Understanding the anatomy of the lumbar spine is key to understanding the pathophysiology and treatments of degenerative lumbar stenosis and spondylolisthesis. The spinal cord ends with the conus medullaris (or conus) at approximately the L1–L2 level. The cauda equina, composed of lumbar and sacral nerve roots, occupies the dural sac below the conus. At each vertebral level in the lumbar spine, an osseous ring composed of the vertebral body anteriorly, two laminas, and two pedicles surround the dural sac.

The ligaments surrounding the spinal cord include the posterior longitudinal ligament that is on the posterior aspect of the vertebral body, and anterior to the dural sac, as well as the ligamentum flavum that runs between adjacent lamina and is located posterior to the dural sac. Importantly, the ligamentum flavum has a broad insertion on the inferior aspect of the cranial lamina and a shorter insertion on the superior aspect of the inferior lamina. This feature is important to note during decompressive procedures. At the level between vertebral bodies, the dural sac is in close proximity to the intervertebral disk anteriorly and the paired facet joints posteriorly, which contributes to the high frequency of stenosis at this level.

Pivotal to linking physical exam findings to anatomic pathology is an understanding of the path of the lumbar nerve roots as they descend through the lumbar spine. Each vertebral level contains a traversing nerve root and an exiting nerve root. In the lumbar spine, nerve roots exit below the vertebra of the same level such that the L4 nerve root exits between L4 and L5 pedicles. The L4–L5 foramen thus contains the L4 exiting nerve root. In the lateral recess at the L4–L5 disk space, the L5 traversing nerve root descends to the neuroforamina at the level below (L5–S1).

The innervation pattern of the lower extremities is critical to linking radiographic and anatomic findings to the physical examination. The lumbar nerve roots flow into the lumbar plexus which gives rise to the following nerves:

The lower lumbar sacral nerve roots give rise to the:

A table of nerve root involvement and associated physical exam findings is provided in Table 19.1. Of note, innervations to muscles are often variable and have contributions from multiple roots. The table provided is a simplification to be used as a guide. The American Spinal Injury Association (ASIA) provides a standardized physical examination for evaluation of spinal trauma that can also be helpful in evaluating degenerative pathology.

An understanding of the cross-sectional anatomy of the lumbar spine is critical to safely and efficiently operating on the spine. The spinous process projects dorsally and caudally, thus the L3 spinous process is commonly at the level of the L3–L4 disk space and the L3–L4 facet joints. Facet joints are a marker for the pedicle of the level below, with the inferior aspect of the L3–L4 facet joint aligning with the level of the L4 pedicle.

Spinal instrumentation with pedicle screws is commonly utilized in the treatment of spondylolisthesis with stenosis. Thus, a review of pedicle anatomy is relevant to the surgical treatment of this common ailment. Pedicles in the lumbar spine are larger relative to the cervical and thoracic spine. The transverse pedicle diameter (width) is usually less than its height and increases gradually
from cranial to caudal. In terms of the sagittal orientation, the pedicles at L3 and L4 are commonly horizontal, and the pedicles above and below those levels are progressively angled cranially and caudally, respectively (Fig. 19.1). In terms of the transverse pedicle angle, pedicles are convergent, and the angle increases as one descends through the lumbar spine starting at approximately 11 degrees at L1 progressing to about 20 degrees at L4, with the L5 transverse angle being approximately 30 degrees.

Spinal stenosis was first described in the early 1800s by Portal, who postulated that a small spinal canal could lead to spinal cord compression and subsequent paraplegia. The first case report came 90 years later when William A. Lane described a 35-year-old woman with progressive paraplegia secondary to spondylolisthesis. The degenerative nature of lumbar spinal stenosis and spondylolisthesis was not described until 1911 by Bailey and Casamajor, and in 1916 by Elsberg.

The etiology of spinal stenosis is degenerative in nature in approximately 80% of adult cases. The pathophysiology of degenerative spinal stenosis and degenerative spondylolisthesis resembles a cascade of events that starts with degeneration of the intervertebral disk. As the disk continues to degenerate, there is an increase in activity of degradative enzymes, and associated decrease in proteoglycans, which results in decreased water content of the nucleus pulposus. The loss of water leads to loss of disk height, and alteration of the normal biomechanics.

In the lower lumbar segments, the intervertebral disk normally bears 70% to 90% of the compressive load placed on the spine. With a loss of disk height, the anterior and middle column no longer bear the same proportion of load through the lumbar spine and part of that force is transferred to the posterior column elements including the facet joints. The supraphysiologic loads placed on the facet joints as a result of degenerating intervertebral
disks lead to progressive facet joint degeneration. Loss of disk height also leads to slack and buckling of the ligamentum flavum and potentially instability between adjacent vertebrae. Once micromotion develops between the two vertebral levels, an environment where listhesis has the potential to develop has been created. As one vertebra shifts anteriorly (anterolisthesis) or posteriorly (retrolisthesis) in relation to the vertebra below, this can further narrow the spinal canal.

Subsequent changes, related to the increased load experienced by the posterior column elements, include facet joint hypertrophy and arthrosis, subchondral sclerosis, ligamentous hypertrophy and calcification, and osteophyte formation. As the degenerative process progresses through this cascade, the spine experiences a period of microinstability as mentioned above, but can regain stability towards the end of the cascade as a result of osteophyte formation around disk and the facet joints.

Lumbar degenerative spondylolisthesis is most common at the L4–L5 level. This is in contrast to isthmic spondylolisthesis, which occurs most frequently at L5–S1. The current theory for why the L4–L5 is a more common site for degenerative spondylolisthesis is that the facet joints at this level have a more sagittal orientation, which limits their resistance to anterior–posterior translation and therefore more prone to subluxation once microinstability develops.

Degenerative spondylolisthesis is more common in the elderly population. Overall incidence of degenerative spondylolisthesis has been reported as 8.7%. It is about five to six times more common in women than in men, and occurs about three times more frequently in black women compared to white women. Degenerative spondylolisthesis rarely results in translation greater than 30% of the anteroposterior length of the inferior endplate. Spondylolisthesis is often in itself asymptomatic until central or foraminal stenosis occurs.

A study from Copenhagen that included 1,533 men and 2,618 women confirmed that the rate of degenerative spondylolisthesis is approximately 8% in women and 3% in men. They found BMI and age to be significant risk factors. Most spondylolisthesis occurred after age 50, with a peak for women 66 to 70 years of age; the peak for men was 50 to 55 years of age. Increased lumbar lordosis was a statistically significant risk factor; however, the mean difference in lumbar lordosis between women that had spondylolisthesis versus those that did not was only 3 degrees and thus lacked clinical significance. There was no association between back pain and spondylolisthesis, suggesting that a substantial number of patients with degenerative spondylolisthesis on imaging are asymptomatic.

Female predominance of spondylolisthesis is unique to degenerative spondylolisthesis, in contrast to isthmic where a male predominance has been observed. The key epidemiologic factors to note are:

If spondylolisthesis is found in a patient who does not fit those factors, other etiologies must be ruled out. The lack of association between low back pain and degenerative spondylolisthesis necessitates that other etiologies of back pain must be ruled out prior to ascribing a patient’s symptoms to radiographic findings.

There are a number of classification systems for spondylolisthesis. The two most common ones are the Wiltse–Newman and the Myerding classifications. The Wiltse–Newman classification groups spondylolisthesis by etiology (Fig. 19.2). The Myerding classification grades spondylolisthesis in terms of percent displacement (grade 1: <25%, grade 2: 25% to 50%, grade 3: 50% to 75%, grade 4: 75% to 100%, grade 5: >100% (spondyloptosis). As indicated above, most degenerative spondylolistheses are grade 1 and rarely exceed grade 2.

Spinal stenosis is defined as narrowing of any part of the spinal canal or neural foramina. Although no formal classification system exists, spinal stenosis is typically grouped in terms of etiology and anatomic location. Etiology is grouped as congenital (split into idiopathic and achondroplastic) and acquired (degenerative, spondylolisthetic, iatrogenic, posttraumatic, and inflammatory) (Fig. 19.3). Anatomic classification refers to the region of stenosis and is divided into central, lateral recess, and foraminal stenosis.

Central stenosis involves narrowing of the central spinal canal and refers to the region between the lateral borders of the cauda equina. Lateral recess stenosis involves the lateral aspect of the central canal, often secondary to facet arthropathy, osteophyte formation, and superior articular process overgrowth. The lateral recess is defined as the region between the lateral border of the cauda equina and the medial aspect of the pedicle. Foraminal stenosis involves narrowing of any part of the neural foramina and is often secondary to disk protrusion, disk collapse, or osteophyte formation. This region is located between the lateral and medial borders of the pedicle.

Degenerative spinal stenosis with or without spondylolisthesis often presents as chronic low back pain in addition to symptoms of radiculopathy and/or neurogenic claudication. The degree of radiculopathy and claudication are variable depending on the severity of the spondylolisthesis, anatomic location of osteophytes, and the severity of facet hypertrophy.