AAOS Comprehensive Orthopaedic Review

Section 7 - Spine

Chapter 70. Lumbar Degenerative Disease and Low Back Pain

I. Prevalence of Lumbar Degenerative Disease

A. In asymptomatic individuals

 

1. One third of asymptomatic individuals will have lumbar MRI scans that demonstrate degeneration.

 

2. 20% of people younger than 60 years of age will have herniated disks.

 

B. In individuals older than 60 years of age

 

1. 57% will have abnormal MRI scans.

 

2. 21% will have herniated disks.

 

3. Abnormal findings are present in almost all people older than age 60 years.



II. Low Back Pain

A. Epidemiology

 

1. 70% to 85% of all individuals will experience low back pain at some time in their lives; usually, it resolves in a matter of weeks.

 

2. The annual incidence of back pain in adults is 15%, and point prevalence is 30%.

 

3. Low back pain is the leading cause of disability in people younger than 50 years of age.

 

4. Back pain occurs with equal frequency in males and females.

 

5. Low back pain occurs in all age groups; however, those between 35 and 50 years of age are most commonly affected.

 

B. Primary causes of low back pain

 

1. Muscle strain or ligament sprain

 

   *Michael Steinmetz, MD, or the department with which he is affiliated has received miscellaneous nonincome support, commercially derived honoraria, or other non-research related funding from Stryker Spine.

 

2. Facet joint arthropathy

 

3. Discogenic pain or annular tears

 

4. Spondylolisthesis

 

5. Spinal stenosis



III. Evaluation

A. History

 

1. Lumbar degeneration can result in back pain with or without radicular pelvic or leg pain.

 

2. The differential diagnosis for spinal causes of back pain is extensive (

Table 1), but an adequate history and examination can narrow the possibilities.

 

3. Various extraspinal conditions also can cause back pain (

Table 2).

 

4. Knowing the history of previous spinal surgery and any associated complications is critical.

 

5. Attention should be paid to any inconsistencies provided by the patient or referring parties and any potential secondary gain issues. If indicated, inquiry into ongoing litigation should be made.

 

B. Neurologic assessment

 

1. Note any weakness. If present, ask the patient to describe examples of the weakness, as this will narrow the scope of the problem.

 

2. The effect of position on symptoms and exacerbating or ameliorating factors should be noted.

 

C. Physical examination

 

1. Observe the patient closely while walking and during transfers, noting any pain, antalgia, or ataxia.

 

2. Perform a meticulous neurologic examination and note any inconsistencies.

 

3. Always perform provocative testing (eg, straight-leg raise, femoral stretch test).

 

[Table 1. Spinal Causes of Back Pain]

D. Imaging

 

1. Radiographs

 

a. AP and lateral radiographs should be the first study used in evaluation of the lumbar spine.

 

i. These views should be obtained in patients who have had low back pain for 6 weeks if there are no red flags. The presence of signs or symptoms indicative of malignancy or infection warrants early radiographic work.

 

ii. Coronal and sagittal alignment as well as the presence or absence of disk degeneration, osseous or soft-tissue abnormalities, and atherosclerosis of the abdominal vasculature should all be noted.

 

b. Oblique views should be obtained in patients suspected of having pars interarticularis defects.

 

c. Flexion and extension views should be obtained in the setting of spondylolisthesis or suspected ligamentous instability. Static radiographs and MRI are not sufficient to diagnose or quantify segmental instability.

 

[Table 2. Extraspinal Causes of Back Pain]

2. Magnetic resonance imaging

 

a. MRI demonstrates spinal soft-tissue anatomy better than any other imaging modality.

 

b. MRI must be used as an adjunct to the history and physical examination; a decision to operate should not be based solely on MRI findings.

 

c. MRI should be obtained in cases of suspected malignancy, infection, and in cases of isolated back pain unresponsive to nonsurgical care for 3 months.

 

d. MRI is indicated for patients who present with or develop focal or diffuse neurologic deficits.

 

e. MRI is not indicated in most patients who present with painful lumbar radiculopathy until they fail 6 weeks of nonsurgical care or they deteriorate clinically (ie, progression of pain, development of neurologic deficits). MRI is indicated in patients who present initially with intractable leg pain and are thus unable to proceed with nonsurgical management.

 

f. Postoperative patients should have MRI with intravenous contrast to help differentiate perineural fibrosis and disk degeneration.

 

i. Scar is vascular and is hyperintense on T1-weighted images.

 

ii. Disk material is avascular and hypointense on T1-weighted images.

 

g. MRI in patients with retained hardware will often generate abundant artifact that can obscure the area of clinical interest.

 

i. The use of fast spin-echo sequences without fat saturation can minimize the artifact.

 

ii. In cases with poorly defined anatomy, a CT with myelography (CT myelogram) may be of use.

 

3. CT myelogram

 

a. CT myelogram is useful in defining patterns of central, lateral recess, foraminal stenosis with and without retained hardware, and fusion status.

 

b. Sagittal and coronal reconstructions are particularly helpful in fusion assessment.

 

c. CT without myelography is very useful in defining structural integrity in cases of neoplasm and infection.



IV. Low Back Pain Associated With Degenerative Disk Disease

A. Intervertebral disk degeneration

 

1. Disk degeneration usually begins in the third decade of life.

 

2. Disk degeneration is characterized by a decline in proteoglycan concentration with resultant loss of hydration, a decreased number of viable cells, a decrease in pyridinoline cross-links, and an increase in pentosidine cross-links. Pentosidine is a cross-link between arginine and glycine, and is a marker of advanced glycosylation.

 

3. In degenerative disk disease (DDD), the size of the outer anulus fibrosis remains constant, but the fibrocartilaginous inner layers of the anulus expand.

 

4. With progression of the DDD, disk height decreases, resulting in alteration of the segmental spinal biomechanics.

 

5. In the early stages of degeneration, both anabolic and catabolic metabolism are increased. The matrix demonstrates net degeneration when the catabolic rate supersedes the anabolic rate.

 

6. The precise cause(s) of disk degeneration are unclear, and there are several potential contributors.

 

a. Comorbidities such as diabetes mellitus, vascular insufficiency, and smoking are potentially associated with disk degeneration.

 

b. There is thought to be a genetic component to disk degeneration, but the precise gene(s) and associated pathophysiology have yet to be elucidated.

 

7. L4-5 and L5-S1 are the disks that typically degenerate first.

 

8. The Kirkaldy-Willis degenerative cascade describes three general stages of disk degeneration following torsional injury:

 

a. Phase I (dysfunctional stage): Significant dysfunction is caused by the acute back pain following the injury.

 

b. Phase II (unstable phase): Long phase of relative instability at the particular vertebral segment, which makes the patient prone to intermittent bouts of back pain.

 

c. Phase III (stabilization phase): Segmental restabilization occurs, and there are fewer episodes of back pain.

 

B. Etiology of low back pain

 

1. The relationship between disk degeneration and low back pain is incompletely understood. Some patients with pronounced disk degeneration have low back pain, but others with the same degree of pathology have no pain at all. Hence, there is no direct correlation between DDD and low back pain.

 

2. Factors that may play a role in the generation of low back pain:

 

a. Altered segmental biomechanics due to disk degeneration.

 

b. Neural hypersensitivity secondary to release of neural mediators (eg, phospholipase A2, nitric oxide, glutamate, substance P, calcitonin gene-related peptide).

 

c. Neurovascular ingrowth into the disk.

 

3. As the disk height decreases, the loading characteristics of the facet joints are altered. As competency of the facet joint capsules is compromised, abnormal motion ensues, causing facet joint degeneration and hypertrophy.

 

C. Acute low back pain

 

1. Differentiating between acute and chronic back pain is important because the natural history, treatment, and prognosis are different.

 

a. Acute low back pain is defined as functionally limiting pain lasting less than 3 months or, most commonly, as back pain lasting 6 weeks to 3 months.

 

b. Chronic low back pain is defined as pain lasting more than 3 months or frequently recurring low back pain.

 

2. Patients with acute low back pain typically present with nonspecific back symptoms and without neurologic symptoms. A specific cause is seldom identified.

 

3. The natural history of most episodes of acute low back pain is that of a self-limiting process. However, a detailed history is critical during evaluation of these patients, and the clinician should always maintain an awareness of red flags that signify serious conditions (

Table 3).

 

4. Physiologic assessment with electromyography (EMG) and/or nerve conduction velocity (NCV) studies of limb pain is rarely necessary to evaluate and treat patients with a radicular component. If the etiology is in question, however, EMG/NCV can be a useful adjunct in the diagnostic arsenal.

 

5. Treatment

 

a. Nonsurgical

 

i. The mainstay of therapy for acute low back pain is nonsurgical.

 

ii. Strong evidence supports the use of acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants; moderate evidence supports the use of analgesics and spinal manipulation for pain relief.

 

iii. Active physical therapy has been shown to have a greater benefit than medical therapy alone.

 

iv. There is insufficient evidence to support the use of alternative treatments including acupuncture, botanical medicine, or dry needle therapy.

 

v. Bed rest and passive modalities should be avoided.

 

b. Surgical

 

i. Surgical management for acute low back pain is reserved for patients with serious underlying pathology.

 

ii. Cauda equina syndrome, infection, neoplasia, and fracture all require emergent surgical consultation and possible decompression/stabilization.

 

iii. In the absence of a progressive neurologic deficit, a deficit that does not improve with time, or intractable pain, surgical management of sciatica due to a herniated nucleus pulposus should follow at least 6 weeks of nonsurgical care.

 

iv. Patients with symptomatic lumbar stenosis should try a nonsurgical course for 8 to 12 weeks.

 

D. Chronic low back pain

 

1. The treatment of chronic low back pain (defined above) is controversial; there is no consensus on surgical versus nonsurgical treatment.

 

2. Important principles in the evaluation of patients with chronic low back pain

 

a. Rule out serious pathology, including neoplasia, trauma, and infection.

 

b. Screen for secondary gain issues or psychological abnormalities and inconsistencies.

 

c. Localize the pain to a specific region of the spine, and characterize the type of pain (mechanical versus myofascial).

 

d. Facet blocks and diskography are helpful adjuncts to the diagnostic process, but they do not replace a rational consideration of the history, examination, and pertinent studies.

 

e. Determine if there is correlative pathology that could account for the pain (eg, segmental instability, pars interarticularis defect, deformity) rather than generalized DDD.

 

f. DDD does not correlate well with back pain, and its presence on imaging studies should not be the sole dictator of surgical planning.

 

3. In the absence of a neurologic deficit, infection, or neoplasia, surgery for chronic low back pain generally should not be considered until a structured 6-month regimen of active physical therapy, NSAIDs, and behavioral modification (smoking cessation, weight loss, activity alteration, etc) has failed to improve the patient's pain.

 

E. Surgical treatment

 

1. Fusion via either an open or minimally invasive approach.

 

a.

Three options:

i. Posterolateral

 

ii. Posterior lumbar interbody fusion (PLIF)

 

iii. Transforaminal interbody fusion (TLIF)

b.

None of these forms of fusion has been shown

 

[Table 3. Red Flags in Acute Low Back Pain Evaluation]

 

to be superior to the others in the surgical treatment of low back pain.

c.

It is unclear currently if minimally invasive fusion surgery is more efficacious than open surgery for low back pain.

 

2. Nonfusion options

 

a. Dynamic stabilization systems and interspinous spacers—These devices are thought to minimize low back pain by unloading or diminishing motion of a spondylotic segment. Their efficacy has not been validated in the literature for the treatment of chronic low back pain.

 

b. Total disk arthroplasty (TDA)

 

i. TDA is currently being studied as an alternative to fusion for the treatment of symptomatic DDD.

 

ii. Theoretical advantages of TDA are preservation of motion and the prevention of adjacent-level degeneration and disease.

 

iii. Based on the randomized clinical trials published to date, single-level TDA appears to be equivalent to lumbar fusion in reducing back pain.

 

iv. TDA is neither indicated nor approved for multilevel use.

 

v. Lumbar TDA has been shown to maintain motion at the surgical level; however, it has not been shown to decrease the incidence of adjacent-segment degeneration or disease. This requires longer-term follow-up.

 

vi. The wear debris characteristics and device-related morbidity are not clearly defined as of this writing. Based on the data available, TDA does not appear to have a more morbid side effect profile compared to lumbar fusion.

 

vii. Long-term evaluation of TDA patients is necessary.



V. Disk Herniations/Herniated Nucleus Pulposus

A. Thoracic disk herniation (TDH)

 

1. Epidemiology

 

a. TDHs represent 0.15% to 4% of cases of symptomatic herniated nucleus pulposus (HNP).

 

b. Most TDHs occur in the caudal third of the thoracic spine.

 

c. Men and women are affected equally.

 

d. Individuals from 30 to 60 years of age are most commonly affected.

 

e. TDH may result in radiculopathy or myelopathy, depending on the site of herniation (lateral/paracentral versus central).

 

[

Figure 1. T2-weighted images that demonstrate a left L5-S1 paracentral disk herniation with an inferiorly migrated fragment in a patient with a left S1 radiculopathy.]

2. Treatment depends on the associated clinical syndrome.

 

a. Nonsurgical treatment—Usually effective for thoracic pain and radiculopathy.

 

b. Surgical treatment—Indicated for myelopathy. The surgical approach is dictated by the location of the herniation.

 

i. Central herniations are often easier to access via a transthoracic approach.

 

ii. Paracentral herniations are often accessible via a posterior approach.

 

B. Lumbar disk herniation (LDH)

 

1. Epidemiology

 

a. Peak incidence is in the fourth and fifth decades of life.

 

b. Only 4% to 6% of LDHs become symptomatic.

 

c. Men are three times more likely to sustain an LDH.

 

d. 1% to 3% of individuals will undergo surgical intervention for an LDH at some point in their life.

 

e. Only 2% to 4% of LDHs are surgical candidates.

 

f. Caudal segments are affected more commonly (L5-S1 more commonly affected than L4-5).

 

2. Natural history

 

a. Within 3 months of symptom onset, approximately 90% of patients will experience symptomatic improvement without surgery.

 

b. Most LDHs, particularly contained ones, will resorb and diminish in size over time.

 

3. Clinical presentation

 

a. An LDH may or may not be associated with an inciting event (eg, load bearing).

 

b. The patient typically presents with varying degrees of back and leg pain.

 

c. Leg pain usually follows the dermatomal path of the affected root(s).

 

d. Radicular pain may be accompanied by motor, sensory, and/or reflex disturbances.

 

e. Presence of sciatica is the most sensitive and specific finding for LDH.

 

f. Cauda equina syndrome secondary to large central LDHs is rare.

 

4. Herniation morphology

 

a. Protrusion—Eccentric bulging through an intact anulus.

 

b. Extrusion—Disk material that crosses the anulus but is continuous within the disk space.

 

c. Sequestered—Herniation that is not continuous within the disk space; also known as a free fragment (Figure 1).

 

5. Physical examination

 

a.

The ipsilateral hip and knee may be flexed and externally rotated to relieve root tension.

 

[

Table 4. Provocative Tests]

[

Figure 2. Neurologic evaluation of the lower extremity.]

b.

Pain with straight-leg raise testing results from increased nerve root tension and lack of normal excursion of the root at the herniation site. A positive crossed straight-leg raise test has a higher specificity than a positive ipsilateral test, but the sensitivity is variable. Table 4 lists relevant provocative testing.

c.

The nerve root(s) affected depends on the level of the herniation and the region within a particular segment where a disk is herniated. Figure 2 lists the motor, sensory, and reflex contributions of roots L4-S1. A radiculopathy can result in sensory, motor, or reflex examination deficits for the affected root. It is critical to understand the anatomy as it relates to normal and abnormal exams.

i. A paracentral disk herniation will affect the traversing nerve root (eg, an L4-5 right paracentral LDH will affect the right traversing L5 nerve root and present as a L5 radiculopathy).

 

ii. A far lateral disk herniation (also known as intraforaminal or extraforaminal), which represents a minority of LDHs, will affect the exiting nerve root (eg, an L4-5 right far lateral LDH will affect the right exiting L4 nerve root).

 

iii. An axillary LDH can affect both the exiting and traversing roots.

 

6. Nonsurgical treatment—see

Table 5.

 

7. Surgical treatment

 

a. Surgery is rarely indicated earlier than 6 weeks from onset of symptoms, but it should not be delayed beyond 3 to 4 months.

 

b. Absolute indications are cauda equina or progressive neurologic deficit, but both are rare.

 

c. Relative indications

 

i. Intractable radicular pain

 

ii. Neurologic deficit that does not improve with nonsurgical care and "tincture of time"

 

iii. Recurrent sciatica following a successful trial of nonsurgical care

 

iv. Significant motor deficit (controversy exists as to what constitutes this) with positive tension signs

 

d. Surgical procedures

 

i. A partial diskectomy remains the standard of care.

 

ii. This can be done with an open approach or through a minimally invasive approach (eg, tubular access).

 

iii. No level I evidence demonstrates superiority of either type of surgery in the long term.

 

e. Outcomes—The most consistent finding postoperatively is improvement in leg pain.



VI. Lumbar Stenosis

A. Overview/epidemiology

 

1. The incidence of lumbar spinal stenosis (LSS) is 1.7% to 8% in the general population; the incidence increases in the fifth decade of life.

 

2. Spinal stenosis simply means a decrease in the space available for the neural elements, and, in the lumbar spine, the cauda equina.

 

3. LSS can be congenital, acquired, or a combination of both. Acquired stenosis can be degenerative, iatrogenic, neoplastic, or traumatic, and it can be associated with disorders such as acromegaly, Paget disease, and ankylosing spondylitis.

 

4. LSS is the most common diagnosis requiring spine surgery in patients older than 65 years of age.

 

5. The natural history of spinal stenosis is not well understood.

 

a. It is typically favorable, with only ~15% deteriorating clinically.

 

b. Improvement occurs in 30% to 50% of patients.

 

[Table 5. Nonsurgical Treatment Options for Lumbar Disk Herniation]

B. Anatomic considerations

 

1. Each spinal segment consists of three joints—the intervertebral disk and two facet joints.

 

2. The spinal canal can be considered as three distinct regions:

 

a. The central canal is defined as the space posterior to the posterior longitudinal ligament, anterior to the ligamentum flavum and laminae, and bordered laterally by the medial border of the superior articular process.

 

b. The lateral recess is defined by the superior articular facet posteriorly, the thecal sac medially, the pedicle laterally, and the posterolateral vertebral body anteriorly.

 

c. The intervertebral foramen is bordered superiorly and inferiorly by the adjacent level pedicles, posteriorly by the facet joint and lateral extensions of the ligamentum flavum, and anteriorly by the adjacent vertebral bodies and disk. Normal foraminal height is 20 to 30 mm; superior width is 8 to 10 mm.

 

C. Pathophysiology

 

1. Lumbar spinal stenosis is the final result of a cascade of events.

 

a. The event that begins the process that eventually results in LSS is thought to be disk degeneration.

 

b. As the disk height decreases, the loading characteristics of the facets are altered.

 

c. Facet joint capsules become incompetent, leading to capsular, ligamentum flavum, and facet hypertrophy.

 

d. The ligamentum flavum also becomes less pliable with age.

 

e. The final result of this continuum of changes is a decrease in the diameter of the spinal canal.

 

2. When the spine is in extension, the spinal canal diameter diminishes as a result of the buckling of the shortened, hypertrophied ligamentum flavum; in flexion, there is a relative increase in the diameter.

 

3. Most authors support a multifactorial etiology of low back pain and leg pain associated with LSS. Mechanical compression, nutritive insufficiency, heredity, structural decompression, individual pain perception, and chemical insult all likely play a role.

 

D. Evaluation

 

1. History

 

a. LSS is typically a disease of exertion.

 

b. Patients typically present with pain; paresthesias; subjective weakness; or "heaviness" in the back, buttock(s), and lower extremity(-ies) that occurs with walking, prolonged standing, walking down hills, and/or descending stairs.

 

c. The symptoms usually start proximally and progress distally, as opposed to vascular disease, in which the opposite occurs.

 

d. Patients usually gain relief by sitting down (unlike vascular insufficiency, in which stopping walking will alleviate symptoms). Patients should be asked how they make the symptoms abate.

 

e. As LSS progresses, patients report being increasingly limited in the distance and intensity of ambulation.

 

f. Common symptoms are pseudoclaudication and standing discomfort (94%), numbness (63%), and subjective weakness (43%).

 

g. The differential diagnosis should always include vascular disease, hip pathology, and peripheral neuropathy.

 

h. Patients with central stenosis often present with pseudoclaudication and are usually older, and those with lateral recess and foraminal stenosis have more of a radicular component and may have pain at rest.

 

2. Physical examination

 

a. The examination in most patients with LSS is normal, but weakness, numbness, and reflex abnormalities can occur.

 

b. A vascular examination must be performed in all patients with suspected LSS.

 

c. A positive lumbar extension test is highly predictive of LSS.

 

E. Imaging

 

1. In patients who do not respond to a nonsurgical approach or deteriorate neurologically, plain radiographs, MRI, and/or myelogram with CT are indicated to delineate the pattern and degree of stenosis (

Figure 3).

 

2. EMG may be helpful to distinguish peripheral neuropathy from LSS.

 

F. Treatment—The decision whether to treat nonsurgically or surgically must be made after consideration of the degree of patient disability, the physical examination, and correlative pathology. The importance of sound clinical acumen in developing an efficacious treatment strategy for patients with LSS cannot be overstated.

 

1. Nonsurgical treatment

 

a. Drug therapy

 

i. Acetaminophen with or without NSAIDs should be used initially.

 

ii. Narcotics and muscle relaxants should be used sparingly and short-term for patients with severe pain.

 

iii. Third-generation anticonvulsants (eg, gabapentin), used to treat neuropathic pain, have been used for some patients with LSS. The efficacy of these medications for LSS is poorly defined, however, and they are not generally recommended.

 

b. Physical therapy—No randomized controlled studies exist that define the effectiveness of physical therapy for symptomatic LSS. Nevertheless, a basic exercise regimen consisting of core strengthening (abdomen, gluteals) with a flexion-based lumbar stabilization program, a flexibility regimen, and aerobic conditioning is recommended.

 

[Figure 3. MRI showing central and lateral recess stenosis from L3-L5.]

c. Steroid injections

 

i. The literature on epidural corticosteroid injections is mixed.

 

ii. They have not been shown to change the natural history of LSS presenting primarily with pseudoclaudication.

 

2. Surgical treatment

 

a. Surgical intervention is indicated in patients whose symptoms fail to improve after a comprehensive nonsurgical regimen.

 

b. Options include laminotomy, laminectomy, and hemilaminectomy; however, a laminectomy is the standard procedure advocated for recalcitrant LSS.

 

c. Several studies indicate that surgically treated patients have more initial symptomatic improvement than do nonsurgically treated patients. However, initial improvements wane as a function of time, presumably due to progression of the degenerative process.

 

d. Multiple studies have shown that both groups of patients improve with time.

 

e. Most studies agree that in the absence of coronal or sagittal plane deformity or segmental instability a decompression without fusion is the proper surgical treatment.

 

f. Indicators of poor outcome after surgery include increased surgical time, single-level decompression, and coexisting comorbidities. (No single comorbidity has been shown to be associated with a worse outcome; they are thought to be additive.)



VII. Spondylolisthesis

A. Five main types of spondylolisthesis

 

1. Degenerative

 

2. Isthmic

 

3. Traumatic (fracture of pars interarticularis)

 

4. Dysplastic (congenital insufficiency of facet joints/disk complex with elongation of the pars interarticularis)

 

5. Iatrogenic (excessive surgical resection of pars interarticularis resulting in pars defect)

 

B. Degenerative spondylolisthesis

 

1. Overview

 

a. Degenerative spondylolisthesis is the anterior translation of a cephalad vertebral body relative to its adjacent caudal vertebra. The articular processes may be sagittally or horizontally oriented or be structurally aberrant. As the disk degenerates, so do the facet capsules and facet joints, thus resulting in segmental instability (

Figure 4).

 

b. Degenerative spondyloslisthesis occurs 6 to 10 times more commonly in women than in men.

 

c. It occurs 5 to 6 times more frequently at L4-5 than other levels, and is associated with sacralization of L5.

 

d. Degenerative spondylolisthesis may result in back pain and/or pseudoclaudication and/or radicular leg pain from associated stenosis.

 

[Figure 4. MRI scan showing degenerative spondylolisthesis and spinal stenosis.]

e. Forward slippage typically will not exceed 30% of the sagittal diameter of the vertebral body.

 

2. Clinical presentation

 

a. Mechanical back pain that is relieved by rest is the most common symptom.

 

b. Leg pain is the second most common symptom. It is usually associated with walking and prolonged standing, and is relieved by rest.

 

3. Physical examination

 

a. The examination is often normal or nonspecific. Decreased and painful lumbar range of motion may be present.

 

b. Hamstring tightness is common and should be distinguished from radicular pain.

 

c. The step-off between the L4 and L5 spinous processes may be palpable in thin patients.

 

4. Nonsurgical treatment

 

a. In the absence of neurologic deterioration, a nonsurgical approach should be initially trialed as outlined above.

 

b. Surgery is reserved for patients not responding appropriately.

 

5. Surgical treatment

 

a. Decompression without fusion

 

i. A meta-analysis of literature on decompression without fusion indicates that 69% of patients treated with decompression alone had satisfactory results.

 

ii. 31% of patients had progression of the slip postoperatively; however, it is unclear if this progression results in poorer outcomes.

 

b. Decompression with fusion

 

i. A meta-analysis of literature on decompression with noninstrumented fusion indicates that 79% of patients report satisfactory outcomes.

 

ii. Bone regrowth following decompression is inversely related to patient outcome. Patients who undergo concomitant fusion have less bone regrowth following surgery, presumably due to the stabilizing effects of fusion.

 

iii. Fusion rates with the use of pedicle screws are higher than in cases where semirigid instrumentation is used or in cases of noninstrumented in situ fusion.

 

iv. Long-term outcome studies indicate that patients who develop successful arthrodesis have better clinical outcomes.

 

C. Isthmic spondylolisthesis

 

1. Overview

 

a. Isthmic spondylolisthesis is the most common type of spondylolisthesis in children and young adults.

 

b. It occurs in 5% of the population.

 

c. It is more common in Eskimos and in young males involved in repetitive hyperextension activities (eg, gymnastics).

 

d. Isthmic spondylolisthesis results from a defect in the pars interarticularis (spondylolysis).

 

e. Associated conditions include spina bifida.

 

f. Isthmic spondylolisthesis most commonly occurs at L5-S1. L4-5 isthmic slips are more prone to progression as the iliolumbar ligament adds stability to the L5-S1 segment.

 

g. Slip progression is most likely to occur in adolescents younger than 15 years of age, usually during the adolescent growth spurt. With skeletal maturity, progression usually does not advance.

 

h. Slip progression occurs in about 20% of adults and coincides with the third decade of life. It is related to progressive disk degeneration that renders the segment relatively unstable.

 

[

Figure 5. The Meyerding classification provides a simple and common quantification of the slip of L5 and S1. A, Grade I defines a slip from 0 to 25%, grade II from 26% to 50%, grade III from 51% to 75%, and grade IV from 76% to 100%. B, To determine the slip angle, a line is drawn parallel to the posterior aspect of the sacrum with a perpendicular line at the level of the cephalad border of the sacrum (because of remodeling), and then a line is drawn at the undersurface of the body of L5. This angle represents the relationship of L5 to the sacrum. C, In higher-grade slips, the sacrum becomes more vertical and the kyphotic deformity increases, as measured by the sacral inclination. D, Sacral slope is defined as the angle between the horizontal reference line and the end-plate line of S1.]

2. Classification—The Meyerding classification for isthmic spondylolisthesis is based on four parameters: slip, slip angle, sacral inclination, and sacral slope (Figure 5).

 

3. Clinical presentation

 

a. Mechanical low back pain

 

b. Altered gait ("pelvic waddle") and hamstring contracture

 

c. Palpable step-off

 

d. Higher-grade slips may present with L5 radiculopathy(ies) due to foraminal stenosis.

 

4. Imaging

 

a. Weight-bearing radiographs may reveal a pars defect or slip.

 

b. Oblique views improve visualization of smaller pars defects.

 

c. Single photon emission CT (SPECT) bone scan is the best test to detect spondylolysis in patients with normal radiographs.

 

d. CT can be used to help define bony morphology.

 

e. MRI is indicated for persistent back pain with or without neurologic component.

 

5. Treatment

 

a. Nonsurgical

 

i. Most patients improve with activity modification and physical therapy (hamstring stretching, lumbar flexibility, and core strengthening).

 

ii. Bracing can be used in children and adolescents if pain is nonresponsive.

 

iii. Most pars defects persist radiographically despite resolution of symptoms.

 

b. Surgical

 

i. In situ posterolateral L5-S1 fusion is indicated for children and adolescents with low-grade (less than 50% slip) spondylolisthesis.

 

ii. Pars repair is indicated for persistently symptomatic patients with spondylosis with minimal DDD, no slippage, and no discogenic component to their pain.

 

iii. Surgical management is indicated for high-grade slips in most children and adolescents irrespective of symptoms. The best method for surgical fusion is controversial.

 

iv. In the adult with persistent symptoms, surgical management is superior to nonsurgical care (

Figure 6).

 

v. For adult grade 1 and 2 slips, the role of anterior column support has not been well defined. Likewise, controversy exists between the benefits of circumferential versus posterolateral fusion alone. For adult grade 3 and 4 slips, evidence supports higher fusion rates with anterior column support.

 

[Figure 6. A, A lateral radiograph of a 32-year-old woman with left leg pain shows a grade II isthmic SPL. Note the retrolisthesis of L4 on L5 (arrow) suggesting degeneration at that level. The asterisk shows the pars defect. B, The PA view shows spina bifida occulta (arrow), which has an association with SPL. C, A sagittal foraminal MRI scan shows severe compression of the L5 root in the foramen (arrow). D and E, Postoperative radiographs obtained 6 months after solid posterolateral fusion with instrumentation. The patient had a classic L4-S1 decompression and is now clinically asymptomatic.]

vi. Partial reduction and transosseous fusions for high-grade spondylolisthesis result in predictably good outcomes.

 

vii. The role of complete reduction has not yet been established.

 

viii. For higher grade slips, it is sometimes necessary to extend fusion to L4 if significant L4-5 degeneration exists or if instrumenting L5 is difficult because of the amount of translation of L5 on S1.

 

ix. A technique that can be used for high-grade slips involves drilling a dorsal to ventral channel from S1 to L5 and placing a strut graft into this tract. This is followed by an instrumented posterolateral fusion.



Top Testing Facts

1. Up to 85% of patients will experience low back pain at some point their lifetime, and it usually resolves in a matter of weeks. The mainstay for treatment of acute low back pain is nonsurgical.

 

2. The vast majority (90%) of symptomatic LDHs improve with nonsurgical management.

 

3. A paracentral disk herniation will affect the traversing nerve root, not the exiting nerve root. For example, an L4-5 left paracentral HNP will result in an L5 radiculopathy, not an L4 radiculopathy.

 

4. An intraforaminal or extraforaminal HNP will affect the exiting root. For example, a far lateral HNP at L3-4 will result in an L3 radiculopathy.

 

5. The absolute indicators for surgical management of LDH are cauda equina and a progressive neurologic deficit. Both are rare.

 

6. Lumbar spinal stenosis is typically associated with exertion. The differential diagnosis includes hip pathology, vascular disease, and peripheral neuropathy.

 

7. The five main types of spondylolisthesis are degenerative, isthmic, traumatic, dysplastic, and iatrogenic.

 

8. In situ posterolateral L5-S1 fusion is indicated for children and adolescents with a low-grade spondylolisthesis.

 

9. Adults with low grade I or II isthmic spondylolisthesis are treated with instrumented L5-S1 fusion; interbody grafting helps with the reduction and increases fusion rates. For grade III slips, it is sometimes necessary to extend the fusion to L4 if there is significant degeneration at L4-5 or if reduction of the L5-S1 slip is not possible.

 

10. A pars repair is indicated for persistently symptomatic patients with spondylosis, minimal DDD, no slippage, and no discogenic component to their pain.



Bibliography

Biyani A, Andersson G: Low back pain: Pathophysiology and management. J Am Acad Orthop Surg 2004;12:106-115.

Carlisle E, Fischgrund J: Lumbar spinal stenosis and degenerative spondylolisthesis, in Spivak J, Connolly P (eds): Orthopaedic Knowledge Update Spine, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2006, pp 299-309.

Fischgrund JS, Mackay M, Herkowitz HN, Brower R, Montgomery DM, Kurz LT: Degerative lumbar spondylolisthesis with spinal stenosis: A prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine 1997;22:2807-2812.

Fritzell P, Hagg O, Wessberg P, Nordwall A: Swedish Lumbar Spine Study Group: Chronic low back pain and fusion: A comparison of three surgical techniques: A prospective multicenter randomized study from the Swedish lumbar spine study group. Spine 2002;27:1131-1141.

Haak M: History and physical examination, in Spivak J, Connolly P (eds): Orthopaedic Knowledge Update Spine, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2006, pp 43-55.

Hanley E, Patt J: Surgical management of lumbar spinal stenosis, in Herkowitz H, Garfin S, Eismont F, Bell G, Balderston R (eds): Rothman-Simeone The Spine, ed 5. Philadelphia, PA, Elsevier Inc, 2006, pp 1015-1024.

Herkowitz HN, Kurz LT: Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg Am 1991;73:802-808.

Kornblum MB, Fischgrund JS, Herkowitz HN, Abraham DA, Berkower DL, Ditkoff JS: Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective long-term study comparing fusion and pseudarthrosis. Spine 2004;29:726-733.

Lin EL, Wang JC: Total disk arthroplasty. J Am Acad Orthop Surg 2006;14:705-714.

Mroz T, Suen P, Payman R, Wang J: Spinal stenosis: Pathophysiology, clinical diagnosis, differential diagnosis, in Herkowitz H, Garfin S, Eismont F, Bell G, Balderston R (eds): Rothman-Simeone The Spine, ed 5. Philadelphia, PA, Elsevier Inc, 2006, pp 995-1009.

Rao R, Bagaria V: Pathophysiology of degenerative disk disease and related symptoms, in Spivak J, Connolly P (eds): Orthopaedic Knowledge Update Spine, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2006, pp 35-41.

Taylor R: Nonoperative management of spinal stenosis, in Herkowitz H, Garfin S, Eismont F, Bell G, Balderston R (eds): Rothman-Simeone The Spine, ed 5. Philadelphia, PA, Elsevier Inc, 2006, pp 1010-1014.

Yu W, Lai Williams S: Spinal imaging: Radiographs, computed tomography, and magnetic imaging, in Spivak J, Connolly P (eds): Orthopaedic Knowledge Update Spine, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2006, pp 57-68.

 

Yue J, Pawardhan A, White A: Acute low back pain, in Spivak J, Connolly P (eds): Orthopaedic Knowledge Update Spine, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2006, pp 281-287.