine, in which the two conditions so often coexist (8).

The most common stenotic conditions are acquired: stenosis due to degenerative changes in the central spinal canal including bulging or herniation of the disc, osteophyte formation and buckling of an hypertrophied ligamentum flavum. An element of stenosis may be associated with a degenerative spondylolisthesis. On occasion, these acquired conditions occur along with developmental
conditions, such as a narrowed or abnormally shaped spinal canal. Purely congenital or developmental spinal stenosis is uncommon and receives but brief mention in this chapter.

TABLE 12-1 Classification of Spinal Canal Stenosis

Congenital-developmental stenosis of the spinal canal
1. Achondroplastic stenosis
2. Normal patient with narrowed spinal canal
Acquired stenosis of the spinal canal
  1. Stenosis due to degenerative changes
  2. Stenosis due to degenerative spondylolisthesis
  3. Iatrogenic—postfusion stenosis
  4. Post-traumatic
  5. Miscellaneous skeletal diseases; e.g., Paget’s disease
Combined A and B

From Arnoldi CC, Brodsky AE, Cauchoix J, et al. Lumbar spinal stenosis and nerve root entrapment syndromes: definitions and classification. Clin Orthop. 1976;115:4–5 with permission.

No better description of the lateral recess zone has been given than in Macnab’s well-read and often quoted article on “Negative Disc Exploration” (21), in which he introduced the term “hidden zone” (Fig. 12-1). Since that time, spinal surgeons have struggled to decompress that zone without removing the inferior facet to cause spinal instability. All too often, in the orthopaedic community, the facet has been saved to the detriment of an adequate decompression of the foramen, whereas in the neurosurgical community, an adequate decompression has been completed at the expense of the facet joint, which has possibly led to subsequent instability.

This chapter concerns itself with the three most common forms of SCS.

SCS with degenerative spondylolisthesis, the most common stenotic condition, occurs most often in women (female-to-male ratio = 6:1) (9,10,20) (Fig. 12-2) and predominantly in the first story of each anatomic segment.
SCS without vertebral body translation is a condition equally distributed among men and women. (Fig. 12-3).
SCS may be due to a combination of a congenitally (developmentally) small spinal canal, superimposed on which are degenerative changes, further narrowing the spinal canal. This condition most commonly occurs in men of large stature and often before age 50 years (Fig. 12-4).

FIGURE 12-1. The hidden zone.

FIGURE 12-2. The three stories of each anatomic segment. (How many times have you seen this schematic!) B: Sagittal MRI of degenerative spondylolisthesis and spinal stenosis showing annular bulging (white arrow) and ligamentum flavum hypertrophy (black arrow) causing stenosis in first story and upper portion of adjacent third story. C: Axial MRI in same patient showing ligamentum flavum hypertrophy, or folding, also contributing to stenosis.

Pathoanatomy: a Summary

To understand the pathoanatomy of SCS, the reader is referred back to Chapter 1 on anatomy, paying specific attention to the first story of the anatomic segment (Fig. 12-2), which is usually the greatest point of acquired stenosis (Fig. 12-5). Aside from the less frequent congenital narrowing of the spinal canal, the three structures that contribute to the canal stenosis are the ligamentum flavum, the facet joints, and the disc space. Notice in Figures 12-2, 12-3, 12-4, 12-5 how this maximum effect is largely confined to the first story and upper reaches of the third story of the level below. This intrasegmental degenerative “napkin-ring” concept is the key to understanding the message of this chapter.

FIGURE 12-3. Spinal canal stenosis without a slipped vertebrae: A: T1 sagittalthe stenosis does not appear that severe. B: T1 axial shows the true extent of the stenosis at L4-L5.

FIGURE 12-4. Spinal canal stenosis without a slip but with a significant congenital narrowing of the spinal canal. Note the “global” nature of the pencil thin canal. This was a young patient tipped into symptoms by a disc herniation at L4-L5 (arrow).

FIGURE 12-5. Adjacent MRI T1 axial slices to show first story spinal canal stenosis (top right). Top left is second story of the fourth anatomic segment; bottom left is third story of fifth anatomic segment; and bottom right is first story of fifth anatomic segment (L5-S1 disc space).

FIGURE 12-6. The three shapes of the spinal canal as seen on CT scan or MRI: round (really triangular), trefoil, oval.

Shape of the Canal

Figure 12-6 illustrates the three basic shapes of the lumbar spinal canal. The most common shapes are round and ovoid. Perhaps 15% of humans have a trefoil canal, and canals of trefoil shape are most vulnerable to the degenerative changes that decrease the space occupied by the neurologic structures.

Degenerative Changes

Degenerative changes can affect the disc, the soft tissue supports, and the facet joints. (7,15,19,24) Annular bulging, ligamentum flavum infolding or hypertrophy, and osteophyte formation encroach on the spinal canal to decrease the space available to the cauda equina (Fig. 12-7).

The hypertrophied ligamentum flavum enfolds to encroach posteriorly and is the major lesion in stenosis of the first story. Further first story canal encroachment occurs when the facet subluxation of a degenerative spondylolisthesis contributes inferior and superior facet bony masses to narrow the space available to the cauda equina (Fig. 12-8). Finally, annular bulging, with or without retrospondylolisthesis, contributes to anterior narrowing of the canal.

In the second story, the anterior canal wall is formed by the inferior half of the vertebral body, which does not contribute to spinal stenosis. The one place in the second story where stenosis is said to occur is the very midline and posterior common meeting point of the superior edges of the lamina and spinous process (Fig. 12-9). This cortical edge can be likened to the wishbone of a chicken and is said to encroach on the midline of the dura at the junction of the second and third stories. But look at Figure 12-9B, this is the second story of Figure 12-7B and there is no stenosis.

The lateral portion of the second story is the foramen. As mentioned previously, superior capsular hypertrophy, especially in degenerative spondylolisthesis, can protrude into this lateral recess/foraminal interval, producing radicular symptoms due to root encroachment in the lateral zone (Fig. 12-10).

Within the third story, there is virtually nothing that can cause acquired spinal stenosis. At the top end of the pedicle (third story) lies the bottom end of the superior facet. If it is hypertrophied, then lateral zone stenosis (subarticular form) can occur, but virtually nothing in the lower portion of the third story of an anatomic segment can contribute to central canal stenosis.

Translation

When one anatomic segment translates on the next, a guillotining effect of the spinal canal occurs. The most common type of translation is degenerative spondylolisthesis, a forward or lateral slip of one anatomic segment on the next. Because of the intact neural arch, it has often been stated that the posterior elements of the cephalad segment impinge on the contents of the spinal canal (Fig. 12-11), when, in fact, the major lesion is still the ligamentum flavum and the facet joints. Lateral spondylolisthesis (Fig. 12-12) has the same effect on the space occupied by the cauda equina. Retrospondylolisthesis or posterior translation impinges least on the space occupied by the cauda equina except that it is usually part of the degenerative changes previously listed (Fig. 12-13).

Congenital/Developmental Narrowing of the Spinal Canal

The vertebral canal reaches its maximum size by 4 years of age. Thereafter, pedicles/vertebral bodies increase in size and the canal may change its shape, but the overall size of the canal changes little. Intrauterine factors such as

infectious diseases and malnutrition may potentially reduce canal size and result in a congenitally narrow canal. Because congenital/developmental stenosis is so prevalent among men of large stature (e.g., the front line of football players), one has to wonder if spurts in vertical height before the age of four somehow reduce the cross-sectional area of the spinal canal. The analogy is a sausage tube held up by one hand maintains its maximal diameter, but when stretched fully by two hands (Fig. 12-14) quickly narrows in diameter. Whatever the insult, the spinal canal can be left in a narrowed state, vulnerable to isolated traumatic events or cumulative trauma causing degenerative changes, which leads to symptomatic SCS (Fig. 12-15).

FIGURE 12-7. A: CT of spinal canal stenosis. The stenotic lesion is greatest in first story of L4 (bottom left). The third and second story of L4 (top) and the second story of L5 (bottom, right) are relatively free of stenosis. B: Sagittal MRI showing a similar picture. Spinal canal stenosis is a lesion in the first and upper reaches of the adjacent third story, produced largely by the buckling of the ligamentum flavum from behind (arrow). C: Axial T1 MRI showing encroachment on space available for cauda equina (arrow) by hypertrophied ligamentum flavum and facet joints.

FIGURE 12-8. Another example of spinal canal stenosis on T1 axial showing the two margins of the posterior vertebral body (arrows) of the “slip” and the ligamentum flavum hypertrophy (open arrow) and facet joint hypertrophy (curved arrow).

FIGURE 12-9. A: The wishbone effect. It seems to be present at surgery, yet so rarely seen on CT or MRI. B: An axial T1 MRI to show the wishbone (arrows); the junction of the spinous process and two lamina. This is an example of a degenerative spondylolisthesis (Figs. 12-2 and 12-3), with no stenosis at the “wishbone.”

FIGURE 12-10. A: Schematic showing effect of capsular encroachment on foraminal zone (B), and medial edge facet hypertrophy on the subarticular zone (A). B: MRI showing actual lesion.

FIGURE 12-11. A: The wishbone effect. It seems to be present at surgery, yet so rarely seen on CT or MRI. B: The so-called guillotining effect on the cauda equina of one posterior arch sliding over its mate. Hatched area is space left for cauda equina.

FIGURE 12-12. Radiograph of a lateral spondylolisthesis (arrow) at the apex of a degenerative scoliosis.

FIGURE 12-13. A retrospondylolisthesis on plain radiograph at L4-L5 (arrows point to the respective corners of the vertebral bodies). Note how L4 is posterior to L5.

Dimension of the Normal Spinal Canal

Porter (24) has done considerable work in measuring the normal lumbar spinal canal. The bony dimensions are fairly constant from L1 to L5 and are listed in Table 12-2.

Measurements in Spinal Canal Stenosis

Verbiest (31) made a major contribution to our knowledge of how much the canal narrows in patients with spinal stenosis. Careful intraoperative measurements (at the level of the disc space, i.e., first story) led him to identify three degrees of canal stenosis: no stenosis, relative stenosis, and absolute canal stenosis. Absolute SCS occurs when a sagittal diameter of less than 10 mm is noted. In a normal canal, the sagittal diameter is
greater than 12 mm and may range up to 20 to 25 mm at L5-S1, normally the largest section of the spinal canal. The normal large diameters at L5-S1 contribute to the fact that SCS is rare at L5-S1 and is the reason why surgical decompression of the L5-S1 segment is so rarely indicated. Relative spinal stenosis occurs when the sagittal diameter is between 10 and 12 mm. Many attempts have been made to relate Verbiest’s intraoperative measurements to plain radiographic films, all with limited success. Measurements applied to anteroposterior (AP) and lateral myelograms, axial computed tomography (CT) scans, and magnetic resonance imaging (MRI) are a better indication of the extent of stenosis (22). Spengler’s group (27), (in a CT scan study), took into account soft tissue encroachment on the spinal canal, to conclude that the space available for the cauda equina should be measured as an area rather than a diameter. An area less than 100 mm² is considered to be indicative of relative spinal stenosis and a cross-sectional area of less than 65 to 70 mm² is indicative of absolute stenosis. As more MRIs are studied, further understanding of the anthropometric aspects of SCS will follow. The use of CT and MRI to reveal both bony and soft tissue encroachment on the space available for the cauda equina have largely made spinal canal measurements obsolete (30).

FIGURE 12-14. In trying to understand congenital stenosis, think of the unstretched sausage tube (left) being stretched through sudden growth (right).

FIGURE 12-15. An example of congenital (global) spinal canal stenosis and an HNP (arrow) that precipitated the patient into a symptomatic state.

Neuropathology

Obviously, narrowing of the spinal canal constricts the dura and cauda equina within. The nerve roots themselves are constricted and often become adherent due to arachnoid changes. In a histologic examination of the roots, Watanabe and Parke (32) found a reduction in the number of
neurons, especially affecting large-caliber fibers. There were varying degrees of degeneration and demyelination with regeneration of nerve tissue. Morphologic assessment of the vessels revealed that the arterioles were absent at the level of the constriction and more coiled on either side of the constriction. Venules were collapsed at the level of the lesion and engorged proximally, and there appeared to be more arterial venous shunts proximal to the stenotic lesion.

TABLE 12-2 Dimensions of the Spinal Canal (Midpedicle Level)

Midpedicle Level	Sagittal (mm)	Corona (interpedicle) (mm)
L1	16	22
L2	15	22
L3	14	23
L4	13	23
L5	14	24

FIGURE 12-16. A synovial cyst (arrow) at a very low grade “slip” L4-L5 contributing to some spinal canal stenosis. Gadolinium enhancement clearly outlines the cyst on axial T1 (top right). The bottom right is a T2 sagittal highlighting the “water” in the cyst.

Synovial cysts are reasonably common in SCS (Fig. 12-16). They arise as outpouchings from the degenerative (synarthrodial) facet joint, and if they enlarge into the canal they may further compress a nerve root. They often become very adherent to the dura and can be difficult to excise because of this.

Pathophysiology

SCS is a chronic rather than an acute compression of the nerve roots in the cauda equina. Although the cauda equina is often considered a peripheral nerve structure, its coverings and vascular anatomy are more like those of a central nervous system structure than those of a peripheral nerve, which makes them more susceptible to compression.

Compression of the cauda equina affects nerve conduction, resulting in the leg symptoms, with it likely that aging nerves are more susceptible to this compressive phenomenon. It is well known that the symptoms of spinal stenosis are exacerbated by activity, specifically involving extension of the back. Thus, any theory to explain the symptoms of spinal stenosis must account for this mechanical component. It is likely that symptoms are caused by a combination of mechanical and ischemic nutritional factors (8,24

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