Lumbar disk disease: pathophysiology, management and prevention

Lumbar disk disease: pathophysiology, management and prevention

Holly S. Gilmer

Back pain is one of the leading reasons for office visits to primary care physicians and one of the most common diagnoses for nonsurgical hospital admissions in adults under 65 years of age. More than 75 percent of persons at some time in their lives have severe low back pain that requires medical attention, with an annual incidence of 7 to 15 percent.

Medical expenses directly related to back pain total more than $8 billion per year. Disability payments and indirect expenses are more than double that amount. Although lumbar disk disease accounts for a small percentage of patients with back pain, it has been estimated that the annual medical cost for treatment of lumbar disk disease alone is nearly $5 billion.[1,2]

Low back pain is the leading cause of disability in persons under age 50 and is second only to heart disease as a cause of disability in persons over age 50. It results in the loss of more than 93 million work days each year.[1,2]

Most patients with low back pain respond to conservative measures such as rest, physical therapy and medication. Since surgery is only rarely necessary for the primary treatment of low back pain and lumbar disk disease, family physicians commonly diagnose and treat this condition and thus should be familiar with the pathophysiology, medical and surgical management and strategies for prevention of lumbar disk disease.[1]

Pathophysiology and Risk Factors

Disk herniation is the protrusion of the gelatinous material of the disk (nucleus pulposus) through the annulus fibrosus (Figure 1). Significant herniation occurs most often through a posterolateral defect, but midline herniation is also common.[3] Patients often seek medical attention for a herniated disk when it protrudes into the spinal canal or neural foramen and compresses a spinal nerve root, resulting in pain and/or paresthesias in the sensory distribution of the nerve. The incidence of disk disease and herniation is highest between levels L3 and S1[1] (Figure 2).

Associated risk factors for lumbar disk disease include advanced age, vigorous exercise for more than 15 years or, in persons over 20 years of age, vigorous exercise for less than one year, sedentary work, history of back trauma, male sex, obesity and cigarette smoking.

Histologic studies have shown that the nucleus pulposus becomes progressively more fibrotic, dehydrated and continuous with the annular region as a person ages; thus, a relatively lower incidence of soft disk herniation is seen in the elderly, compared with the incidence of degenerative disk disease.[4]

Prolonged sitting imposes mechanical stress on the spinal column and contributes to general deconditioning of the lumbar musculature. Repeated microtrauma may lead to cumulative degeneration of the lumbar disk; a history of back injury has been found to be a statistically significant factor in symmetric degeneration of the disk. A history of back trauma also correlates with an increased incidence of annular rupture.[1]

Lumbar disk herniation frequently coexists with cervical disk disease. A recent retrospective study[2] of 200 patients who had cervical diskectomy found that 31 percent required lumbar disk surgery.

Psychosocial disturbance may play a role in the etiology or treatment of back pain.[2,4]

Lumbar disk disease progresses as a series of pathophysiologic events, beginning with asymptomatic fissuring and fragmentation within the disk.[1] The nucleus pulposus gradually prolapses through the annulus fibrosus, followed by herniation of the disk into the spinal canal or the neural foramen.[2]

Clinically, the stage of intra-disk breakdown is asymptomatic because of the relatively low nerve supply to the nucleus pulposus. The annulus fibrosus is well innervated, however, and thus its rupture, with prolapse of the herniating nucleus pulposus, is usually manifested as mild to severe back pain, often with radiation to the pelvis and legs. This back pain typically involves multiple exacerbations and remissions.

After the disk fragment has herniated through the annulus and into the spinal canal, the back pain often diminishes significantly, because there is no longer any tension on the annulus. As the disease progresses, unilateral or bilateral leg pain in a radicular pattern characteristically replaces back pain as the chief complaint. Radicular, or sciatic, pain is an important sign of disk herniation and, if possible, should be distinguished from referred leg pain, which indicates that the disk is still confined by the annulus. Lumbar intervertebral disk herniation may also be asymptomatic if nerve root compression is not present.[2 3,5]

Several theories have been proposed for the etiology of the chronic pain associated with disk herniation. Compression of the nerve root results in neural ischemia, neural edema and fibrosis formation. All of these changes may then stimulate the nervi nervorum, resulting in chronic pain.[1]

Chronic inflammation has also been suggested as an etiology of back pain, in addition to chronic mechanical pressure on the annulus and nerve root entrapment. However, because entrapment syndromes are characterized by numbness, while inflammation is almost always associated with pain, it has been argued that chronic inflammation is a more probable cause of back pain. Supporting this theory is the fact that some patients experience a dramatic reduction of pain when given anti-inflammatory drugs. During surgery, an appearance of chronic inflammation in the region of the herniated disk is commonly noted.

Chronic inflammation in the region of a herniated disk may be autoimmune in origin. The annulus pulposus is normally isolated from the body’s immune system until a traumatic or disease-associated event results in growth of granulation tissue. As the nucleus pulposus becomes accessible to the vascular system, an autoimmune response occurs, leading to chronic inflammation in the area.

The mechanical trauma that results in fissuring within the disk and herniation through the annulus fibrosus could stimulate a reparative response, allowing ingrowth of granulation tissue and contact with the immune system. The liberation of phospholipase [A.sub.2] from a herniated disk could also cause direct inflammation in the surrounding region.

The autoimmune theory for disk degeneration is supported by the frequent coexistence of cervical and lumbar disk disease at various levels.[1-6] Nerve endings have also been described in the granulation tissue of degenerate disks, which before herniation had been without innervation. It is possible that normal mechanical stresses on the nonsensory disk become painful because of the ingrowth of these new nerve endings.[1,2-4,7]

Clinical Presentation and Diagnosis

Patients with herniated lumbar disks may present with back pain, referred leg pain, radicular leg pain, sensory changes, leg weakness or a combination of these Symptoms.[2] Back pain caused by a herniated disk may be mild, acute and incapacitating, or chronic and persistent. It may be intermittent or constant.

The most common presenting symptom is severe pain in the lower back and/or leg that develops immediately or within a few hours after an injury. It is not unusual for the pain to begin 24 hour-s or more after a forgotten minor traumatic incident.

The patient may give a history of heavy lifting or twisting, rather than injury. The pain is accentuated by flexion of the spine while moving or sitting, or by increased abdominal pressure (i.e., coughing, sneezing or straining). It may be accompanied by severe muscle spasm.[1] The muscles (primarily the erector spinae) may become ischemic from prolonged contraction, adding to the pain. Pain relief occurs with rest or unloading of the spine.

Referred pain may be localized to the greater trochanter, buttocks and posterior thigh. Referred pain from a herniated disk almost never spreads below the knee.[1] Radiation below the knee suggests radiculopathy rather than referred pain. L5 radiculopathy typically produces shooting pain from the posterolateral thigh down the lateral aspect of the calf to the ankle, in the lateral malleolar region. S1 radiculopathy causes pain that radiates down the posterior thigh and calf to the heel, with paresthesias of the lateral two toes[3] (Table 1 and Figure 3a).


Symptoms of bilateral weakness, fatigue, paresthesias, dysesthesias and numbness are more indicative of bony abnormalities of the spine, such as degenerative spinal stenosis, than of disk disease.[8] Computed tomographic (CT) scanning, magnetic resonance imaging (MRI) or myelography are useful in distinguishing between these two types of spinal pathology.

On physical examination, tenderness to pressure is present, usually on one side and at one level. There is often prominent muscle spasm, leading to decreased joint mobility at the affected segment. Functional scoliosis may also be present.[1,3] Numbness, weakness or reflex changes may be found over a specific anatomic root distribution.[8]

Most commonly, deficits are localized to the L5 or S1 nerve roots. Weakness in extension of the great toe and in dorsiflexion, along with hypesthesia of the dorsum of the foot, indicates dysfunction at the L5 level (Table 1 and Figure 3b).

Compromise of the S1 nerve root results in a decreased ankle jerk reflex, weak plantar flexion and hypesthesia of the posterolateral calf and lateral foot[3] (Table 1 and Figure 3c).

The straight-leg-raising test is positive in 95 percent of patients with a herniated disk.[2] The test is positive if pain occurs in a radicular pattern when the leg is elevated 60 degrees or less, indicating nerve root irritation.

Straight-leg raising of the asymptomatic leg sometimes produces pain in the affected leg. The test is only positive in about 25 percent of patients with evidence of disk herniation at surgery. However, when present, it is much more specific for the diagnosis of herniated disk than the standard straight-leg-raising test.[2]

In the past, the two most commonly used imaging studies for diagnosis of lumbar disk disease were myelography and CT. Myelography has an estimated sensitivity and specificity of 95 to 100 percent in the detection of herniated lumbar disks and has traditionally been the gold standard for the diagnosis of lumbar disk disease.[9] CT has a similar sensitivity and specificity and is considered a valid study for diagnosing disk herniation.[3] Myelography followed immediately by CT has been demonstrated to be slightly more sensitive and specific than CT or myelography alone.[1,3]

Myelography has significant side effects related to the use of contrast agents, including nausea, vomiting headache and neck stiffness. More severe complications of myelography are anaphylaxis, seizure and, rarely, death.

MRI is an emerging primary modality for diagnosing herniated lumbar disk (Figures 4a and 4b). It has been proposed as the imaging study of choice for detecting disk herniation. In a recent study[1] comparing MRI and CT, CT with myelography, and myelography alone, MRI had a comparable accuracy, with similar rates of false-negative and false-positive results. MRI has the advantages of being painless and noninvasive, with no radiation exposure and no known side effects. In addition, MRI is capable of detecting both early and advanced disk degeneration.[10]

Diskography with disk injection aids in diagnosing disk herniation by reproducing the patient’s pain pattern through injections at the level of the disk. The mechanism of action of the injections is unclear, but they probably produce radicular pain by stimulating the already sensitized peridiskal tissues. Although recognized as highly sensitive, the technique is controversial because it is invasive and because a cause-and-effect relationship between the disk injections and the patient’s pain has never been established.

Disk injection pain has demonstrated relatively low accuracy in the diagnosis of herniated lumbar disks, because of a very low sensitivity. However, because disk injection pain is quite specific for herniated disk, it is useful in combination with diskography, which is highly sensitive but not specific.

Diskography with CT also demonstrates high sensitivity and specificity in the detection of recurrent herniated disks.[9] The high specificity of this method is particularly helpful in distinguishing between the extensive scar tissue often found in the region of a previously ruptured disk and actual disk material. Diskography with CT is recognized as the preferred method of diagnosing far lateral or foramen herniations.[3,9] Rare complications of diskography are disk rupture or disk space infection.[9]

Ultrasonography is currently being investigated as a safe, convenient and noninvasive method of diagnosing herniated lumbar disk. On ultrasound, ventral echoes containing reflected waves are attenuated at the level of a herniated disk, resulting in irregular images. As yet, ultrasonography has a reported accuracy of only 78 percent in diagnosing herniated disk, compared with better than 90 percent for myelography.[1] Further investigation is needed before ultrasonography alone can be considered a valid tool for the diagnosis of disk disease.

Epidural venography has also been used successfully as a method of screening for herniated disks. If the venogram is negative, the patient does not have a herniated disk in the lower three segments. Stress radiographs may show misaligned spinous processes and loss of lumbar lordosis. However, in general, plain films are more useful in ruling out other possible causes of back pain, such as tumors, fractures or degenerative bone deformities, than in diagnosing a herniated lumbar disk.[2,11]

Electromyography detects abnormalities in the electrical activation of a muscle that are caused by nerve compromise. This technique is best used as a confirmatory study at least three weeks after the onset of symptoms. Electromyography is particularly helpful in ruling out metabolic, ischemic or hereditary neuropathy.[3,11] It is generally not considered necessary in the diagnosis of simple herniated lumbar disks, unless the combination of a thorough history, physical examination and CT (with or without myelography or diskography) or MRI is nondiagnostic.

Clinical Course

Over the course of lumbar disk degeneration and herniation, symptoms may progress to severe dysfunction, and an episodic pattern of remission and relapse over weeks to months tends to become established. During periods of back pain, any movement may be nearly unbearable. Remissions become fewer and shorter. Neurogenic claudication commonly occurs as a result of nerve root compression by a herniated disk. This disorder is characterized by unilateral or bilateral sensory and motor changes at multiple levels, as well as the clinical signs of disk herniation.

Cauda equina syndrome, with compromised bowel and bladder function caused by the herniated disk, is a serious complication of lumbar disk herniation. It is uncommon, occurring in 1 to 16 percent of cases. Compression in the cauda equina area by the disk usually results in severe low back pain radiating into both legs, with saddle anesthesia and leg weakness. Paresthesias and numbness may occur in both legs.

Sexual dysfunction is also common in cauda equina syndrome and is manifested by impotence and decreased penile, vaginal or rectal sensation.

A recent review[1] of the charts of 31 patients with cauda equina syndrome revealed no clear prognostic predictors of recovery of motor, sensory, bowel, bladder or sexual function, although a correlation was seen between loss and recovery of perianal sensation and bladder function. For this reason, it is extremely important to assess perianal sensation in patients with suspected cauda equina syndrome. This study did not establish any positive association between time elapsed from diagnosis of cauda equina syndrome to surgery and recovery of function. However, development of the symptoms of cauda equina is considered a surgical emergency because loss of vital functions may occur.

Differential Diagnosis

Severe back pain, leg pain or sciatica may occur in several conditions other than lumbar disk herniation. Back pain accompanied by significant weight loss may indicate the presence of a primary or metastatic tumor. Plain film is the most helpful study for evaluating this problem.

Severe, tearing pain with dizziness and diaphoresis is typical of an expanding aortic aneurysm. Burning pain originating in a duodenal ulcer may radiate to the back. Acute, localized back pain suggests a vertebral fracture.

Fever or meningeal symptoms with intermittent or constant low back pain are typical signs of vertebral osteomyelitis. Like the pain of lumbar disk disease, osteomyelitic pain may increase with exercise and be relieved by rest. It may radiate into the hip or buttocks, with decreased range of motion and flexion contracture. Paraplegia from osteomyelitis has been reported. Plain film is sometimes diagnostic, but because the development of radiographic findings lags behind the onset of symptoms by one to two months, a bone scan should be performed if osteomyelitis is suspected.

If a bone scan and plain radiographs are negative, a CT scan or MRI may detect bony changes that have been missed on other studies. Exacerbation of pain with recumbency, prolonged morning stiffness or visceral pain should lead to evaluation for other disorders. The erythrocyte sedimentation rate may be helpful in differentiating inflammatory conditions from noninflammatory conditions. Sciatic pain may be caused by bony abnormalities such as spondylolisthesis (slippage of one vertebral body in the spinal column), spondylolysis or degenerative spondylosis caused by arthritis.

Irritation of the sciatic nerve has been known to occur simply from chronic local pressure, such as that caused by a wallet in the back pocket. Rare conditions such as synovial cysts, congenital nerve root abnormalities, primary neural tumors or epidural abscesses may also mimic radicular pain.[1,8]



The initial management of a patient with a suspected herniated disk should include a plain film of the lumbosacral spine, with anteroposterior and lateral views. This step is most useful in ruling out conditions such as spondylolisthesis, osteomyelitis and metastatic disease. Medical management of suspected herniated lumbar disk in the absence of neurologic deficits consists of offering the patient reassurance and recommending bed rest on a firm

mattress with a bed board.[1] It is believed that bed rest is beneficial because the supine position minimizes intradiskal pressure. Patients should be Cautioned not to spend the time in bed sitting up to read or watch television, because the sitting position increases intradiskal pressure to a level even higher than it is in the standing position.

Prolonged bed rest causes muscle weakness, cardiovascular decompensation and bone demineralization. For these reasons, bed rest should be prescribed for no longer than two weeks, and usually for just a few days. Brief periods of standing and walking during the prescribed bed rest period should be recommended to prevent deconditioning.[2]

If the disk herniation occurs following an injury, immediate application of ice to the lumbar region may reduce inflammation and pain. Ice should be applied for a maximum of 10 minutes at a time. After the first 24 hours, heat, in the form of warm baths or heating pads, may be more beneficial. Heat should be applied for no longer than 20 minutes at a time.

If progressive neurologic dysfunction is not a factor, an initial trial of conservative therapy is indicated, including reduced activity and occupational therapy, with training in isometric exercises and safer ways to engage in the activities of daily living. The best exercise and mobilization program is directed toward gradual strengthening of the abdominal and back muscles and improved general physical fitness. Of course, activities known to exacerbate back pain, such as heavy lifting, repetitious axial rotation or bending, should be avoided.[1-3,8,11]

Analgesics and muscle relaxants are components of conservative therapy, but their use should be limited to less than two weeks. Narcotics and muscle relaxants should not be prescribed for patients with chronic pain syndromes (duration of pain of more than three months).[2] Traction, rigid orthoses, epidural anesthetic injections, facet injections and even intradiskal steroid injections are sometimes used, although evidence for their use is generally lacking. Finally, psychologic testing or counseling may be indicated in some situations.[1,11]

If the patient’s pain does not subside and radicular pain becomes the chief complaint, a CT scan or MRI should be performed. Disk herniation is often clearly demonstrated on CT scan alone, eliminating the need for further studies. However, if the CT scan is not diagnostic, lumbar myelography should be followed by a CT scan or MRI.

A herniated disk that is clearly delineated on imaging studies is not an absolute indication for surgery. It is usually safe to continue conservative therapy as long as pain is the principal problem and progressive neurologic, motor or bowel and bladder dysfunction are not present. Exceptions to this rule are patients with large extruded disk fragments, who should be treated promptly with surgical removal of the fragments to avoid perithecal or perineural fibrosis (arachnoiditis). Although a recent prospective study[1] of extruded lumbar disks that were treated nonsurgically noted resolution of back pain and sciatica without evidence of perithecal or perineural fibrosis or other complications, the evidence is probably not sufficient to justify exposing patients to this risk.

Conservative therapy should be continued for a significant period of time, because of the high incidence of spontaneous resorption of herniated disk material and subsequent resolution of radicular pain.[2,3] It is theorized that resorption of a herniated disk occurs when the disk is extruded and exposed to the vascular supply of the epidural space. Cellular elements in the epidural space probably promote phagocytosis of the foreign disk material. Separation of the extruded disk fragment from its nutrient supply may cause desiccation of the disk, thereby decompressing the nerve.[12] Decreased radicular pain probably occurs as a result of chronic stretching of the nerve over the herniated nucleus pulposus, resulting in stress relaxation of the nerve.[3]

In comparisons of the efficacy of conservative therapy and surgery, no significant difference in recovery of function has been reported between patients whose herniated disks resolved spontaneously and those whose herniated disks were surgically removed.[12]


Chemonucleolysis is a technique involving injection of intervertebral disks with chymopapain (Chymodiactin). The technique is reserved for patients with a documented herniated disk who have failed to respond to conservative therapy.[1,2] Since chymopapain acts on the entire disk, the injection inflicts more damage to the disk, than surgery.

In 70 to 80 percent of patients treated with chymopapain, radicular pain resolves within six weeks of the injection.[1] More than 50 percent of patients, however, experience increased back pain and muscle spasm after the injection, and nearly 80 percent have incapacitating back pain for up to three months after treatment.[3] Although chemonucleolysis is considered an acceptable treatment modality, surgery is generally preferred, because it confers more complete pain relief with fewer side effects.


Only 5 to 10 percent of patients with radicular pain require surgery. Surgery should be considered if symptoms have not been significantly alleviated after six weeks of conservative therapy.

Although intractable back and radicular pain are indications for surgery, the operation may be deferred for longer than six weeks if the patient prefers. The length of time elapsed without relief, however, is probably the one best indication that the pain will not remit without surgery.[1]

In patients with a symptomatic herniated disk, spontaneous remission of symptoms tends not to occur as often in older persons as in younger persons, and surgery is often the only alternative in the elderly. Although a trial of conservative treatment is indicated for elderly patients, they tolerate lumbar surgery well, and if conservative therapy fails, the physician should not be reluctant to recommend surgery for an elderly patient.”

Surgery should never be performed for an asymptomatic herniated disk, since it is not necessary to alleviate nerve compression. Surgery is also contraindicated in syndromes of back pain without accompanying radicular pain, paresthesias or numbness, because the pain will not be relieved. In these instances, the patient would be exposed unnecessarily to the risks of surgery with no possible benefit.

Surgical alternatives for herniated lumbar disks include laminectomy with or without open diskectomy, central or lateral decompression, microdiskectomy, percutaneous diskectomy and fusion. Satisfactory outcomes have been reported in up to 91 percent of patients with a definite diagnosis of herniated lumbar disk.[1,2,13]

Most lumbar disk surgery is directed toward either removing pressure on compressed spinal nerves or stabilizing affected segments of the spine by arthrodesis. The most common surgery for lumbar disk disease is lumbar laminectomy, in which a portion of the vertebral lamina is removed (Figure 5). Removal of the herniated disk, or diskectomy, is called for when the annulus shows unmistakable signs of a soft, herniated desk.[11] Often, adequate decompression of the spinal cord or nerve can be achieved by microdiskectomy. In this procedure, a hemilaminotomy is done through a tiny skin incision, and herniated disk material is removed with the aid of an operating microscope.[3,14]

In percutaneous diskectomy, disk material is removed blindly through a needle, thus decompressing the spinal nerve. This technique is rarely used today because of its imprecision and relatively low success rate (50 to 70 percent).[3,9] With the use of more sophisticated optical equipment, this procedure is called diskoscopy and has a slightly more dependable success rate.

Recently, excellent results have been reported for the treatment of disk degeneration by diskectomy, followed by posterior lumbar interbody fusion, anterior lumbar interbody fusion or anteroposterior fusion.[1,2] Although the patients receiving this treatment did not have herniated disks, they had nonspecific back, thigh, buttock and leg pain caused by stretching of the annulus by a degenerating lumbar disk. The approach remains an experimental procedure for patients with chronic, intractable back pain who have degenerative disk changes identified by MRI or diskography.

Because joint instability is increased when the disk space is interrupted, fusion is nearly always called for in cases of a herniated disk with preexisting joint slippage (spondylolisthesis). Fusion may also be performed in cases of previously failed lumbar disk surgery,[1,3] but the prognosis for improvement after two or three operations has been poor. A recent retrospective analysis of published series of back surgery with and without fusion showed that fusion offered no statistically improved benefit to the clinical outcome.[15]

Although the surgical approach to lumbar disk disease is largely successful, some patients continue to experience pain after surgery. Other patients have a pain-free interval immediately after the surgery, followed by return of pain.[1] The pain-free interval varies from a few weeks to several years.

Since only herniated nucleus pulposus is removed during standard diskectomy operations, recurrent disk herniations involving the residual nudeus pulposus are possible. Rare complications include incomplete nerve root decompression, facet joint injury, arachnoiditis and disk space infection.[1,2,3]

Failed spinal fusion may present with disk rupture or spinal stenosis and pseudoarthrosis. Finally, in any kind of back pain syndrome, malingering or hysterical patients, or those with compensatory or secondary gain comprise a large percentage of the patients who do not recover with conservative or surgical treatment.[1,8] Therefore, it is judidous to require patients with chronic disk pain to undergo psychologic evaluation before attempting further surgery.


Reassurance and patient education are an extremely important part of prevention. Patients should be advised that the prognosis in disk herniation is good, with a 90 to 95 percent recovery rate for conservative therapy alone, and that permanent disability is rare.

Risk factors, such as obesity and smoking, should be eliminated. A program of weight control, regular exercise and posture correction, along with use of a firm mattress plus bed board, may reduce the frequency and severity of recurrent disk herniations.

Instruction in proper methods of lifting, performing manual labor and resting should also be given. Endurance exercises, such as speed walking, stationary bicycling and swimming have been found to be beneficial in promoting recovery and preventing recurrence. Isometric flexion exercises are often helpful for patients with chronic pain.[2,3,8]


[1.] Vlok GJ, Hendrix MR. The lumbar disc: evaluating the causes of pain. Orthopedics 1991;14:419-25. [2.] Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990; 112:598-603. [3.] Spencer DL. Lumbar intervertebral disc surgery. In: Bridwell KH, DeWald RL, eds. The textbook of spinal surgery. Vol 2. Philadelphia: Lippincott, 1991:675-93. [4.] Miller JA, Schmatz C, Schultz AB. Lumbar disc degeneration: correlation with age, sex, and spine level in 600 autopsy specimens. Spine 1988;13:173-8. [5.] Gordon SJ, Yang KH, Mayer PJ Mace AH Jr, Kish VL, Radin EL. Mechanism of disc rupture. A preliminary report. Spine 1991;16:450-6. [6.] Jacobs B, Ghelman B, Marchisello P. Coexistence of cervical and lumbar disc disease. Spine 1990;15:126-4. [7.] Saal JS, Franson RC, Dobrow R, Saal JA, White AH, Goldthwaite N. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990;15:674-8. [8.] Bassam BA. Low back syndromes. The challenge of accurate diagnosis and management. Postgrad Med 1990;87:209-15,218. [9.] Jackson RP, Becker GJ, Jacobs RR, Montesano PX, Cooper BR, McManus GE. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus. I. A comparison of computed tomography (CT), myelography, CT-myelography, discography, and CT-discography. Spine 1989;14:1356-61 [Published erratum appears in Spine 1990;15:591. [10.] Jackson RP, Cain JE Jr, Jacobs RR, Cooper BR, McManus GE. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus. II. A comparison of computed tomography (CT), myelography, CT-myelography, and magnetic resonance imaging. Spine 1989;14-1362-7. [11.] Hill GM, Ellis EA. Chemonucleolysis as an alternative to laminectomy for the herniated lumbar disc. Experience with patients in a private orthopedic practice. Clin Orthop 1987;12(225):229-33. [12.] Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990;15:683-6. [13.] Wiltse LL. Surgery for intervertebral disk of the lumbar spine. Clin Orthop 1977;6(129):22-45. [14.] Thomas AM, Afshar F. The microsurgical treatment of lumbar disc protrusion. Follow-up of 60 cases. J Bone Joint Surg [Br] 1987,69:696-8. [15.] Turner JA, Ersek NW, Herron L, et al. Patient outcomes after lumbar spinal fusions. JAMA 1992;268:907-11.

HOLLY S. GILMER, M.D. is a first-year resident in the Department of Neurosurgery at the University of California, Davis, Medical Center, Sacramento. Dr. Gilmer graduated from the University of Michigan Medical School, Ann Arbor.

STEPHAN M. PAPADOPOULOS, M.D. is an assistant professor of surgery at the University of Michigan Medical School. After graduating from the University of Texas Medical School, Houston, he completed a residency in neurosurgery at the University of Michigan Medical School and a fellowship in spinal surgery at the Barrow Neurological Institute, Phoenix.

GERALD F. TUITE, M.D. is a resident in neurosurgery at the University of Michigan Hospitals, Ann Arbor. Dr. Tuite graduated from Northwestern University Medical School, Chicago.

COPYRIGHT 1993 American Academy of Family Physicians

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