LUMBAR SPONDYLOSIS

LUMBAR SPONDYLOSIS

Kilian, Robert, and Lambl first described spondylolysis accompanied by spondylolisthesis in the literature in the mid 1800s.

The number of different spinal abnormalities contributing to development of spondylolisthesis was appreciated only after Naugebauer's anatomic studies in the late 1800s.

PATHOPHYSIOLOGY

Spondylolysis is a defect in the pars interarticularis that may or may not be accompanied by forward translation of one vertebra relative to another (spondylolisthesis).

Wiltse, Macnab, and Newman developed a classification to help outline causes of vertebral translation in an anterior direction.

Their categories include the following:

• Type I: Congenital spondylolisthesis

• Type II: Isthmic spondylolisthesis

• Type III: Degenerative spondylolisthesis

• Type IV: Traumatic spondylolisthesis

• Type V: Pathologic spondylolisthesis

Type I: Congenital spondylolisthesis is characterized by presence of dysplastic sacral facet joints allowing forward translation of one vertebra relative to another. Orientation of facets in an axial or sagittal plane may allow for forward translation, producing undue stress on the pars, resulting in a fracture.

Type II: Isthmic spondylolisthesis is caused by the development of a stress fracture of the pars interarticularis.

Type III: Degenerative spondylolisthesis is commonly caused by intersegmental instability produced by facet arthropathy. This variation usually occurs in the adult population and, in most cases, does not progress beyond a grade I spondylolisthesis (see grading system below).

Type IV: Traumatic spondylolisthesis can, in rare instances, result from acute stresses (trauma) to the facet or pars.

Type V: Any bone disorder may destabilize the facet mechanism producing pathologic spondylolisthesis. Iatrogenic spondylolisthesis, lastly, may occur if an overzealous surgeon performs too great of a facetectomy.

The most commonly used grading system for spondylolisthesis is the one proposed by Meyerding in 1947. The degree of slippage is measured as the percentage of distance the anteriorly translated vertebral body has moved forward relative to the superior end plate of the vertebra below.

Classifications use the following grading system:

v  Grade 1: 1- 25% slippage

v  Grade 2: 26-50% slippage

v  Grade 3: 51-75% slippage

v  Grade 4: 76-100% slippage

v  Grade 5: Greater than 100% slippage

FREQUENCY

Wiltse and Beutler each reported an incidence of 6-7% for isthmic spondylolysis. Up to 5% of children aged 5-7 years have been found to

have spondylolysis, many of whom are asymptomatic. The incidence increases up to the 7% by age 18.

Athletic activities requiring repetitive hyperextension and rotation or repetitive combined flexion-extension predispose some athletes to developing pars defects.

Gymnasts, linemen in college football, weight lifters, javelin throwers, pole-vaulters, and judoists are most commonly affected. 

 Approximately 82% of cases of isthmic spondylolisthesis occur at L5-S1.

Another 11.3% occur at L4-L5. Congenital defects, including spina bifida occulta, have been linked to occurrence of isthmic spondylolisthesis.

Scoliosis has been found to occur along with spondylolysis as well.

Roughly 50% of all cases of spondylolysis are not associated with spondylolisthesis.

Degenerative spondylolisthesis occurs more frequently with increasing age. The L4-L5 interspace is affected 6-10 more times than any other level. Sacralization of L5 is frequently seen with L4-5 degenerative spondylolisthesis.

MORTALITY/MORBIDITY

• Increased mortality is not associated with spondylolisthesis. While some patients may have persistent low back pain, significant disability is rare unless the patient has severe neurologic compromise that has not been addressed.

• The most common morbidity is persistent low back pain or nerve impingement. Because disk degeneration is accelerated at the sight of level of the spondylolysis, diskogenic pain may occur. Degenerative spondylolisthesis produces characteristic arthritic symptoms that may worsen with age.

SEX

Beutler et al noted a 2:1 male-to-female ratio of occurrence in asymptomatic patients with spondylolysis.

• Females with isthmic spondylolytic lesions appear to be more prone to progressive displacement and may need surgical intervention more often than males.

• Congenital spondylolisthesis (dysplastic type) occurs with a 2:1 female-to-male ratio with symptoms beginning around the adolescent growth spurt. These comprise about 14-21% of all cases of spondylolisthesis.

• Degenerative spondylolisthesis occurs more commonly in females with a 5:1 female-to-male ratio. The incidence increases after age 40 years.

AGE

• Acute isthmic spondylolysis often occurs during the first and second decades of life. Most cases occur before the patient reaches age 15 years. In rare cases, acute spondylolysis may be seen in early adulthood. Younger patients are at higher risk than older patients for developing progressive spondylolisthesis. The risk for progression in adults is rare when the lesion is at L5. In contrast, lesions at L4-5 may progress into adulthood because of increased sagittal rotation, shear translation, and axial rotation at this segment.

• Congenital/dysplastic spondylolisthesis has been documented in children as young as 3.5 months. More commonly, congenital spondylolistheses go undiagnosed until later in life after an individual has been ambulating for quite some time.

• Degenerative spondylolisthesis occurs most commonly after age 40 years.

CLINICAL

HISTORY

• Isthmic spondylolisthesis

  • Symptoms often occur around the time of an adolescent growth spurt.

  • Some report acute onset of focal low back pain during activity, while others have more insidious onset.

  • Radiating pain may extend to the buttocks or thigh. Pain may be more significant and have mechanical characteristics with higher grades of spondylolisthesis.

  • In most cases, patients do not complain of symptoms suggesting neurologic deficit with lower grades of spondylolisthesis. Radicular pain becomes more common with larger slips. Complaints of radiating pain below the level of the knee associated with numbness and tingling in a dermatomal distribution would suggest the presence a radiculopathy resulting from either the foraminal stenosis that occurs with spondylolisthesis or a concomitant herniated disk. Nerve root impingement from the fibrocartilaginous bar that forms at the sight of the lysis may occur. High degrees of spondylolisthesis may present with neurogenic claudication or symptoms suggesting cauda equina impingement.

  • The patient's pain usually is provoked by activity, particularly back extension activities.

  • Patients with acute spondylolysis tend to demonstrate poor tolerance of activities requiring excessive spine loading, including running and jumping. Sitting usually is better tolerated.

  • A large percentage of patients with spondylolysis are asymptomatic. Progression of a spondylolisthesis also may occur without symptoms.

• Degenerative spondylolisthesis

  • The pain begins insidiously and may be achy in character. Pain is located in the low back and posterior thighs.

  • Neurogenic claudication may be present as well, with lower extremity symptoms being made worse with activity and better with rest.

  • Symptoms are often chronic and progressive, although patients may experience periods of remission.

• Dysplastic spondylolisthesis: Symptoms present much like isthmic spondylolisthesis, but neurologic compromise is more likely.

• Traumatic spondylolisthesis

  • Patients present with acute pain associated with trauma.

  • If a slip is severe enough, cauda equina compression may occur and present with classic symptoms including bowel and bladder dysfunction, radicular symptoms, or neurogenic claudication.

• Pathologic spondylolisthesis: Symptoms may be insidious in onset and associated with radicular pain/claudication.

PHYSICAL

• Isthmic spondylolisthesis

  • Hamstring tightness is observed almost universally, even in low-grade spondylolisthesis.

  • Lumbar spasm may be present.

  • A palpable step-off is noted with slips equal to or greater than grade 2.

  • With higher degrees of spondylolisthesis, an increased lumbosacral kyphosis is seen (50% or greater) along with a compensatory thoracolumbar lordosis. Truncal shortening may be present. With severe slips, the rib cage may rest on the iliac crest.

  • Dermatomal weakness may be present if a radiculopathy or an element of stenosis is present.

  • A waddling gait may be noted secondary to hamstring tightness producing a shortened stride length.

  • If spondylolisthesis is not present, spondylolysis presents with paraspinal spasm, pain provocation with lumbar spine extension, and tight hamstrings.

• Degenerative spondylolisthesis

  • These patients present with less prominent physical findings. Pain often is provoked with lumbar spine extension.

  • If lumbar stenosis is present, then reflexes may be diminished. Radicular findings also may be present.

• Congenital / dysplastic spondylolisthesis: Physical findings are similar to those described above for isthmic spondylolisthesis.

• Traumatic and pathologic spondylolisthesis

  • These patients also present with similar findings.

  • A good neurologic evaluation is important.

CAUSES

• A genetic predisposition to isthmic spondylolisthesis is believed to be linked with patients having a thin pars or subtle hypoplastic facet joints. Family members have a reported incidence of 28-69%. Activities requiring lumbar extension stress increase the risk. Patients with spina bifida occulta are known to have a higher occurrence.

• Degenerative spondylolisthesis is caused by facet degeneration accompanied by disk degeneration most commonly at the level of L4-L5. Some studies identify sagittally oriented facets as more prone to arthritic change.

• Congenital spondylolisthesis is due to dysplastic sacral or lower lumbar segments. Dysplastic facets or abnormal orientation of the facet joints are the cause for spondylolisthesis.

• Traumatic spondylolisthesis is rare. In theory, severe hyperextension stress placed on the pars could produce fracture and instability. One should keep in mind that hyperflexion-distraction forces can cause facet dislocation and spondylolisthesis.

• Pathologic spondylolisthesis can occur as a result of any bone lesion that might weaken the posterior elements. Generalized skeletal diseases including osteomalacia, syphilitic disease, and Von Recklinghausen disease are some reported causes. Bony destructive lesions, including tumor or infection, are other potential causes.

DIAGNOSIS

LABORATORY STUDIES

• Laboratory studies do not help in diagnosing spondylolytic spondylolisthesis. Workup is radiographic in nature.

IMAGING STUDIES

• Radiography

  • Initial workup includes anteroposterior, lateral (done while standing), and spot view radiographs of the lumbar spine and lumbosacral junction. Oblique views may provide additional information but are not obligatory. Flexion/extension views increase the sensitivity of radiographic studies and give the clinician some idea of the degree of instability that may be present. Percentage of slip and slip angle (calculated by measuring the angle formed by a line drawn from superior endplate inferiorly and the inferior endplate at the segment of involvement) are clinically valuable.

    • Radiographic studies allow visualization and grading of spondylolisthesis but may not always reveal the presence of an isolated spondylolysis (without spondylolisthesis). The 'Scottie dog' whose neck is broken can be seen on the oblique films when there is a classic spondylolysis.  

• Bone scan

  • Bone scan with single-photon emission computed tomography (SPECT) imaging is helpful and often helps to direct management.

  • If the bone scan is positive, then the lesion is metabolically active. The physician may consider bracing, since healing is still in progress. A cold scan in the context of documented spondylolysis indicates that healing is complete; therefore, bracing is of limited utility.

  • Computed tomography (CT) scan

  • CT scan performed with 1 mm sections, including coronal and sagittal reconstructions, allows for better visualization of the spondylolytic defect.

  • CT scan not only documents the presence and severity of spondylolysis, but it can help rule out more serious causes for a positive bone scan.

  • Myelogram/CT studies are helpful in delineating the severity of central stenosis. Nerve root cut-off often is observed in the presence of radiculopathy.

• Magnetic resonance imaging (MRI)

  • MRI may visualize edema in the marrow around the sight of an acute spondylolytic defect.

  • MRI also is helpful in identifying the presence of nerve root compression as a result of foraminal or central canal stenosis.

OTHER TESTS

• Electromyography may provide 1 more modality for identifying a concomitant radiculopathy or polyradiculopathy (ie, stenosis), which may be present as a result of spondylolisthesis.

TREATMENT

PHYSICAL THERAPY

Most patients with low-grade isthmic spondylolisthesis and degenerative spondylolisthesis can be treated conservatively.

If an isthmic lesion is acute, the patient should be restricted from provocative activities or sports until they are asymptomatic.

Physical therapy is an integral part of the patient's rehabilitation process. The most accepted protocol includes activity and exercise that reduces extension stress.

The goals of exercise are to improve abdominal strength and increase flexibility.

Since tight hamstrings are almost always part of the clinical picture, appropriate hamstring stretching is important. Instruction in pelvic tilt exercises may help reduce any postural component causing increased lumbar lordosis.

Myofascial release may play a role as well in reducing pain from the surrounding soft tissues.

If conservative treatment is indicated for congenital spondylolisthesis, the above principles apply.

Traumatic spondylolisthesis most often requires surgical stabilization.

SURGICAL INTERVENTION

Surgical treatment is indicated when any type of spondylolisthesis is accompanied by a neurologic deficit. Persistent disabling back pain after conservative management may be considered an indication.

High-grade slips (greater than 50%) more commonly require surgical intervention. Traumatic spondylolisthesis is rare but almost always requires surgical stabilization.

OTHER TREATMENT

v Bracing for acute isthmic spondylolysis/spondylolisthesis is controversial, but it has been shown in some studies to reduce symptoms and to facilitate healing. Most sources discuss use of a thoracolumbosacral spinal orthosis or modified Boston Brace for low-grade slips or for isolated spondylolytic lesions (without spondylolisthesis). Some sources advocate more extensive bracing with inclusion of most of the thorax (to the nipple line) and the thighs. Recommend use of the device for 3-6 months.

v Steroid injections for pars pain have been advocated by some physicians. Epidural steroid injections may help radicular pain or neurogenic claudication.

v Matsudaira et al tested the effectiveness of limaprost, an oral prostaglandin E1 derivative, against that of etodolac, a nonsteroidal anti-inflammatory drug (NSAID), in improving the health-related quality of life in patients with symptomatic lumbar spinal stenosis. In a randomized, controlled trial, 66 patients suffering from central stenosis with acquired, degenerative lumbar spinal stenosis, along with neurogenic intermittent claudication and bilateral leg numbness related to the cauda equina, were administered a daily dose of limaprost (15 μg) or etodolac (400 mg) for 8 weeks. The results indicated that limaprost was more effective than etodolac in improving patients' physical functioning, vitality, and mental health, and in reducing pain and leg numbness.

MEDICATION

The goal of medication in care of spondylolysis or spondylolisthesis of any type is to mitigate pain. NSAIDs are used most commonly while narcotic analgesics are used for breakthrough pain.

NONSTEROIDAL ANTI-INFLAMMATORY MEDICATIONS

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but may inhibit cyclo-oxygenase activity and prostaglandin synthesis.

Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

IBUPROFEN (Ibuprin, Motrin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult: 200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric: <6 months: Not established

6 months to 12 years: 4-10 mg/kg/dose PO tid/qid

>12 years: Administer as in adults

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

NAPROXEN (Naprosyn, Naprelan, Anaprox, Aleve)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Adult: 500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d 

Pediatric: <2 years: Not established

>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

ETODOLAC (Lodine, Lodine XL)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclo-oxygenase, which results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.

Adult: 200-400 mg PO q6-8h prn; not to exceed 1200 mg/d

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely, and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if there is persistent leukopenia, granulocytopenia, or thrombocytopenia

SULINDAC (Clinoril)

Decreases activity of cyclo-oxygenase and in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Adult: 150-200 mg PO bid or 300-400 qd; not to exceed 400 mg/d

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely, and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if there is persistent leukopenia, granulocytopenia, or thrombocytopenia; caution in anticoagulation defects or are receiving anticoagulant therapy

ANALGESICS

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

ACETAMINOPHEN (Tylenol, Feverall, Tempra)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Adult: 650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d

Pediatric: <12 years: 15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d

>12 years: 650 mg PO q4h; not to exceed 5 doses in 24 h

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in patients with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose

HYDROCODONE & ACETAMINOPHEN (Vicodin, Lortab)

Drug combination indicated for moderate to severe pain.

Adult: 1-2 tab or cap PO q4-6h prn pain

Pediatric: <12 years: 10-15 mg/kg/dose acetaminophen PO q4-6h prn; not to exceed 2.6 g/d acetaminophen

>12 years: 750 mg acetaminophen PO q4h; not to exceed 10 mg hydrocodone bitartrate per dose or 5 doses/24 h.