The Lumbar Region

Clinical Considerations

Certain individuals develop a painful degenerative lumbar kyphosis that is characterized by disc and vertebral body wedging and weakness of lumbar paraspinal muscles. This condition may be related to a prolonged working posture in flexion. For example, a higher incidence of this condition has been found in Japanese dairy farmers when compared with Japanese field farmers. The working posture of the former group calls for long periods of forward flexion while squatting. This posture is maintained for the majority of each working day throughout the workers’ careers, which can last for many decades (Takemitsu et al., 1988). Such prolonged flexion is thought to cause remodeling of the vertebral bodies of the lumbar region so that they are shorter anteriorly than posteriorly.

The lumbar lordosis is often significantly increased in achondroplasia. This can lead to a marked compensatory thoracic (thoracolumbar) kyphosis, which can be severe in some cases (Giglio et al., 1988).

A high incidence of scoliosis (64%) exists in the lumbar region of individuals with Marfan syndrome. Other lumbar vertebral anomalies associated with Marfan syndrome include a high incidence of transitional lumbosacral segments (18%), concavity of both the superior and inferior aspects of the vertebral bodies (biconcavity), and longer than normal transverse processes (Tallroth et al., 1995).

Clinical Considerations

Osteophytes of the lumbar vertebral bodies can be large. They are much more prominent laterally than anteriorly (the opposite of what is commonly found in the thoracic region), and usually they are completely absent anteriorly at the L3-4 and L4-5 levels. This seems to be associated with the pulsing action of the abdominal aorta and proximal portions of the common iliac arteries (Edelson & Nathan, 1988).

Fractures of the secondary centers of ossification associated with the superior and inferior vertebral end plates, the ring apophyses (also known as anular apophyses; see Chapters 2 and 12), have been reported. These fractures are rare but occur most frequently during adolescence. The signs and symptoms of apophyseal ring fractures resemble those of IVD protrusions. Such fractures may be unnoticed on conventional x-ray films. Sagittally reformatted computed tomography (CT) is currently the imaging modality that shows these fractures to best advantage (Thiel, Clements, & Cassidy, 1992).

Accessory Processes

The accessory processes are unique to the lumbar spine. Each accessory process projects posteriorly from the junction of the posterior and inferior aspect of the TP with the corresponding lamina. These processes serve as attachment sites for the longissimus thoracis muscles (lumbar fibers) and the medial intertransversarii lumborum muscles (Standring et al., 2008). (See Figure 4-5, B, for the attachment of the medial intertransversarii lumborum muscles to the accessory processes.)

Superior Articular Processes

Left and right superior articular processes are formed on every vertebrae of the lumbar spine (see Fig. 7-2). Each superior articular process possesses a hyaline cartilage–lined superior articular facet that is oriented in a vertical plane. That is, these facets are not angled to the vertical plane like the superior articular facets of the cervical and thoracic regions.

All the lumbar superior articular facets face posteriorly and medially. The articular surface of a typical superior articular facet can be gently curved with the concavity facing medially (Figs. 7-3 and 7-4), or the articular surface can be angled abruptly. When the articular surface is angled abruptly, two relatively distinct articulating surfaces are formed. One surface faces posteriorly and forms almost a 90-degree angle with the second surface, which faces medially. As with the curved facet, the concavity faces posteriorly and medially. In either case (curved or angled articular surface), the shape conforms to the inferior articular facet of the vertebra above. The hyaline cartilage of the central region of the superior articular facet (the area of greatest concavity) increases in thickness with age, probably because this region receives much of the load during flexion of the spine (Taylor & Twomey, 1986). Also, the articular processes may fracture as a result of age-related degeneration (Kirkaldy-Willis et al., 1978).

The orientation of the superior articular facets varies from one vertebral level to another (see Fig. 7-4). A line passed across each superior articular facet, on transverse CT scans, shows that the L4 superior facets (and therefore the L3-4 Z joints) are more sagittally oriented than the L5 facets. Also, the S1 superior facets (and therefore the L5-S1 Z joints) are more coronally oriented than the L4 and L5 facets (Van Schaik, Verbiest, & Van Schaik, 1985). (See Zygapophysial Joints for further detail on the orientation of the superior and inferior articular facets.) The angle of the L4-L5 Z joint (i.e., the angle of the superior articular facets) has been found to become more sagittally oriented with age, which may explain the higher incidence of degenerative spondylolisthesis (forward slippage of L4 on L5) at this level in individuals more than 60 years of age (Wang & Yang, 2009). The left and right articular facets are usually symmetrical in orientation (unlike the thoracic facets) (Masharawi et al., 2004) with the exception of the facets that form the L5-S1 articulation where left to right asymmetry (tropism) occurs rather frequently. However, the right facets of L1-L4 are slightly longer from superior to inferior than the left facets (Masharawi et al., 2005).

The mamillary processes (see Fig. 7-2), which project posteriorly from the superior articular processes of lumbar vertebrae, are unique to the lumbar spine. Each mamillary process is a small rounded mound of variable size. Some are almost indistinguishable, whereas others are relatively prominent. The mamillary processes serve as attachment sites for the multifidi lumborum muscles.

Mamillo-Accessory Ligament

A mamillo-accessory ligament (Bogduk, 1981; Lippitt, 1984) is found between the mamillary and accessory processes on the left and right sides of each lumbar vertebra. Occasionally one or more of these ligaments may ossify in the lower lumbar levels (L3-5). The incidence of ossification increases in frequency from L3 to L5. Ossification of these ligaments at L5 occurs at a frequency of 10% (Bogduk, 1981) to 26% (Maigne, Maigne, & Guervin-Surville, 1991). Maigne and colleagues (1991) studied 203 lumbar spines and found that ossification of this ligament at L5 occurred twice as often on the left. They offered no reason to explain why the ligament ossified more frequently on this side. However, they believed the ossification was the result of osteoarthritis, because they found no evidence of ossification on the spines of children and young adults. These authors also stated that an ossified mamillo-accessory ligament could occasionally be seen on standard lumbar x-ray films.

The mamillo-accessory ligament has been described as a tough, fibrous band that may represent tendinous fibers of origin of the lumbar multifidi muscles or fibers of insertion of the longissimus thoracis pars lumborum muscle (Bogduk, 1981). Regardless of its precise structure, the reported purpose of the mamillo-accessory “ligament” is to hold the medial branch of the dorsal ramus of the above spinal nerve (e.g., the L2 medial branch is associated with the L3 mamillo-accessory ligament) against (a) the bone between the base of the superior articular process and the base of the transverse process and (b) the Z joint, which is slightly more medial (Fig. 7-5). The medial branch of the dorsal ramus gives off articular branches to the capsule of the Z joint as it passes deep to the mamillo-accessory ligament. The medial branch then continues medially across the vertebral lamina to reach the multifidus muscle (Bogduk, 1981). Therefore the medial branch of the dorsal ramus (posterior primary division) is held within a small osteofibrous canal along the posterior arch of a lumbar vertebra. The medial branch could possibly become irritated or even entrapped within this tunnel, which would result in low back pain. However, more investigation is necessary to determine if such irritation or entrapment occurs and, if so, its frequency (Bogduk, 1981; Maigne, Maigne, & Guerin-Surville, 1991).

Inferior Articular Processes

The inferior articular processes of lumbar vertebrae are convex anteriorly and laterally. They possess inferior articular facets that cover their anterolateral surface. As with the superior articular facets, the inferior ones vary in shape. Even though articular processes vary from one vertebral level to another, and even from one side to another, superior and inferior articulating processes of one Z joint conform to one another. This conformation is such that each inferior articular facet usually fits remarkably well into the posterior and medial concavity of the adjoining superior articular facet. The exception to this is that the inferior articular processes and their facets are less vertically oriented and angle slightly anteriorly to the frontal plane. This orientation (“disharmony” with the superior articular processes) likely enhances motion of the lumbar region (Masharawi et al., 2004).

General Considerations

The Z joints have been positively identified as a source of back pain (Mooney & Robertson, 1976; Yamashita et al., 1990; Bogduk, 1992; Dreyfuss & Dreyer, 2001). In addition, Rauschning (1987) states that these joints “display typical degenerative and reparative changes which are known to cause osteoarthritic pain in peripheral synovial joints.” Therefore the lumbar Z joints are highly significant clinically. Because these joints are discussed in detail in Chapter 2, this section focuses on the unique and clinically significant aspects of the lumbar Z joints.

The lumbar Z joints are considered to be complex synovial joints oriented in the vertical plane (Standring et al., 2008). They are fashioned according to the shape of the superior and inferior articular facets (see previous discussion). Therefore the lumbar Z joints are concave posteriorly and even have been described as being biplanar in orientation (Taylor & Twomey, 1986). That is, they have a coronally oriented, posterior-facing, anteromedial component and a large, sagittally oriented, medial-facing, posterolateral component. Taylor and Twomey (1986) state that the lumbar Z joints are coronally oriented in children and that the large sagittal component develops as the individual matures. The sagittal component limits rotation, whereas the coronal component limits flexion. More specifically, the shape of the lumbar Z joints allows a large amount of flexion to occur in the lumbar region, yet the size of the lumbar Z joints is what eventually limits flexion at the end of the normal range of motion. Therefore the long contact surfaces between the coronal component of the superior articular processes and the adjacent inferior articular processes finally limit flexion by “restraining the forward translational component of flexion” (Taylor & Twomey, 1986).

Even though the size of the Z joints eventually limits flexion, approximately 60 degrees of flexion is able to occur in the lumbar region before the bony restraints of the lumbar articular processes prevent further movement. However, the size and shape of the Z joints dramatically limit rotation. By limiting rotation, the Z joints protect the IVDs from rotational injury. During rotation of the lumbar region, distraction (or gapping) occurs between adjacent lumbar articular facets (superior facet of vertebra below and inferior facet of vertebra above) on the side of rotation. For example, right rotation results in gapping of the facets on the right side. Also during rotation, the two opposing facets of the opposite side are pressed together. This causes them to act as a fulcrum for the distracting facets on the side of rotation (Paris, 1983; Cramer et al., 2003). Side posture spinal adjusting, performed by chiropractors and other health practitioners, also causes gapping of the Z joints. The gapping action produced by such adjustive procedures is thought to break-up fibrous adhesions that develop in Z joints that are moving less than normal (are hypomobile) (Cramer et al., 2000, 2002, 2003, 2010).

Extension of the lumbar region is limited by the inferior articular process on each side of a lumbar vertebra contacting the junction between the lamina and superior articular process of the vertebra below. This junction between the lamina and superior articular process is known as the pars interarticularis.

Variation of Zygapophysial Joint Size and Shape

A considerable degree of variation exists between individual Z joints at different lumbar levels and between the left and right Z joints at the same vertebral level. The shapes range from a slight and gentle curve, concave posteriorly; to a pronounced, dramatic, and posteriorly concave curve; and in some cases to a joint in which the posterior and medial components face one another at an angle of nearly 90 degrees. Generally, the Z joints of the upper lumbar levels are more sagittally oriented than those of the lower lumbar levels (see Fig. 7-4). This makes the lower lumbar joints more susceptible to recurrent rotational strain (Kirkaldy-Willis et al., 1978). However, Z joint osteoarthritis is more prevalent in lower lumbar (L3-L4, L4-L5, and L5-S1) Z joints (particularly at L4-L5) when they are more sagittally oriented (Kalichman et al., 2009).

Biomechanical Considerations

The articular facets do not absorb any of the compressive forces of the spine when humans are sitting erect or standing in a slightly flexed posture. The IVD and vertebral bodies absorb almost all the compressive loads under these conditions. However, when a person stands erect (slight extension), the facets resist approximately 16% (range, 3% to 25%) of the compressive forces between vertebrae. Disc degeneration may lead to increased stress on the Z joints, causing them to resist up to approximately 47% of the loads. This results in pain, not from the articular cartilage, but usually from pressure on the subchondral bone of the articular processes, entrapment of soft tissue between the articular facets, or added strain on the articular capsules (Dunlop, Adams, & Hutton, 1984; Yang & King, 1984; Hutton, 1990). In addition, beyond the limit of normal physiologic flexion, the inferior articular process is forced over the superior articular process, and the compressive loads carried by the facets again increase from those carried in the neutral position (Shirazi-Adl & Drouin, 1987).

The superior and inferior articular processes of the Z joints also resist anterior shear forces. The articular processes carry approximately one third of the anterior shear forces during forward flexion, whereas the IVDs carry approximately two thirds of the shear loads (when the load is applied suddenly). However, because of the viscoelasticity of the IVD, if a shear load is applied slowly, the vertebra above creeps further forward than when shear loads are applied rapidly. Thus the shear forces on the articular processes are increased with slowly applied and long-lasting loads in forward flexion (e.g., bending forward for long periods to weed a garden).

Articular Capsules

An articular capsule covers the posterior aspect of each lumbar Z joint (see Fig. 7-5), and the ligamentum flavum covers the anteromedial aspect of the Z joint. The articular capsule is tough, possesses a rich sensory innervation, and is well vascularized (Giles & Taylor, 1987; Ashton et al., 1992).

The bundles of collagen fibers that form the thick outer fibrous layer of a typical lumbar Z joint capsule are oriented in different directions, depending on whether the fibers are located in the superior, middle, or inferior aspect of the capsule. The superior fibers attach laterally to the groove that is located between the mamillary process and posterior ridge of the superior articular process. From here the fibers of the superior capsule course medially across the superior joint recess, attaching to the medial aspect of the laminae of the superior-most vertebrae forming the Z joint. Fibers of the middle part of the Z joint capsule course more horizontally (lateral to medial), beginning from their attachment to the posterior aspect of the mamillary process (on the posterior aspect of the superior articular process) (Yamashita et al., 1996). These fibers then cross the Z joint gap and attach to the medial part of the lamina of the suprajacent vertebra. The fibers just described extend a considerable distance medially and become continuous with the lateral fibers of the interspinous ligament. Finally, the fibers of the more inferior aspect of the capsule course from superomedial to inferolateral, covering the joint space and the inferior end of the inferior Z joint recess. The superomedial fibers attach to the medial and inferior part of the lamina. The bundles of collagen fibers of this inferior aspect of the capsule are longer and thicker than those of the superior aspect of the capsule (Yamashita et al., 1996).

The orientation of the fibers within the tough outer layer of the capsule helps to limit forward flexion (Paris, 1983). The medial-to-lateral arrangement of the fibers in the central part of the Z joint may tend to stabilize the joint during axial rotation, while allowing movement in flexion and extension (Yamashita et al., 1996). The contribution of the lumbar Z joint capsule in stabilizing and perhaps even in helping to limit motion during axial rotation also has been supported by biochemical studies that show evidence of increased capsular resistance to tension in regions of the capsule that would receive the greatest stretch during this motion (Boszczyk et al., 2001). The collagen fibers of the superior and middle aspects of the Z joint are shorter than those of the inferior aspect of the capsule and are thought to be under more tensile stretch than the inferior aspect of the capsule. The posterosuperomedial-most corner of the capsule (just inferior to the superior Z joint recess) is thought to be the area of the capsule that receives the highest tensile stretch (Yamashita et al., 1996). In fact, Yamashita and colleagues (1996) stated that the lumbar Z joint capsules undergo “extensive stretch under physiological loads.”

The collagen fibers of the inferior aspect of the lumbar Z joint capsules are thicker and more heavily innervated than those found in the superior and middle aspects of the capsules. This may be because the inferior aspects of the capsule can be compressed (therefore requiring increased thickness), and even pinched (thus resulting in pain from additional nociceptive nerve endings), during full extension of the lumbar region (Yamashita et al., 1996).

Laterally, fibers of each articular capsule frequently are continuous with the articular cartilage lining the superior articular facet. A gradual transition occurs from the fibrous tissue of the capsule to fibrocartilage and finally to the hyaline cartilage of the superior articular facet (Taylor & Twomey, 1986).

Each capsule has a relatively large superior and inferior recess that extends away from the joint. The capsular fibers (or fibers of the ligamentum flavum, anteriorly) surrounding these recesses are relatively thin and loose, and there may be openings through which neurovascular bundles enter the recesses (Taylor & Twomey, 1986). Paris (1983) states that effusion within the Z joint may enter the superior recess and as little as 0.5 ml of effusion may cause the superior recess to enter the anteriorly located IVF. Once in the IVF, this expanded superior capsular recess may compress the dorsal root ganglion or the exiting spinal nerve, resulting in radiculopathy (see Chapter 11 for a full discussion of radiculopathy). Such a distinct protrusion of the superior recess of the Z joint capsule constitutes an example of a large Z joint synovial cyst (Xu et al., 1991; Bougie, Franco, & Segil, 1996).

Xu and colleagues (1991), in a study of 50 pairs of lumbar Z joints from an elderly population, found that the capsules varied greatly in thickness and regularity. They found that the capsules were “irregularly thickened, amorphous, and calcified in 22 cases.” In addition, they found that in most subjects the synovium of the joint space extended 1 to 2 mm outside the boundaries of the joint in one or more locations. These synovial extensions, which could be considered to be small synovial cysts, maintained communication with the joint space, and were found on both the anterior and posterior aspects of the joint. Anteriorly the spaces most often extended along the posterior border of the ligamentum flavum (64% of Z joints). Sometimes a synovial joint extension extended directly into the ligamentum flavum (8% of cases). Posteriorly the synovial cysts usually extended either laterally along the superior articular process (7% of cases) or medially along the inferior articular process (29%). Extensions were found on both the inferior and superior articular processes in 41% of the Z joints, and no synovial extensions were found in 23% (7% of individuals) of the Z joints. Xu and colleagues (1991) believed that the synovial joint extensions (synovial cysts) probably were more common in the older population (e.g., the specimens in their study) than in younger age groups. They stated that their findings may explain why Z joint arthrography (visualization of the Z joint on x-rays after injection with radiopaque dye) could be successful even when the joint space was not entered with the injecting needle (i.e., the needle could enter a synovial extension).

In another study, Xu, Haughton, and Carrera (1990) visualized the synovial joint extensions (cysts) with magnetic resonance imaging (MRI). Their positive identification of these synovial joint extensions was aided with the injection of paramagnetic contrast medium (gadodiamide, Winthrop Pharmaceuticals). Their imaging was performed on dissected spines using small surface coils, long acquisition times, and thin slice thicknesses. Therefore clear delineation of these extensions is probably still beyond the resolving capabilities of MRI scans obtained in a typical clinical setting. However, Xu and colleagues (1991) thought their results helped to explain the variable appearance of the facet joints on MRI scans. They stated that “the inhomogeneity detected at MR imaging and computerized tomography in the ligamentum flavum near the facet joint most likely represents extension of the joint capsule between the ligamentum flavum and the articular processes…” (Xu et al., 1991).

The superior and inferior recesses are filled with fibrofatty pads. These pads are well vascularized and are lined with a synovial membrane. They also protrude a significant distance into the superior and inferior aspects of the Z joint. Engel and Bogduk (1982) state that adipose tissue pads probably develop from undifferentiated mesenchyme of the embryologic Z joint. Furthermore, they note that in certain instances, mechanical stress to the joint may cause an adipose tissue pad to undergo fibrous metaplasia, which results in the formation of a large fibroadipose meniscoid (an adipose tissue pad with a fibrous tip composed of dense connective tissue, to be differentiated from the normal synovial folds described in Ch 2). The authors believed that both the adipose tissue pads and the normally found synovial folds, or meniscoids, “play some form of normal functional role” (see Fig. 7-5).

In addition, “fringes” of synovium extend from the capsule to the region between the articular facets. These fringes fill the small region in which the facets do not form a complete union.

Sometimes a fatty synovial fold develops a relatively long fibrous tip that extends a considerable distance between the joint surfaces, where it may become compressed (Taylor & Twomey, 1986). Such protruding synovial folds (again, different from the normal synovial folds) have been associated with the early stages of degeneration (Rauschning, 1987). Rauschning (1987) typically found hemarthrosis and effusion into the Z joints when the meniscal folds of this type were torn or “nipped” between the joint surfaces.

Occasionally the aging process causes a piece of articular cartilage to break from the superior or inferior articular facet. The piece usually breaks along the posterior aspect of the Z joint, parallel to the joint space. However, the attachment to the articular capsule usually is maintained. The result is the presence of a large, fibrocartilaginous meniscoid inclusion within the joint. Taylor and Twomey (1986) reported that the formation of this type of meniscoid is partially caused by the regular pulling action on the posterior articular capsule by the multifidi muscles that originate from these capsules. The attachment of the capsule to the periphery of the articular cartilage may then result in the cartilage tears found to run parallel with the joint surface. Again, the torn cartilage fragment is capable of developing into a Z joint meniscoid, which can become interposed between the two surfaces of the joint. The authors also noted that the posterior aspect of the Z joint may open when the multifidi and other deep back muscles relax, allowing the meniscoids and other joint inclusions to bow into the joint space and become entrapped (Kos, Hert, & Sevcik, 2002). The result of this type of entrapment could be (a) loss of motion (locked back), resulting from the cartilage being lodged between two opposing joint surfaces; (b) pain, because the meniscoids remain attached and therefore might put traction on the pain-sensitive joint capsule; or (c) both decreased motion and pain.

As described in Chapter 2, the Z joint articular capsule receives sensory innervation from the medial branch of the posterior primary division of three consecutive spinal nerves. The sensory receptors in the Z joint capsule are both free nerve endings (for nociception) and mechanoreceptors (for proprioception). Consequently, the Z joint capsules not only are potential sources of low back pain (i.e., are potential “pain generators”) but also are likely to play a role in lumbar proprioception (Ianuzzi, Pickar, & Khalsa, 2011). Using nerve tracing techniques in rats, Suseki and colleagues (1997) found that some sensory neurons innervating the lower lumbar Z joint capsules arise from the L1 and L2 dorsal root ganglia. These sensory fibers course through the lumbar sympathetic chain and then through gray communicating rami to reach the lower lumbar Z joints. These authors felt that this innervation of lower lumbar spinal tissues by sensory nerves arising from upper lumbar dorsal root ganglia might help to explain the clinical finding that pathology of lower lumbar spinal tissues sometimes can be described by patients as referring to regions innervated by higher lumbar segments (e.g., radiation into the inguinal region from a painful L5-S1 Z joint).

The pain-sensitive articular capsule and the synovial lining of the ligamentum flavum of each lumbar Z joint normally are held out of the joint by three structures. First, the multifidus lumborum muscles take part of their origin (several originate from each vertebra) from the posterior aspect of each articular capsule (Taylor & Twomey, 1986). These muscles pull the capsule out of the joint’s posterior aspect. Second, the ligamentum flavum pulls the synovium out of the joint’s anterior aspect. Third, when the joint surfaces are compressed, the Z joint synovial folds push the capsule out of the joint (Paris, 1983). If either of the two mechanisms associated with the articular capsule fails to function properly, the result could be painful pinching of the capsule, with subsequent acute low back pain and muscle tightness (spasm).

In addition, recall that the Z joint folds possess nociceptive fibers (Giles, 1987, 1988; Giles & Taylor, 1987). Consequently, entrapment within a Z joint of these innervated folds may be a primary source of back pain and muscle tightness (spasm) even without traction of the capsule. Chapter 2 describes Z joint synovial folds and other Z joint inclusions in further detail.

Narrowing of the IVD space results in increased pressure on the articulating surfaces of the Z joint. This pressure is further increased with extension of the lumbar region. Disc space narrowing also causes or increases the severity of impingement of synovial folds. Therefore increased pressure on the subchondral bone of the articular processes and increased impingement of articular tissues (soft tissue “nipped” between the facets) may be two causes of back pain in patients with decreased height of one or more IVDs (Dunlop, Adams, & Hutton, 1984).

Zygapophysial Joint Degeneration

A strong correlation has been found between increasing age and degeneration of the Z joints (Peterson, Boulton, & Wood, 2000). Kirkaldy-Willis and colleagues (1978) stated that such changes include inflammatory reaction of the synovial lining of the Z joint, changes of the articular cartilage, development of loose bodies in the Z joint, and laxity of the joint capsule. All these result in joint instability. Changes of the Z joints (left and right) of any given vertebral level frequently are accompanied by degenerative changes in the IVD of the same level (Kirkaldy-Willis et al., 1978; Peterson, Boulton, & Wood, 2000). Disc degeneration leads to increased rotational instability of the Z joints, resulting in further degeneration of these structures. This process of degenerative changes of the IVDs leading to degeneration of the Z joints also has been supported with computer models of spine function (Goel et al., 1993). The Z joint degenerative changes usually take the form of increased bone formation (e.g., arthrosis, spur formation), which can compress the exiting spinal nerve (Epstein et al., 1973; Rauschning, 1987). Much less frequently, degenerative change manifests as erosion of the superior articular process (Kirkaldy-Willis et al., 1978). This can lead to degenerative spondylolisthesis. Figure 7-6 shows the process of Z joint and disc degeneration and the interrelation between the two.

Individuals with low back pain secondary to trauma have been found to have more advanced degeneration of the Z joints than low back pain patients who do not experience trauma, although no difference between pain and disability has been found between these two groups of patients. In addition, as low back pain increases, the number of lumbar Z joints showing signs of degeneration and the severity of the degeneration also increase (Peterson, Boulton, & Wood, 2000).

The articular cartilage lining of the lumbar Z joints usually become irregular with age (Taylor & Twomey, 1986). The cartilage of the posterior aspect of the joint frequently is worn thin or even may be completely absent. The articular cartilage of the anterior aspect of the joint usually remains thick but may show many fissures (known as cartilaginous fibrillation) that extend from the articular surface of the cartilage deep to the attachment of the cartilage to the subchondral bone. These types of articular cartilage changes often are more pronounced at the most superior and inferior aspects of the joint (Taylor & Twomey, 1986).

As mentioned, osteophytes (or bony spurs) often develop with age on the superior and inferior articular processes. Frequently this occurs along the periphery of the Z joint along the attachment sites of the ligamentum flavum or the articular capsule. The osteophytes most often develop at the attachment site of the ligamentum flavum on the anteromedial aspect of the superior articular process and extend into the posterolateral aspect of the vertebral canal and also into the IVF. Taylor and Twomey (1986) found that fat-filled synovial pads developed in the region of osteophytes associated with the Z joints. These pads formed a cushion between the osteophytes and inferior articular process. The authors also occasionally found that a prominent pad had developed within the inferior recess of the Z joint. This pad was found to lie between the tip of the inferior articular process and the lamina at the base of the subjacent vertebra’s superior articular process. This is where the inferior articular process contacts the lamina during extension of the lumbar spine. This fat pad often was found to become thickened and sclerotic with age, probably in response to the mechanical stimulation of the inferior articular process.

Pars Interarticularis

The region of the lumbar lamina located between the superior and inferior articular processes is known as the pars interarticularis. This region can be fractured rather easily, a condition known as spondylolysis. As mentioned, at the levels of L4 and L5 loads probably are transferred from the vertebral bodies to the pars interarticularis by means of the pedicles. As the trabeculae in the L4 and L5 pedicles pass posteriorly, they are most highly concentrated where they extend into the pars interarticularis. Because trabeculae develop along the lines of greatest stress, the trabecular arrangement leading to the pars interarticularis of the L4 and L5 pedicles has been used to explain the frequency of spondylolysis at these levels.

As a result of bilateral spondylolysis, the vertebral body, pedicles, TPs, and superior articular processes can displace anteriorly. This anterior displacement is known as spondylolisthesis. Spondylolysis and spondylolisthesis are most common at L5. However, they may occur at any lumbar level. (The subsection entitled Spondylolysis and Spondylolisthesis of the section Fifth Lumbar Vertebra found later in this chapter describes these conditions in more detail.)

General Considerations

The vertebral foramina in the lumbar region generally are triangular in shape, although they are somewhat more rounded in the upper lumbar vertebrae and more triangular, or trefoil, in the lower lumbar vertebrae. The triangular shape of the vertebral foramina of the middle and lower lumbar vertebrae is reminiscent of the shape of these openings in the cervical region; however, the lumbar foramina are smaller than those of the cervical region. On the other hand, the lumbar vertebral foramina are larger and more triangular than the rounded foramina of the thoracic region.

The maximum midsagittal diameter in the horizontal plane of the lumbar vertebral foramina is reached by the age of 4 years. Therefore if development is delayed in early childhood, “catch-up growth” does not occur for this dimension. However, the distance between the pedicles (interpedicular distance) increases until adulthood. Thus the lumbosacral vertebral canal becomes more trefoil in appearance with age, reaching its adult dimensions in the early to mid-twenties (Papp, Porter, & Aspden, 1994).

The size of the lumbar vertebral canal ranges from 12 to 20 mm in its anteroposterior dimension at the midsagittal plane. The transverse diameter ranges from 18 to 27 mm, and averages 23.2 to 24.4 mm (Dommisse & Louw, 1990; Ebraheim et al., 1997b). Flexion of the lumbar region significantly increases the size of the vertebral canal at the level of the IVDs (both cross-sectional area and midsagittal diameter) and lumbar extension significantly decreases canal size (Inufusa et al., 1996; Schmid et al., 1999; Madsen et al., 2008). Stenosis has been defined as a narrowing below the lowest value of the range of normal (Dommisse & Louw, 1990). Because of the clinical significance of the vertebral canal, Table 7-3 has been included as a ready source of the dimensions of this region. However, care must be taken when using published values of morphometric measurements of anatomic structures to make clinical decisions. For example, the midsagittal diameter of the vertebral foramina is smaller in Asians than in Europeans or North Americans (You-Lu & Wu, 1988; Lee et al., 1995).

Lumbar epidural adipose tissue has been found to be histologically different from adipose tissue in other regions of the body (e.g., subcutaneous adipose tissue). Epidural fat is less solid than subcutaneous fat. The adipocytes are almost identical in size and shape throughout epidural adipose tissue. In addition, epidural adipose tissue has less connective tissue within it and the connective tissue present forms “gliding planes” separated by distinct “slits.” The adipocytes of subcutaneous fat are irregular and varied in shape, there is much more connective tissue, and no gliding planes separated by slits are found. The epidural fat in fetuses completely surrounds the dura mater and is evenly distributed from superior to inferior in the lumbar vertebral canal. However, in the adult spine, the lumbar epidural fat is found almost exclusively along the posterior aspect of the dura mater and is most prominent at the level of the IVDs. The epidural fat is isolated into these “pads” by thin connective tissue membranes that are located on the anterior surface of the adipose tissue. These thin connective tissue membranes lie against the posterior surface of the spinal dura mater, and attach laterally to the lateral aspects of the left and right ligamenta flava and intervertebral foramina, and attach superiorly and inferiorly to the suprajacent and subjacent laminae, respectively. Each adipose tissue pad is connected by a small connective tissue pedicle to the posterior midline. Therefore in horizontal section, the pads are triangular in shape with their apex pointing posteriorly and their base resting anteriorly against the posterior spinal dura mater. The size (volume) of the pads increases from the L1-2 to the L4-5 level. These anatomic features suggest a functional role of the epidural adipose tissue—a role designed to aid in the smooth passage of the dura mater during flexion and extension movements across the bony and ligamentous structures of the posterior aspect of the vertebral canal (Beaujeux et al., 1997).

It should be recalled that the conus medullaris of the spinal cord extends to about the L1 to L2 vertebrae in adults (approximately S1 in fetuses, L3 in neonates, and L1 to L2 within the first few months to 2 years of life) (Wilson & Prince, 1989; Macdonald et al., 1999; Malas et al., 2000). (See Chapter 3 for a full discussion of this topic.) Inferior to the level of the conus medullaris the vertebral canal (Figs. 7-7 and 7-8) contains the cauda equina. The cauda equina is bathed in the cerebrospinal fluid of the subarachnoid space. The subarachnoid space in the lumbar vertebral canal is large compared with that in the cervical and thoracic regions. Because of its size, the subarachnoid space below the level of the conus medullaris (L1 to L2 vertebral foramen) is known as the lumbar cistern. Also within the lumbar vertebral canal are the meninges: pia mater, attached to rootlets; arachnoid; and dura mater, which surrounds the arachnoid and to which the arachnoid is closely applied. In addition, adipose tissue, vessels, and nerves are located within the epidural space of the vertebral canal. Clinicians who specialize in diagnostic imaging frequently use the term thecal sac when collectively referring to the dura mater, arachnoid, and subarachnoid space within the vertebral canal. This term is not restricted to the lumbar region and is used when referring to these structures in the cervical and thoracic regions as well.

Dural Attachments within the Vertebral Canal

The dura mater of the lumbar spine has a series of attachments to neighboring vertebrae and ligaments. These attachments are found at each segmental level and are usually located at the level of the IVD (Rauschning, 1987). They have been called the dural attachment complex (Dupuis, 1988), meningovertebral ligaments (Bashline, Bilott, & Ellis, 1996), or Hoffmann ligaments (Rauschning, 1987; Dupuis, 1988). A centrally placed set of connective tissue bands attaches the anterior aspect of the dura mater to the posterior aspect of the lumbar vertebral bodies and the posterior longitudinal ligament. This set of bands has been called midline Hoffmann (meningovertebral) ligaments (Dupuis, 1988). These are the most numerous and the most robust of the meningovertebral ligaments (Bashline, Bilott, & Ellis, 1996). A second set attaches the anterior and lateral aspects of the dura mater to the lateral, flared extension of the posterior longitudinal ligament, which is attached to the IVD (Fig. 7-9). These bands have been called the lateral Hoffmann (meningovertebral) ligaments (Dupuis, 1988), and are less common and less robust than the midline meningovertebral ligaments (Bashline, Bilott, & Ellis, 1996). A third set of connective tissue bands attaches the exiting dural root sleeves with the inferior pedicles forming the IVFs. These are known as the lateral root ligaments, and may act to limit medial and superior mobility of the nerve root. These meningovertebral ligaments are the least common (i.e., not found at all lumbar vertebral levels) and least robust, but are still found in all specimens (Bashline, Bilott, & Ellis, 1996) (see Connective Tissue Attachments of the Dura to the Borders of the Intervertebral Foramina later in this chapter). These three types of meningovertebral ligaments are variable in distribution, size, and length (varying in length from a few millimeters to as long as 2.5 cm) (Bashline, Bilott, & Ellis, 1996). Posterior Hoffmann (meningovertebral) ligaments also have been identified. They are much less common than the others and course from the posterior aspect of the dura mater to the ligamentum flavum and the posterior aspects of the neural canal (Bashline, Bilott, & Ellis, 1996). A single fibrous band (most common), or pair of fibrous bands, has been identified passing between the posterior aspect of the dura, at the level of the superior aspect of the superior articular process of S1, and the ligamentum flavum at the L5-S1 vertebral level. The ligamentous band(s) was (were) found in 10 of 14 (71%) lumbar spine surgery patients (Solaroglu, Okutan, & Beskonakli, 2011).

Although meningovertebral ligaments have been identified in the thoracic and cervical regions, they are much less common and substantive than those of the lumbosacral region (Scapinelli, 1990; Bashline, Bilott, & Ellis, 1996). However, sturdy attachments of the cervical dura mater to the ligamentum nuchae and rectus capitis posterior minor muscle have been found (see Chapter 5).

It should be recalled that irritation of the anterior aspect of the lumbar spinal dura mater has been found to result in pain felt in the midline, radiating into the low back and superior aspect of the buttock (Edgar & Ghadially, 1976). This pattern of referral is also seen in irritation of the posterior longitudinal ligament (see Ligaments and Intervertebral Discs of the Lumbar Region). Bashline and colleagues (1996) speculated that with bulging or protrusion of the IVD, the presence of midline and lateral meningovertebral ligaments would cause traction of the dura mater and the related nerve roots, increasing back and lower extremity pain. They later verified that a bulging IVD can cause traction of the dura mater by means of meningovertebral ligaments (Bashline, Bilott, & Ellis, 1996). They further speculated that the absence of meningovertebral ligaments at some levels in some individuals may be one reason why disc bulges of the same size in two individuals, or at two different levels in the same individual, may present with dramatically different signs and symptoms. The abundance of meningovertebral ligaments in the lumbar region, coupled with the higher incidence of disc bulging and protrusion in this region, would make the lumbar region the most susceptible to this phenomenon. Bashline and colleagues (1996) further speculated that the greater number of anterior meningovertebral ligaments in the lumbar region may result from the greater volume of the lumbar vertebral canal, allowing for more ligaments of greater size. Another possible reason given was to provide additional stabilization of the dural sac in the more inferiorly located lumbar region than in other regions of the vertebral column (attachment of the dura to the bones of the cranial vault stabilizes the dura superiorly). The authors also hypothesized that these ligaments would pull the dural sac anteriorly with spondylolisthesis resulting in pain in this condition (Bashline, Bilott, & Ellis, 1996). In addition, calcification of some of these ligaments has been noted. Such calcification could potentially cause mechanical irritation of the anterior aspect of the dura mater and the underlying nerve roots (Spencer, Irwin, & Miller, 1983; Bashline, Bilott, & Ellis, 1996). In addition, Spencer and colleagues (1983) believed that the commonly seen “cap” of bone present along the posterior aspect of lumbar vertebral bodies could result from the attachment of meningovertebral ligaments causing a type of “traction spur.”

Spinal Canal Stenosis

Narrowing of the vertebral canal (spinal canal) is most often known as spinal canal stenosis, or, simply, spinal stenosis. Many variations of this condition exist in the lumbar region, several of which are discussed in this section. The possible pathologic condition that can result from spinal canal stenosis and that is common to all the variations is compression of one or more of the nerves that course through the vertebral canal. Such compression can lead to pain and dysfunction, probably caused by ischemia of the entrapped nerves (Lancourt, Glenn, & Wiltse, 1979). Lumbar spinal canal stenosis affects the nerves of the cauda equina or the dorsal and ventral roots as they leave the vertebral canal and enter IVFs.

Spinal stenosis is usually characterized by diffuse and bilateral low back pain accompanied by radicular pain (see Chapter 11) that radiates along the posterior aspect of one or both thighs and extends to or below the knees. In addition to low back and radicular pain, a patient with spinal stenosis usually experiences weakness of the lower extremities that occurs after prolonged standing with the lumbar region in extension or after walking (neurogenic claudication) (Amundsen et al., 1995). Takahashi and colleagues (1995) and Takahashi, Shima, and Porter (1999) measured epidural pressure by means of epidural transducers in patients with spinal stenosis. The epidural pressures were found to be low when patients were sitting or lying down and were high when patients were standing. Flexion decreased epidural pressure and extension increased it. The epidural pressure was found to be the highest during extension while standing. The increased pressures also were positively associated with neurologic symptoms of cauda equina compression.

Subdivisions of spinal stenosis include lateral recess stenosis and foraminal (intervertebral foraminal) stenosis. The exiting nerve roots travel through the narrower lateral aspect of the vertebral canal, known as the lateral recess, before entering the IVF. As the roots pass through this region of the vertebral canal, pressure may be placed on them. This is known as lateral recess stenosis. Another type of stenosis includes narrowing of the IVF. This condition is known as foraminal stenosis.

General Considerations

The bony and ligamentous canals called the intervertebral foramina (singular, foramen) are described in Chapter 2. However, several features of the lumbar IVFs are unique. In addition, these regions have been the subject of extensive descriptive and clinical investigation. The relationship between the lumbosacral nerve roots and their surrounding tissues is important in the proper diagnosis of low back pain and pain radiating into the lower extremity (Hasue et al., 1983). This section therefore focuses on the unique aspects of the anatomy of the lumbar IVFs, the pertinent conclusions of previous and current studies of the IVF, and the clinical relevance of this fascinating area.

Many features of the region of the lumbar IVFs are different from those of the rest of the spine because of the unique characteristics of the lumbar and sacral spinal nerves (Fig. 7-11). Because the spinal cord ends at generally the level of L1 to L2, the lumbar and sacral dorsal and ventral roots must descend, sometimes for a considerable distance, within the subarachnoid space of the lumbar vertebral canal. This region of subarachnoid space is known as the lumbar cistern. The exiting nerves (dorsal and ventral rootlets or roots) leave the lumbar cistern by entering a sleeve of dura mater. This usually occurs slightly inferior to the level of the IVD at the level above the IVF that the roots eventually will occupy. For example, the L4 roots enter their dural sleeve just beneath the L3-4 disc and then course inferiorly and laterally to exit the L4-5 IVF. More specifically, on leaving the subarachnoid space of the lumbar cistern, the exiting dorsal and ventral roots pass at an oblique inferior and lateral angle while retaining a rather substantial and very distinct covering of dura mater. This covering, known as the dural root sleeve, surrounds the neural elements and their accompanying radicular arteries and veins until they leave the confines of the IVF (see Fig. 2-15). The largest lumbar dural root sleeve (proximal to the dorsal root ganglion) is L5 (5.6 mm diameter) and the smallest is L1 (3.5 mm diameter) (Torun et al., 2008).

Frequently the dorsal and ventral rootlets that arise from the spinal cord do not all unite to form dorsal and ventral roots until they are well within the dural root sleeve (Rauschning, 1987; Dupuis, 1988). In addition, the dorsal and ventral roots combine to form the spinal nerve while within the distal aspect of the funnel-shaped dural root sleeve. This latter union occurs at the level of the IVF. The exiting spinal nerve has been found to be larger than the combined size of the individual dorsal and ventral roots (dePeretti et al., 1989). On reaching the lateral edge of the IVF, the dural root sleeve becomes continuous with the epineurium of the spinal nerve.

Many authors (Vital et al., 1983; Bose & Balasubramaniam, 1984; Rauschning, 1987; Lee, Rauschning, & Glenn, 1988) have described the region beginning at the exit of the neural elements from the lumbar subarachnoid cistern and continuing to the lateral edge of the IVF as having significant clinical importance. Perhaps because of the clinical significance of this region, several terms have been used to describe it, including lumbar radicular canal (Vital et al., 1983), nerve root canal, or simply root canal (Rauschning, 1987) (Fig. 7-12). The term nerve root canal (NRC) is used in the following paragraphs when discussing the course of the dural root sleeve and its contents, and the term IVF is used to describe the terminal part of the NRC that lies between the pedicles of two adjacent vertebrae.

Within the dural root sleeve an interneural complex of fibrous connections (Dupuis, 1988) anchors the neural elements (rootlets and roots) to the surrounding dura mater of the NRC. More specifically, these connections course from the dura and inner arachnoid mater of the sleeve to the pia mater surrounding the rootlets and roots. Recall that farther laterally the root sleeve unites with the spinal nerve to form its epineurium.

Connective Tissue Attachments of the Dura to the Borders of the Intervertebral Foramina

The external surface of the dural root sleeve is usually attached by one or more connective tissue bands to the inferior pedicle of the IVF (see Fig. 7-9). This connective tissue attachment is called the lateral root ligament (Dupuis, 1988). It limits the medial and upward mobility of the root sleeve and its contents (Rauschning, 1987). Fibrous connections from the lateral aspect of the IVF to the exiting spinal nerve have also been identified (Hasue et al., 1983; dePeretti et al., 1989). Grimes and colleagues (2000) found four connective tissue attachments from the dural root sleeve to the adjacent borders of the IVF at all lumbar levels. One such attachment passed posteriorly to the lateral-most aspect of the ligamentum flavum as it blended with the Z joint capsule. Another connective tissue attachment was found to extend superiorly to the pedicle above, and a third formed a mirror image to the second by extending inferiorly to the pedicle below. Finally, another connective tissue attachment extended anteriorly to the posterior aspect of the IVD (Grimes, Massie, & Garfin, 2000). An appropriate term for these connective tissue attachments would seem to be “intraforaminal meningovertebral ligaments,” after Bashline and colleagues (1996), who used the term meningovertebral ligaments to refer to Hoffmann’s ligaments connecting the dura mater to surrounding tissues within the vertebral (spinal) canal. These intraforaminal structures were found to stabilize the neural structures within the IVF and to resist considerable traction applied to the spinal nerve and anterior primary division distal to the connective tissue attachments (dePeretti et al., 1989; Grimes, Massie, & Garfin, 2000). Because the fibrous attachments have been found to give considerable resistance to traction of the anterior primary divisions, they serve to spare the lumbar roots from traction injuries. The dural root sleeve also provides resistance to traction. In fact, the dural root sleeve ruptures before avulsion of the rootlets from the conus medullaris occurs. These resistive forces, when combined with the fact that the rootlets and roots forming the spinal nerves are of excess length within the dura mater, indicate that the IVF seems to provide an almost insurmountable protective barrier to traction forces placed on the exiting spinal nerves (dePeretti et al., 1989).

Entrapment of the Neural Elements

Unfortunately, the exiting neural elements are not as well protected from pressure injuries as they are from traction injuries. Compression, or entrapment, of neural elements as they pass through the NRC or the IVF is of extreme clinical importance (Lancourt, Glenn, & Wiltse, 1979). Also a detailed understanding of this region is essential because treatment may differ depending on the cause of entrapment. The clinician should attempt to localize a lesion as precisely as possible to determine the structure causing the problem and to identify the specific neural elements being affected (Rauschning, 1987). These neural elements include the dorsal and ventral roots and their union as the spinal nerve. Causes of such compression include degenerative changes of the superior articular processes and posterior vertebral bodies, protrusion of the IVD, and pressure from the superior pedicle of the IVF (McNab, 1971; Hasue et al., 1983; Vital et al., 1983) (see Chapter 11).

Occasionally osteophytes from the Z joints and vertebral bodies can become so large that they can almost completely divide the IVF into two smaller foramina, one on top of the other (Kirkaldy-Willis et al., 1978). Such changes may result in entrapment of the exiting spinal nerve. However, osteophytes of the superior articular processes forming the Z joints cause venous obstruction of the intervertebral veins more often than compression of nerves in the IVF. This leads to “compression, congestion, and resultant dilation of foraminal veins.” The venous changes are also associated with intraneural and perineural fibrosis, focal demyelination, and edema of the nerve roots. These neural changes probably result from ischemia secondary to poor venous return from the nerve roots upstream to the venous obstruction (Hoyland, Freemont, & Jayson, 1989).

Because of the clinical importance of the NRCs and the IVFs, a more accurate anatomic description is necessary.

Anatomy of the Nerve Root Canals

The sizes of the NRCs vary considerably from the upper to lower lumbar segments. They are smaller in length at the level of L1 and L2 because, after exiting the lumbar cistern, the L1 and L2 nerves course almost directly laterally to reach the IVF. This led Crock (1981) to state that the concept of a nerve root canal at L1 and L2 is useless, because the beginning of the dural root sleeve lies against the inferior and medial aspect of the IVF’s upper pedicle. Therefore no true dural “canal” exists for these nerve roots.

Table 7-5 lists the obliquities and lengths of the lumbar NRCs. Other authors (e.g., Ebraheim et al., 1997b) have found a more superior-to-inferior course of the NRCs (i.e., lower obliquity values than those presented in the table). The NRCs become progressively longer from L1 to S1 as the dural root sleeves generally exit at a more oblique inferior angle (i.e., lower obliquity values in Table 7-5). Therefore the NRCs of L5 and S1 are the longest in the lumbar region and the most susceptible to damage from pathologic conditions of surrounding structures (Crock, 1981). Tables 7-6 and 7-7 describe the relationships of the L5 and S1 NRCs, respectively. Many, if not most, of the types of borders described in Table 7-6 for the L5 NRC also apply to the L3 and L4 NRCs as well.

All the exiting rootlets or roots course over an IVD either just before entering their dural root sleeve (L1 and L2) or, in the case of L3-S1, directly in the region where they enter the dural root sleeve. However, only the S1 dural root sleeve (and contents) passes completely over an IVD (the L5 disc). The S1 NRC passes through a movable, narrow opening between the L5 disc anteriorly and the L5-S1 ligamentum flavum posteriorly. Therefore the S1 nerve is exposed to possible compression both anteriorly (disc protrusion) and posteriorly (ligamentum flavum bulging or buckling, hypertrophy of superior articular process of sacrum) in this region (Rauschning, 1987).

Anomalies of the Neural Elements and the Dural Root Sleeves

Anomalies of the rootlets as they come off of the spinal cord are common. Such anomalies occur much more often with the dorsal rootlets than the ventral rootlets (Kikuchi et al., 1984). The anomalies take the form of rootlets of one spinal cord segment passing to the root of the nerve below or above. Such anomalies could conceivably result in the perception of radicular symptoms different from the normal pain pattern.

Anomalies of the roots making up the cauda equina while within the lumbar cistern also are quite common. These usually consist of nerve bundles from one root passing to a neighboring root. The clinical implications of this type of anomaly are the same as those just discussed for anomalous rootlets.

Congenital anomalies associated with the dural root sleeves also occur with some frequency. Hasue and colleagues (1983) found anomalies in 5 of the 59 cadavers (8.5%) in their study. Several types of anomalies have been identified (Hasue et al., 1983; Neidre & MacNab, 1983; Kikuchi et al., 1984; Aota et al., 1997; Bogduk, 2005) (Fig. 7-13). The first type is known as conjoined nerve roots and is the most common type of dural sleeve anomaly (see Fig. 7-13, C). With this anomaly, roots of adjacent spinal cord segments share the same dural root sleeve for a short distance. The roots then separate into their own dural root sleeve and exit the appropriate IVF. Conjoined nerve roots cause one set of dorsal and ventral roots (or both sets) to take a tortuous course, possibly making them more susceptible to traction across a bulging disc or narrow NRC.

The second type of root sleeve anomaly is the most dramatic. The dorsal and ventral roots of two distinct spinal cord levels, within their appropriate root sleeves, exit the same IVF, leaving the adjacent IVF devoid of exiting roots (see Fig. 7-13, B). In a variation of this anomaly, an additional dorsal and ventral root and their covering dural root sleeve pass through the same IVF with the neural and dural structures that normally pass through the IVF. In this instance, all of the IVFs have roots within them, and one IVF has two pairs of roots passing through it (see Fig. 7-13, D). The nerves within an IVF containing more than one set of roots in these types of anomalies are more susceptible to entrapment. Entrapment of two sets of roots within one IVF might lead to radicular symptoms of more than one dermatome (see Chapters 9 and 11).

In the third type of dural root sleeve anomaly, a communicating branch, surrounded by its own dural sheath, passes from one NRC to its neighbor before either primary root exits its normal IVF. The result of this anomaly could be similar to that of roots sending connecting branches to neighboring roots, causing dispersion of radicular symptoms to include an adjacent segment (e.g., L5 compression may result in some pain or paresthesia in the distribution of L4). However, because it runs within its own dural root sleeve, the neural elements within the “bridging sleeve” are more vulnerable to compression either when they are inside a lateral recess or as they pass behind an IVD. This type of anomaly also can occur in conjunction with the variation of the second type of anomaly mentioned. In this case a communicating branch is found between two dural root sleeves as they both exit the same IVF (communicating branch shown in Fig. 7-13, D).

Anomalies of the nerve roots and dural sleeves can be a sole cause of radicular symptoms. They also can augment radicular symptoms from other causes (Hasue et al., 1983). Even though the incidence of symptoms as a result of such NRC anomalies is thought to be rare, they should be kept in mind when patients have unusual distribution patterns of radicular pain (Bogduk, 2005).

Terminology Associated with the Nerve Root Canals and the Intervertebral Foramina

Terminology with regard to the exiting roots can be confusing. Some authors (Vital et al., 1983) describe the beginning of the NRC (that portion posterior to the IVD directly above the level of the IVF of exit) as the retrodiscal portion of the NRC (see Fig. 7-12, B). As the nerve continues to descend more laterally in what is described by many as the lateral recess, the nerve lies medial to the pedicle that forms the upper border of the IVF that the nerve roots eventually exit. This region is sometimes called the parapedicular portion of the NRC (Vital et al., 1983). The portion of the IVF occupied by the uniting dorsal and ventral roots and the exiting spinal nerve is called the IVF proper. Table 7-8 describes the borders of the retrodiscal, parapedicular, and IVF proper subdivisions of the NRC. This table is included to help clarify the regions where the nerve roots and (mixed) spinal nerve are most vulnerable to various types of pathologic conditions.

Moving from the upper to the lower lumbar region, the parapedicular portion (lateral recess) of the NRC widens in the transverse plane (i.e., left to right), becomes shorter from top to bottom, and becomes narrower from anterior to posterior (average, 12 mm at L2 and 8 mm at L5) (Vital et al., 1983); therefore this part of the NRC becomes more like a true lateral recess, or gutter, as one descends the lumbar spine.

The position of the entire lumbar region affects the NRC and the neural elements (Vital et al., 1983). The anteroposterior dimension of the retrodiscal space narrows in the upright posture. This is because of slight posterior bulging of the IVD and slight anterior buckling of the ligamentum flavum. During flexion of the lumbar region, the neural elements become stretched and pressed against the anterior walls of the retrodiscal and parapedicular spaces. Also, the IVF proper increases in height and width during flexion. Extension of the lumbar region results in slackening of the neural elements. They also move against the posterior wall of the lateral recess during extension. In addition, the IVF becomes significantly shorter from superior to inferior and anterior to posterior during extension (Mayoux-Benhamou et al., 1989).

A different set of terms was introduced by Rauschning (1987) and Lee and colleagues (1988) (see Fig. 7-12, C). These authors used the term entrance zone when referring to the region that begins as the roots enter the dural root sleeve and continues through the lateral recess. Other authors use the terms lateral recess, lateral canal, subarticular gutter, or lateral nerve canal when referring to this region (Rauschning, 1987). This area corresponds to the combination of the retrodiscal and parapedicular regions previously described. The most common cause of stenosis in the entrance zone is hypertrophic osteoarthritis of the Z joint, usually of the superior articular process. Other causes include congenital variations of the Z joints or a congenitally short pedicle. Also, a bulging anulus fibrosus (e.g., L3 anulus compressing the L4 nerve) or osteophytic spurs from the superior vertebral end plate coursing along the anulus could compress the neural elements in the entrance zone.

Rauschning (1987) and Lee and colleagues (1988) use the term midzone or pedicle zone when referring to the region of the NRC located between the two adjacent pedicles that constitute an IVF (see Fig. 7-12, C). This area was described previously as the IVF proper (Vital et al., 1983) (see Fig. 7-12, A). The dorsal root (spinal) ganglion and ventral root are located within this region and can be compressed here. Because of its large size, the dorsal root ganglion is more susceptible to minor compression than the ventral root. Osteophyte formation along the ligamentum flavum (anterior to the pars interarticularis) and hypertrophy of fibrous tissue along a fracture of the pars interarticularis were cited by Lee and colleagues (1988) as being the most common causes of stenosis in the middle zone. They also believed that clinicians may overlook stenosis of this region because the middle zone is difficult to evaluate with diagnostic imaging procedures. They stated that neural entrapment of the middle zone may result in symptoms of activity-related, intermittent, neurogenic claudication. They also noted that some patients progress until they experience constant pain and diminished sensation even during times of rest. These unprovoked resting symptoms may be caused by spontaneous action potentials arising from compressed or entrapped ganglionic cells (Lee et al., 1988).

The term exit zone, or foramen proper, was used by Rauschning (1987) and Lee and colleagues (1988) to refer to the almost two-dimensional opening (“doorway”) formed by a parasagittal plane passed along the lateral edge of the two pedicles that help to form an IVF (see Fig. 7-12, C). The most common causes of stenosis in this region were cited as “hypertrophic osteoarthritic changes of the facet joints (Z joints) with subluxation and osteophytic ridge formation along the superior margin of the disc” (Lee, Rauschning, & Glenn, 1988).

Clinical Conditions Related to the Nerve Root Canals

Narrowing of the IVD, particularly at the L5-S1 level, causes narrowing of the IVF at the same level (L5-S1 IVF in this case) and also narrowing of the NRC of the nerve exiting at the IVF below (the S1 NRC in this case). Crock (1981) stated that the remaining anulus fibrosus of the disc may bulge posteriorly, bringing the posterior longitudinal ligament along with it. The superior articular facet of the segment below (S1) moves superiorly and anteriorly, again compressing the NRC (S1). The combination of posterior anulus bulge along with anterior displacement of the superior articular facet of the vertebra below can result in dramatic narrowing of the NRC that runs between these two structures (Rauschning, 1987). Osteophyte (bony spur) formation is fairly common, both from the vertebral body along the attachment of the anulus fibrosus and from the superior articular process along the attachment of the ligamentum flavum. These spurs can further compress the neural and vascular elements of the NRC (Rauschning, 1987). In addition, a bony ridge may develop along the anterior and inferior surface of the lamina. This can compress the more medial NRC (that of the nerve exiting at the IVF of the level below, S1 in this instance) and also the lateral and distal (inferior) aspect of the NRC of the nerve exiting at the same level (in this case, L5).

The L5 NRC is related to both the L4-5 (at its origin) and the L5-S1 (at its exit) IVDs. Therefore with suspected entrapment of the L5 nerve, a differentiation between compression from an L4 or L5 disc bulge or protrusion, or from another structure along the L5 NRC, must be made (Bose & Balasubramaniam, 1984).

Congenital hypertrophy of the L5-S1 articular processes and facets may cause localized obstruction of the L5-S1 IVF. Osteoarthritis of the L5-S1 facets may cause the same condition, but usually such arthritis tends to cause obstruction more medially, affecting the descending S1 NRC (Crock, 1981).

Intervertebral Foramina Proper

When viewed from the side, the lumbar IVFs face laterally. A typical lumbar IVF is sometimes described as being shaped like an inverted teardrop or an inverted pear (Fig. 7-14). The specific dimensions of the lumbar IVFs are given in Chapter 2 (see Tables 2-6 and 2-7).

The spinal nerve is located in the upper third of each lumbar IVF. As it enters the IVF, the spinal nerve is close to the medial and inferior aspect of the superior pedicle that forms the upper boundary of the IVF (Crock, 1981). Here the nerve is accompanied by a branch (or sometimes branches) of the lumbar segmental artery; by the superior intervertebral (segmental, or pedicle) veins, which connect the external and internal vertebral venous plexuses; and by the sinuvertebral nerve (Rauschning, 1987). The spinal nerve occupies approximately one third of the IVF in the lumbar region. However, the spinal nerve can be as close as 0.4 mm (range, 0.4 to 0.8 mm) to the bony anterior and posterior IVF borders (Giles, 1994). This allows crowding by the articular facets during extension (Bose & Balasubramaniam, 1984; Rauschning, 1987). The inferior aspect of the IVF is usually narrowed to a slit by the anulus fibrosus, which normally bulges slightly posteriorly. The inferior aspect of the IVF is also narrowed by the posteriorly located ligamentum flavum. The inferior intervertebral (segmental, discal) veins usually lie in this narrow space. As with the superior intervertebral (pedicle) veins, the inferior veins also unite the internal (epidural) vertebral venous plexus with the external vertebral venous plexus and the ascending lumbar vein.

The lateral borders of the IVFs are covered with an incomplete layer of transforaminal fascia (Paz-Fumagalli & Haughton, 1993). This fascia condenses in several locations at each IVF to form the accessory ligaments of the IVF (see Chapter 2). An exiting spinal nerve could be affected by these structures as it leaves the IVF (Bachop & Janse, 1983; Bachop & Ro, 1984; Bose & Balasubramaniam, 1984; Rauschning, 1987; Bakkum & Mestan, 1994; Qian, Qin, & Zheng, 2011). In addition to compression by accessory ligaments or transforaminal fascia, Rauschning (1987) states that lateral disc herniations and bony structures such as the TPs (usually of L5, but at higher lumbar levels on rare occasions) “may compress, kink, or constrict the lumbar nerves beyond the foraminal outlet.” The author calls this region the extraforaminal region or the postcanal zone.

Also, the lateral borders of the L1 through L4 IVFs are associated with the origin of the psoas major muscle. In fact, because of the posterior origin of the psoas major muscle from the front of the TPs and its anterior origin from the lumbar vertebral bodies and IVDs, the psoas major almost completely surrounds the lateral opening of the first four lumbar IVFs. Therefore the anterior primary divisions (ventral rami), by necessity, run through the substance of the psoas major muscle, frequently uniting with neighboring ventral rami within the muscle to form the branches of the lumbar plexus. In addition to the protection given by the dural root sleeve and the meningovertebral (Hoffmann) ligaments (see previous discussion and Fig. 7-9), the psoas major muscle may provide some protection for the dorsal and ventral roots during traction of the peripheral nerves of the lumbar plexus (dePeretti et al., 1989). Such traction may occur as a result of hyperflexion or hyperextension of the lower extremity.

The boundaries of the IVF can be imaged well with both MRI and CT (Cramer et al., 1994) (Fig. 7-15; see also Fig. 7-14). Occasionally ossification of the superior attachment of the ligamentum flavum results in foraminal spurs, which can be seen on CT. These spurs are considered to be normal variants; may project well into the IVF, posterior to the dorsal root ganglion; are frequently bilateral; and are usually asymptomatic (Helms & Sims, 1986).

Changes in Dimensions of the Intervertebral Foramina

Flexion of the lumbar region has been shown to significantly increase the height and width of the IVFs by separating the pedicles (increases height), by decreasing the normal bulging of the anulus fibrosus of the IVD (increases IVF width), and by decreasing the thickness of the ligamentum flavum (increases IVF width) (Fujiwara et al., 2001). Extension significantly decreases the height and width of the IVFs and increases pressure within the IVF (Morishita et al., 2006) by having the opposite effects as flexion (Fujiwara et al., 2001). Flexion increases the cross-sectional sagittal area of the IVF from the neutral position by 12%, whereas extension decreases the area of the IVF from the neutral position by 15% (Inufusa et al., 1996); other investigators have found even greater changes in cross-sectional IVF area (up to 44%) during flexion and extension (Schmid et al., 1999). Distraction (traction) has been found to increase IVF size in cadavers (Schlegel et al., 1994), and compression decreases the height of the IVFs (Nowicki et al., 1990). Titanium cages (BAK Interbody Fusion System) implanted in the IVDs during interbody fusion spine surgery also have been shown to increase IVF volume at L4-5 and L5-S1 (Chen et al., 1995). Many of the pathologic conditions described as affecting the NRC, such as anterior osteophytes on the superior articular processes of the Z joints, also can diminish the dimensions of the IVF proper (Bailey & Casamajor, 1911; Giles, 1994). In addition, recall that the IVD forms a part of the anterior border of the IVF. Because of this, a far lateral IVD prolapse can cause a significant decrease in the anterior-to-posterior dimension of the IVF, resulting in a dramatic change of shape of the spinal nerve in the IVF and the development of fibrotic adhesions in and around the spinal nerve (Hadley, 1948). In addition, a decrease in disc height also results in a decrease of the vertical dimension of the IVF (Crock, 1981; Cinotti et al., 2002). In fact, a decrease in IVF height of only 4 mm, when combined with lumbar extension, can cause compression of the dorsal root ganglion or the spinal nerve within the IVF (Revel et al., 1988). This is most likely because the dorsal root ganglion and spinal nerve normally can be as close as 0.4 mm to the bony anterior and posterior borders of the IVFs (Giles, 1994). Cinotti and colleagues (2002) found that a decrease in the sagittal diameter of the vertebral (spinal) canal was related to a decreased width of the IVF at the same level (usually resulting from decreased length of the pedicles). This relationship of decreased spinal canal size with decreased IVF size; along with the close relationship of disc degeneration, acquired spinal canal stenosis, IVF stenosis, and decreased IVF height, led Cinotti and colleagues (2002) to conclude that IVF stenosis should be suspected whenever spinal canal stenosis is present. In a related study, Morishita and colleagues (2006) found increased L5-S1 IVF pressures during lumbar extension. They then combined IVF pressure measurements with electrophysiologic recordings taken during spinal surgery and concluded that a double compression of the L5 nerve roots occurred at (1) the vertebral canal and (2) the IVF, during extension in patients with lumbar spinal stenosis. For these reasons, having access to the normal size of the lumbar IVFs as they appear on MRI scans can be clinically useful. (These values are presented in Chapter 2 in the section Intervertebral Foramen, Tables 2-6 and 2-7.)

L5 Nerve Root Canal and L5 Intervertebral Foramina

The anatomy of the L5 NRC is unique, and because of this the L5 roots and nerve are susceptible to compression in many different locations. This canal is longer and runs at a more oblique anterior angle than the rest of the lumbar NRCs. Also, the lateral recess of the L5 vertebra is the deepest laterally and often the narrowest from anterior to posterior of the entire spine. This narrow lateral recess may lead to compression of the L5 nerve in some instances (Rauschning, 1987). Hasue and colleagues (1983) found histologic evidence of compression (intraneural fibrosis) of the L5 dorsal root. Compression occurred between the superior articular process of S1 and the posterior aspect of the vertebral body of L5 (Hasue et al., 1983).

After leaving the lateral recess, the L5 roots and their dural root sleeve continue along the L5 NRC by wrapping around the posterior and lateral aspect of the L5 vertebral body. The roots continue around the posterolateral aspect of the L5 IVD and unite to form the spinal nerve. The L5 nerve, which is the largest of the lumbar nerves, exits the lateral border of the L5 NRC (the IVF proper), which is the smallest IVF of the lumbar spine (Olsewski et al., 1991; Cramer et al., 2003). This makes the L5 nerve particularly susceptible to compression within its IVF.

The anterior primary division (APD) of L5 is given off at the most lateral aspect of the IVF and then passes along a depression on the front of the sacral ala. The APD frequently is bounded anterosuperiorly in this region by the corporotransverse ligament (Bachop & Janse, 1983; Bachop & Ro, 1984; Rauschning, 1987). The corporotransverse ligament passes from the vertebral body and IVD of L5 to the TP of L5. Several investigators (Nathan, Weizenbluth, & Halperin, 1982; Olsewski et al., 1991; Briggs & Chandraraj, 1995) report that the inferior band of the iliolumbar ligament, known as the lumbosacral ligament (LSL), consistently courses from the vertebral body and TP of L5 to the ala of the sacrum (see Fig. 7-23). The descriptions of the corporotransverse ligament by Bachop and Janse (1983) and Bachop and Ro (1984) are consistent with what Nathan and colleagues (1982) consider to be the fibers of origin of the LSL. This indicates that the fibers of origin of the LSL are much more substantial than those fibers found more inferiorly and laterally, and that frequently a distinct tough, fibrous band, the corporotransverse ligament, is formed in the region of origin of the LSL.

After passing beneath the corporotransverse ligament and the LSL, the APD of L5 continues inferiorly (Nathan, Weizenbluth, & Halperin, 1982; Bachop & Janse, 1983; Bachop & Ro, 1984; Olsewski et al., 1991). Therefore the corporotransverse ligament of Bachop and the LSL significantly extend the osteoligamentous canal of the L5 NRC, and the most inferior aspect of the LSL forms the anterior and inferior boundary of the L5 osteoligamentous canal. Nathan and colleagues (1982) state that the gray communicating ramus from the sympathetic chain to the APD of L5 pierces the LSL. Previous studies had shown that, throughout the spine, osteophytes from vertebral bodies frequently exert pressure on the sympathetic trunk, rami communicantes, and spinal nerves. This was found to be particularly true with the neural elements of L5 (Nathan, Weizenbluth, & Halperin, 1982). Finally, just inferior to the LSL, a branch of the APD of L4 joins the APD of L5 to form the lumbosacral trunk.

The unique characteristics of the L5-S1 NRC, the IVF proper, and the lateral osteoligamentous canal of the L5 APD make the L5 nerve “extremely vulnerable to compression by any of the structures forming the tunnel. A tight LSL, osteophytes on the border of the L5-S1 disc or a combination of the two may impinge on the nerve and compress it against the ala of the sacrum” (Nathan, Weizenbluth, & Halperin, 1982). Olsewski and colleagues (1991) reported that the APD of L5 was observed to be compressed by the LSL in 11% of the 102 cadaveric specimens they studied by gross dissection. Histologic evidence of compression (e.g., perineurial and endoneurial fibrosis, peripheral thinning of myelin sheaths, and shift to a smaller fiber diameter) was shown in 3% of L5 APD specimens studied by Olsewski and colleagues (1991), and in 9% of the specimens studied by Briggs and Chandraraj (1995). Osteophytes extending posterolaterally from both the inferior surface of the L5 body and the upper border of the body of the sacrum were found to narrow the L5 osteoligamentous canal further in 1 of 59 spines (2%) studied by Olsewski and colleagues (1991). This was found to contribute to compression of the APD of L5. Nathan and colleagues (1982) found such osteophytes “frequently” and also noted that the L5 nerve was “very often” entrapped or compressed to some degree by osteophytes or the LSL while passing through the osteoligamentous tunnel. Briggs and Chandraraj (1995) found that IVD narrowing also contributed to compression of the L5 APD; they felt that the reason for this may be the addition of fibers to the LSL in response to instability in the region after IVD degeneration.

Compression of the L5 APD by the corporotransverse ligament or the LSL could result in pain along the distribution of L5 nerves to include the L5 dermatome (lateral aspect of the leg distally to the great toe [Floman & Mirovsky, 1990]) and possible loss of motor function of the muscles primarily innervated by the L5 APD (motor paresis of the extensor hallucis longus muscle is found in 5% to 11% of patients with L5 nerve root compression [Jönsson & Stromqvist, 1995]). Referred pain may be experienced in the lumbar region (see Chapter 11), although this has not been fully documented. Myelography, discography, standard CT scans, and transverse plane MRI scans would all be negative (Olsewski et al., 1991). Far lateral parasagittal MRI scans (farther lateral than standard MRI protocols) may show the relationship between the L5 nerve and the corporotransverse ligament and the LSL (Nowicki & Haughton, 1992). Perhaps far lateral parasagittal MRI would be a useful diagnostic procedure for patients exhibiting L5 dermatomal and motor symptoms and signs when other imaging modalities do not reveal a possible cause of entrapment (see Fig. 2-25). Further investigation in this region is warranted. In the meantime, “in the patient presenting with L5 root signs, if the myelogram, discogram, and CT scan do not reveal any defect, then the possibility of extraforaminal compression must be considered as a possible source of the clinical signs” (Olsewski et al., 1991).

Because of the unique anatomy of this region, several distinct conditions, besides those already described, can affect the L5 nerve roots, the L5 spinal nerve, or the APD of L5. For example, because the neural elements of L5 are related to the L5 IVD for a relatively long distance, far lateral L5 IVD protrusion (lateral to the IVF) may affect the L5 spinal nerve or the APD of L5. Another example of the unique vulnerability of the L5 neural elements is spondylolisthesis after spondylolysis (see Fig. 7-17). This condition may result in compression of the L5 nerve along its course from behind the L5 disc to the nerve’s lateral relation with the corporotransverse ligament and the L5 TP, both of which lie above the nerve (Bachop & Janse, 1983; Bachop & Ro, 1984; Rauschning, 1987).

A 20% or greater anterior shift of a spondylolisthetic L5 vertebra may result in compression of the APD of L5 between the TP of L5 and the sacral ala (Wiltse et al., 1984). Such compression is usually unilateral but occasionally may be bilateral. Also, both asymmetric degeneration of the L5 IVD and degenerative lumbar scoliosis result in lateral tilting and rotation of L5. As with spondylolisthesis, this also can result in compression of the L5 nerve between the TP of L5 and the sacral ala. Such far lateral compressions of the L5 nerve have been called the “far-out syndrome (Wiltse et al., 1984) of Wiltse” (Dommisse & Louw, 1990). Wiltse and colleagues (1984) stated that the lateral entrapment caused by either degenerative scoliosis or asymmetric disc degeneration probably was most common in elderly patients, whereas lateral entrapment as a result of spondylolisthesis was found most frequently in a somewhat younger group of adult patients. The authors also stated that far lateral entrapment occasionally could occur at levels higher than L5 and may be accompanied by the radiographic findings of marked scoliosis with closely approximated TPs of two adjacent vertebrae. CT was found to be the imaging modality of choice to view the region of entrapment. A “wide window” setting for the CT scan was necessary to view the laterally placed TPs. CT images reformatted in the coronal plane were particularly useful in evaluating the relationship between the L5 TPs and the sacral ala (Wiltse et al., 1984).

Nathan and colleagues (1982) found that branches of the iliolumbar artery and relatively large veins always accompanied the APD of L5 beneath the LSL. Using examples of neuralgias and pareses of cranial nerves caused by compression of these nerves by adjacent arteries, they hypothesized that likewise the APD of L5 could become entrapped within its osteoligamentous tunnel by branches of the iliolumbar artery and accompanying veins. This would be particularly feasible when the APD of L5 already was partially compressed within a narrow tunnel or by osteophytes extending posterolaterally from the inferior border of the L5 body.

Spondylolysis and Spondylolisthesis

Spondylolysis is a defect of the lamina (Fig. 7-17) between the superior and inferior articular processes. This region is known as the pars interarticularis. Controversy exists as to whether this defect is most frequently caused by trauma or if it is hereditary (Schwab, Farcy, & Roye, 1997). Causes of pars (isthmic) defects include lytic or stress fractures of the pars interarticularis (probably the most common cause), elongated but intact pars (not spondylolysis), and acute fracture of the pars (Day, 1991). The lesions range from subtle hairline fractures to the large gaps seen in spondylolisthesis (Ward et al., 2007). The fifth lumbar vertebra is the segment most vulnerable to acute pars fracture (Ebraheim et al., 1997a). Athletes whose sport requires them to rapidly alternate between flexion and extension of the lumbar region are commonly afflicted with acute fractures of the pars interarticularis (McGill, 1997). Bilateral spondylolysis may result in forward slippage of that portion of the vertebra located anterior to the laminar defect (i.e., vertebral body, pedicles, TPs, superior articular processes). This leaves the inferior articular processes, a portion of the laminae, and the spinous process behind. Such forward displacement of the structures anterior to the spondylolysis is known as spondylolisthesis and is found in 5% to 6% of lumbar spines (Standring et al., 2008; Herman, Pizzutillo, & Cavalier, 2003) (see Fig. 7-17). Although most common at L5, spondylolisthesis occurs with some frequency at L4 and may be seen at any level of the lumbar spine. Other causes of spondylolisthesis include (a) improper formation of the posterior vertebral arch, known as the dysplastic type of spondylolisthesis; (b) degeneration and subsequent erosion of the superior articular process; (c) fracture of part of the posterior arch other than the pars interarticularis (e.g., pedicle fracture); and (d) pathologic conditions of the bone forming the posterior arch (e.g., Paget’s disease).

Even though spondylolysis is probably most often due to acute or stress fracture, there is also a genetic predisposition, with a 30% to 70% prevalence in family members of individuals diagnosed with spondylolysis (Faingold et al., 2004). The genetic component is supported by the findings that both an increased sacral kyphosis and an increased slope of the superior S1 bony end plate are associated with L5-S1 spondylolisthesis in children and adolescents (Wang et al., 2008). (See Chapter 8 section titled The Sacrum for additional information.) In addition, the distance between the lateral aspect of the left and right inferior articular processes is narrower in individuals with L5 spondylolysis. This distance normally increases from L4 to L5. When the distance does not increase (most likely a genetically inherited trait), the inferior articular process of L4 and the superior articular process of S1 have a “pincher effect” on the pars interarticularis of L5 during activities that involve hyperextension (e.g., gymnastics and swimming using butterfly and breast-strokes). This pincher effect predisposes these indivduals to L5 spondylolysis (Ward et al., 2007).

Sometimes the pars defect fills with connective tissue. The connective tissue attachment has been termed the spondylolysis ligament (Wiltse, 1962) and contains several zones of fibrous and cartilaginous tissues (Nordström et al., 1994). Einstein and colleagues (1994) found that this “ligament” was innervated by nerves that met the criteria of pain-sensitive (nociceptive) fibers (e.g., immunoreactivity to calcitonin gene–related peptide [CGRP] and vasoactive intestinal peptide), indicating that deformation of the ligament during spondylolisthesis could result in low back pain. Of course, several other tissues (e.g., IVD, muscles, ligaments) that are stretched because of spondylolisthesis also could generate pain as well (Einstein et al., 1994).

Frequently a “rounding defect” occurs on the anterosuperior aspect of the vertebral segment, or usually the sacrum, below the level of spondylolisthesis. This convex, curving defect is thought to increase the slippage of the spondylolisthetic segment. The rounding defect may be due to damage of the anular apophysis caused by pressure from the spondylolisthesis above (Higashino et al., 2007).

Standard x-ray films and CT remain the imaging modalities of choice for visualizing spondylolysis. However, parasagittal MRI does help to reveal a defect of the pars, which appears as a decrease in signal intensity perpendicular to the plane of the articular facets on these images (Grenier et al., 1989a). Occasionally, rather than the development of a spondylolisthesis, the posterior segment created by bilateral spondylolysis moves further posteriorly. When such posterior displacement occurs, it can frequently be identified on sagittal plane MRI scans (Ulmer et al., 1995).

Spondylolisthesis is graded by the degree to which the affected vertebral body is anteriorly displaced in relation to the vertebral (or sacral) body located immediately inferior to it. For example, a 25% spondylolisthesis represents forward displacement of a vertebral body (measured at the posterior and inferior border of the vertebral body) along one fourth of the length of the vertebral body (or sacral body) directly inferior to it. Spondylolisthesis also can be graded on a scale of 1 to 5 (Meyerding classification), with each grade representing up to 25% of anterior slippage. A grade 5 (original classification only went to grade 4) describes a vertebral body that has been displaced completely off of the vertebra (or usually, the sacrum) directly beneath it, a condition known as spondyloptosis (Maxfield, 2010).

Although spondylolysis with spondylolisthesis has been implicated as a cause of spinal canal (specifically, lateral recess) stenosis at the level of the pars interarticularis defect, Liyang and colleagues (1989) reported an increase in vertebral canal dimensions at the level of spondylolisthesis in 1 cadaveric spine, which was included in their study of 10 normal spines. Spondylolisthesis at L5 also may result in entrapment of the L5 nerve as it passes laterally, in front of the pars interarticularis, to exit the L5 IVF. The entrapment is caused by the portion of the pars located above the fracture site. This is the part of the pars that is displaced anteriorly with the vertebral body and pedicles. By moving anteriorly, it can compress the L5 nerve (Kirkaldy-Willis et al., 1978).

Degenerative spondylolisthesis (DS) is a condition in which the superior articular processes undergo erosion with age rather than the usual increase in bone formation that frequently occurs in these processes with age. This erosion results in the vertebrae above (usually L4, the next most common is L3) moving anteriorly, bringing its posterior arch with it. The shape and orientation of the superior articular processes and facets also appear to play a role in DS. First, sagittally oriented facets are associated with DS (Kalichman et al., 2009). Second, the cephalad aspects of the superior articular processes are more sagittally oriented and the caudad aspects of the same facets are more coronally oriented in not only the DS segment but also the adjacent lumbar segments. This unique orientation and shape of the articular facets throughout the lower lumbar spine in individuals with DS indicates that there may be a genetic predisposition to the development of this condition (Toyone et al., 2009).

The amount of anterior slippage (olisthesis) with DS ranges from 8% to 43% (Postacchini & Perugia, 1991). The consequence of this anterior slippage of the entire vertebra, including the posterior arch, is spinal canal stenosis with possible compromise of the cauda equina (Kirkaldy-Willis et al., 1978). As mentioned, most frequently L4 moves anteriorly on L5, and the inferior articular processes of L4 entrap the L5 and S1 nerve roots against the posterior aspect of the vertebral body of L5 (Dommisse & Louw, 1990).

At the opposite end of the clinical spectrum for the pars interarticularis: the pars can occasionally enlarge as a result of degeneration. This is significant at the level of L5 because it can lead to entrapment of the S1 nerve as it courses along the lateral aspect of the vertebral canal (lateral recess).