Lumbar-Spondylosis – OrthoPaedia

Lumbar Spondylosis

Lumbar spondylosis, or degeneration of the lumbar discs and facet joints, is a common feature of aging. This degeneration often presents without causing symptoms beyond a routine back ache. However, the tissue overgrowth, ligamentum flavum hypertrophy, and bony osteophytes that accompany the degenerative process can also cause narrowing of the lumbar spinal canal (spinal stenosis). These processes can compress the neural elements causing leg pain, lower extremity numbness, buttock pain, and weakness.

Structure and Function

The five lumbar vertebrae, designated L1 to L5, lie between the rib cage and the pelvis (see Figure 1). The central canal lies behind the body of each vertebra and is bordered by the pedicles and the laminae (see Figures 2 and 3). There is an intervertebral disc between the adjacent vertebra. There are also superior and inferior articular processes that make up the facet joint: the inferior articular process of the vertebrae above lying either dorsally (cervical and thoracic spine) or medially (lumbar spine) to the superior articular process of the vertebrae below.

Figure 1: The lumbar spine, highlighted in red: anterior view (left) lateral oblique (center) and posterior view (right). (Courtesy of Wikipedia)

Figure 2: A lumbar vertebral body with superior view to the left and mid-sagittal view to the right. The central canal is denoted with a red star. The superior articular processes that make up the anterior side of the facet joints are circled in blue. The disc lies between the vertebral bodies, as shown. (Modified from Radiopaedia.org, rID: 82813/Gray’s Anatomy)

Figure 3: Colorized version of a superior view of a vertebra, highlighting the general area of the pedicles in blue, the laminae in green, and the spinous process in orange. The remaining bone, comprising the vertebral body, the articular processes, and transverse processes, are shown in red.

Along the vertebral column, there are anterior and posterior longitudinal ligaments adjacent to the vertebral bodies (see Figure 4). Posteriorly, the ligamentum flavum runs between adjacent lamina. Hypertrophy of the ligamentum flavum can compress the canal or the neural foramen and put pressure on the nerve roots.

Figure 4: The ligaments of the lumbar spine. To the left is the original from Gray’s Anatomy. To the right the potential sources of compression are shown in color: the disc in purple, the bony elements (see text) in black, the posterior longitudinal ligament in blue, and the ligamentum flavum (Latin for "yellow ligament") is shown (of course) in yellow.

Osteophytes (bone spurs) can form near the neural foramen as part of the degenerative process. These bone spurs may grow into the spinal canal resulting in central or lateral recess stenosis or grow into the foramen causing foraminal stenosis.

When the disc degenerates, it becomes flatter. This will shrink the size of the foramen inherently. As the disc space narrows, this will also alter the geometry of the facet joints. This can stimulate facet joint osteoarthritis with resultant osteophytes, further exacerbating the problem of narrowed space.

Facet instability and disc degeneration can produce a slippage of one vertebral body relative to the one below. This so-called degenerative spondylolisthesis further reduces the canal and foraminal dimensions. This type of slippage is distinguished from isthmic spondylolisthesis in which there is a defect of the pars interarticularis. (The pars interarticularis, or pars for short, is the part of a vertebra located between the inferior and superior articular processes of the facet joint. See https://orthopaedia.com/page/Spondylolysis-and-Spondylolisthesis) In degenerative spondylolisthesis there is no defect in the pars, and because the pars remains intact, the slip is often less than 25% of the width of the vertebral body and rarely greater than 50%. (With isthmic spondylolisthesis, where the pars interarticularis defects are often bilateral, slips greater than 50% are more commonly seen.)

The spinal cord terminates at roughly the L1 vertebral level, but the nerve roots that branch off the lower end of the spinal cord (the conus medullaris) remain within the central canal until they exit at their appropriate neural foramen. The nerves branching off beneath the termination of the spinal cord are said to resemble a horse's tail, hence the name cauda equina.

Thus, lumbar stenosis can compress all or part of the cauda equina. This compression can produce pain, paresthesia, and weakness in the pelvis and lower extremities. This can result in numbness in the legs and decreased walking distances.

Patient Presentation

Patients with degenerative joint disease without stenosis are usually asymptomatic, but can report back pain or difficulty bending. If stenosis is present, patients may report buttock or lower extremity symptoms as well.

Osteophytes emanating from the vertebral bodies or facet joints may impinge on isolated nerve roots, causing pains or paresthesias suggestive of a disc herniation. Hypertrophy of the ligamentum flavum and disc prolapse additionally combine to narrow the spinal canal.

The back pain of lumbar spondylosis is often described as “mechanical”, meaning that motion provokes the pain. Yet spondylosis can at times produce pain at rest as well: degeneration-induced instability of the vertebral bodies can initiate compensatory muscle spasm to limit motion and the pain from this muscle spasm might endure throughout the day, even at rest. This phenomenon can make diagnosis more difficult, as pain at rest normally suggests a cause outside of arthritis.

Lumbar stenosis can cause neurogenic claudication. (The word claudication comes from a Latin verb claudicare, meaning ‘to limp’, but in modern parlance refers to lower extremity pain and not a limp, per se.) The adjective “neurogenic” is used to distinguish this pattern of symptoms from vascular (or “classic”) claudication, which is caused by peripheral arterial insufficiency. Both types of claudication are produced by ischemia: in neurogenic claudication the spinal nerve roots are ischemic, whereas in vascular claudication, the leg muscles themselves are deprived of blood flow.

One way to differentiate the two types of claudication is that neurogenic claudication alone can be relieved by bending over. Patients with neurogenic claudication report that riding a bicycle or walking while pushing a shopping cart produces surprisingly little pain, despite the exertion. Spinal flexion tends to maximally open the spinal canal, whereas extension of the spine as seen with upright standing tends to compress the central canal. (This is analogous to Phalen’s maneuver compressing the carpal tunnel, with pressure relieved by holding the wrist in a neutral position.)

The location of the symptoms may be informative too. Neurogenic claudication usually causes symptoms proximally, primarily in the buttock and posterior thigh. Vascular claudication, mediated by decreased blood flow to the muscles, appears first distally in the calf.

On examination, patients with vascular claudication may show signs of arterial insufficiency such as cool, brittle, shiny skin on the legs, and weak or absent pulses. In contrast, patients with neurogenic claudication are more likely to have normal skin color, texture, and temperature in their lower extremities and normal palpable pulses.

Historically, students have been taught that vascular claudication can be identified by its “dose-dependent” symptoms, meaning that the pain of vascular claudication is initiated and worsened with movement and ameliorated by rest, in a crescendo/decrescendo pattern. By contrast, symptoms of neurogenic claudication were taught to be less related to the duration of activity and more to spinal position (flexion and extension). Although one recent study [doi: 10.1503/cjs.016512] found that the “classic symptom attributes used to differentiate neurogenic from vascular claudication are at best weakly valid independently,” the constellation of symptoms can be a useful diagnostic guide.

Objective Evidence

Lab studies are usually not indicated unless there is concern for an infectious or neoplastic process. An electromyelogram (EMG) with nerve conduction studies can often help differentiate lower lumbar radiculopathy due to stenosis from peripheral neuropathy due to diabetes.

Radiographs in the setting of spondylosis (see Figures 5 and 6) may show disk-space narrowing, facet-joint hypertrophy, spondylolisthesis, end-plate sclerosis, and osteophytosis.

Figure 5: Lateral radiograph of the lumbar spine showing degenerative narrowing of the L5/S1 disc space (red arrow) contrasted to the normal space (shown in green) at the levels above. (Courtesy of https://doi.org/10.1155/2012/413913 Diagnostic Testing for Degenerative Disc Disease by Michael W. Hasz)

Figure 6: Lateral radiograph of the lumbar spine showing degenerative spondylolisthesis of L4-5 level (red arrow). (Courtesy of Minimally invasive versus traditional open transforaminal lumbar inter body fusion for the treatment of low-grade degenerative spondylolisthesis, a retrospective study. Sci Rep 10, 21851 (2020). https://doi.org/10.1038/s41598-020-78984-x)

Advanced imaging such as CT and MRI can confirm the diagnosis of spinal stenosis and can show both narrowing of the central canal and neural foramina. The central canal is considered stenotic when measured to have less than a 100 mm2 cross-sectional area or less than a 10 mm A-P diameter on CT scan.

CT is more sensitive for detecting bony abnormalities such as facet joint hypertrophy and osteophytes; MRI (see Figure 7) is more sensitive for detecting spinal stenosis from ligamentous hypertrophy and disc degeneration.

Figure 7: A sagittal T2-weighted MRI image demonstrating the darker discs at the L4-L5 and L5-S1 levels (blue stars), indicating dissection and degeneration, contrasted with the brighter signal within the L3-L4 disc, denoted by the yellow star. The normal posterior disc border at L3-L4 is contrasted with the protrusion of the L4-L5 disc (shown by red line). (Courtesy of https://doi.org/10.1155/2012/413913 Diagnostic Testing for Degenerative Disc Disease by Michael W. Hasz)

Figure 8: A matched pair of sagittal and axial views. The pair in the blue box above shows age-normal degenerative changes. The axial view shown at right is taken at the level of the blue line coursing through the disc in the figure at left. The space of the canal and recesses is shown by the yellow circle. Stenosis is seen below in the red box. In the sagittal view to the left, the decreased anterior-to-posterior space is outlined by the orange bracket. To the right, the smaller space of the stenotic canal and recesses is shown by the orange circle. (Images courtesy of Nader M. Hebela.)

It is important to note that many people over the age of 60 may show signs of spinal stenosis on imaging even if they have no symptoms. Thus, although these imaging modalities are sensitive, they are not clinically specific.
Lastly, CT myelogram is an option for patients who cannot undergo an MRI. In a CT myelogram, dye is injected intrathecally. Radiographs and a CT scan are obtained to reveal neural structure impingement as well as bony abnormalities.

Epidemiology

Degenerative change in the spine is a universal phenomenon of aging. Approximately 10% of the adult population suffers from symptomatic lumbar spondylosis, with women and men affected equally. The peak incidence of seeking care for lumbar spondylosis occurs around the age of 65. Although degeneration increases with age, older people tend to be less active. These processes may offset, such that the objective increase in degenerative disease may not necessarily cause increased subjective symptoms. Lumbar spondylosis with stenosis most commonly occurs at the L4-5 level.

Differential Diagnosis

The differential diagnosis of lumbar spondylosis is based on the presenting symptoms. If the chief complaint is back pain, the following musculoskeletal diagnoses must be considered: muscular strains, disc disease, degenerative arthritis, inflammatory arthropathies, and less likely, infection and malignancy. (In patients at risk, osteoporotic compression fracture is also on the differential diagnosis.) If the chief complaint is claudication, the main diagnostic entities to consider are vascular insufficiency, diabetic neuropathy, and large central disc herniations.
Note also that back pain can have a non-musculoskeletal cause. Abdominal aortic aneurysms, gynecologic disorders such as endometriosis and tubal pregnancy, gastrointestinal disorders such as ulcers and pancreatitis, and kidney stones may present with back pain.

Red Flags

The compression of multiple nerves in the cauda equina often leads to unilateral or bilateral lower extremity pain and sensorimotor changes. Rarely, these changes can cause bowel/bladder dysfunction, manifest as incontinence or urinary retention (with overflow incontinence and increased post-void residuals).
Night pain can be present with lumbar degenerative disc disease/degenerative joint disease, as noted, but severe night pain - enough to wake the patient - especially if there are systemic complaints such as fever or weight loss, should raise suspicion of spinal infection or metastasis.

Treatment Options and Outcomes

Needless to say, not all back pain requires medical treatment. Diagnostic investigations may discover incidental findings that are not the true cause of symptoms. Furthermore, surgical treatment is typically reserved for symptomatic neurologic compression, which manifests as lower extremity symptoms, and not isolated back pain.

If pain requires intervention, a non-operative approach is the best first option. Such treatment includes a period of relative (but not complete) rest, use of NSAIDs, hot or cold compresses, and physical therapy. Physical therapy is aimed at core strengthening and muscular rehabilitation. Stationary biking (and other exercises that incorporate lumbar flexion) are usually better tolerated by patients than exercises like walking or jogging that require lumbar extension.

Steroid injections and hyaluronic acid injections can be trialed prior to considering a more aggressive approach.

In cases of progressive neurologic deficits or unremitting and extremely debilitating pain, a patient may elect to proceed with a surgical procedure.

Laminectomy, which involves the partial or total excision of a lamina, may be used to remove osteophytes and fibrotic ligaments. Fusion can be performed in cases of spinal instability or degenerative spondylolisthesis (see Figure 9), although more recent studies are beginning to question the benefits of fusion versus laminectomy and decompression alone.

Figure 9: Lateral radiograph of the lumbar spine, Fusion of the degenerative L4-5 anterolisthesis shown above in Figure 6. (Courtesy of Minimally invasive versus traditional open transforaminal lumbar inter body fusion for the treatment of low-grade degenerative spondylolisthesis, a retrospective study. Sci Rep 10, 21851 (2020). https://doi.org/10.1038/s41598-020-78984-x)

Various types of decompressions can be performed, including laminectomy, laminotomy, or foraminotomy (Figure 10). The decision on which procedure to do depends on the location of the symptomatic neural compression.

Figure 10: A schematic superior view of a normal lumbar vertebral body (top left) with a patent canal, shown in yellow. A similar view with lumbar spondylosis in which soft tissue and bony overgrowth along with disc protrusion produce a highly stenotic canal shown in red (top right). Shown at bottom left is a bilateral laminectomy (green arrows), with a wider decompression sacrificing the articular processes shown to the right (pink star). This more extensive resection provides greater decompression, but the absence of the facets necessitates the addition of surgical fusion to stabilize the spine.

Laminotomy, which removes only a small part of the lamina, can be used as an alternative to laminectomy.
Another alternative to laminectomy is interspinous distraction, although studies suggest that the benefits of this treatment do not persist over time.

Alternative therapies for lumbar spondylosis include yoga, transcutaneous electrical nerve stimulation (TENS), chiropractic, aromatherapy, acupuncture, and deep tissue massage.

Surgery has been associated with greater symptomatic improvement as compared to non-operative treatment at one to eight years, but this difference narrows through the years. Improvements in function and patient satisfaction are also noted with surgery, although recurrence of spinal stenosis adjacent to the level of decompression can occur. Reoperation and secondary procedures are needed in about 15% of cases. Common surgical complications include superficial and deep wound infections, dural tears, and blood loss requiring transfusion. Neurologic injuries, including sensory and motor dysfunction, are also possible complications but are seen less frequently.

Risk Factors and Prevention

Age is the greatest risk factor in the development of lumbar degenerative spondylosis. Obesity (which increases the load on the spine), family history, and trauma or injury to the back are also known associations with these degenerative conditions as well as spinal stenosis. Specific occupations and sports that involve bending or heavy lifting can increase the risk of degenerative joint disease (DJD) and degenerative disc disease (DDD). Women are at a greater risk of developing DJD and spinal stenosis than are men. DJD, DDD, spondylolisthesis, spondylolysis, and congenitally shortened pedicles predispose an individual to spinal stenosis. The last scenario, known as congenital stenosis, usually becomes apparent in the 2nd through 4th decades. Shortened pedicles, though also seen in the general population, are a common feature of achondroplasia. Prior surgical interventions such as laminectomy and fusion are additional risk factors. Lastly, certain endocrinopathies and iatrogenic causes, such as Cushing’s syndrome, Paget’s disease, acromegaly, and exogenous steroid use, are associated with spinal stenosis.

Weight loss, proper technique when bending and lifting, and exercising good posture can help prevent the development of DJD and DDD. Physical activity that promotes core strengthening and back flexibility may also be beneficial.

Miscellany

Short-legged dog breeds, including dachshunds, basset hounds, corgis, and shih tzus, are very commonly affected by lumbar degenerative disc stenosis. Up to a quarter of dachshunds acquire the disease.

Key Terms

Spondylosis, degenerative disc disease (DDD), degenerative joint disease (DJD), facet joint arthritis, osteophytes, spinal stenosis, central stenosis, foraminal stenosis, neurogenic claudication, laminectomy, foraminotomy

Skills

Describe the process of disc and joint degeneration and understand how both conditions can lead to spinal stenosis. Differentiate neurogenic and vascular claudication. Identify the imaging findings associated with degenerative spondylosis.