Lumbar Degenerative Disk Disease 

Updated: Aug 03, 2020
Author: Rajeev K Patel, MD; Chief Editor: Stephen Kishner, MD, MHA 


Practice Essentials

As humans age, they endure both macrotraumas and microtraumas and undergo changes in body habitus that alter and redistribute biomechanical forces unevenly on the lumbar spine. Natural progression of degeneration of the lumbar segment with motion proceeds with characteristic anatomic, biomechanical, radiologic, and clinical findings in lumbar degenerative disk disease (LDDD).[1, 2]  Magnetic resonance imaging (MRI) is currently the criterion standard imaging modality for detecting disk pathology. Physical rehabilitation with active patient participation is a key approach to treatment of patients with diskogenic pain.

Descriptions of treatment for low back pain (LBP) date to Hippocrates (460-370 BCE), who reported joint manipulation and use of traction. Onset of LBP often is associated with bipedal ambulation. Theories propose that this transformation in the mechanics of locomotion is the inciting evolutionary event that made the lumbar spine susceptible to degenerative disease. Degeneration is universal to structures that make up the functional spinal unit, composed of two adjacent vertebral bodies and the intervertebral disk. The disk and two zygapophyseal joints at the same level function as a trijoint complex.

Symptoms of lumbar degenerative disk disease

Symptoms, usually isolated in the low lumbar region and buttocks, can vary, with referral to the lower thoracic and/or upper lumbar region, abdomen, flanks, groin, genitals, thighs, knees, calves, ankles, feet, and toes.

Diskogenic pain is usually described as aching; however, a wide spectrum of adjectives can be reported, from soreness to stabbing pain.

Workup in lumbar degenerative disk disease

Imaging studies used in the evaluation of LDDD include the following:

  • Radiography - Plain radiographs can be helpful in visualizing gross anatomic intervertebral disk changes
  • Computed tomography (CT) scanning - CT scanning can be used to identify uniform, symmetrical degenerative changes of the disk that result in a diffuse annular disk bulge, seen as diffuse peripheral extension of disk material; CT scanning also may demonstrate endplate degenerative changes, including sclerosis and cortical irregularity with erosions
  • Magnetic resonance imaging (MRI) - MRI is currently the criterion standard imaging modality for detecting disk pathology; it has demonstrated degenerative changes in three times as many motion segments as contrast-enhanced CT scanning

Management of lumbar degenerative disk disease

Physical therapy

Physical rehabilitation with active patient participation is a key approach to treatment of patients with diskogenic pain.

Relative rest, which restricts all occupational and avocational activities, for up to the first 2 days after an acute episode, may be indicated to help calm initial pain. Passive modalities are valuable during the initial 48 hours of relative rest to aid in pain relief.

The physical rehabilitation program should also include training in proper body mechanics and lumber ergonomics during various functional, occupational, and avocational activities. Manual techniques may be applied to increase soft tissue pliability when secondary myofascial tightness is present. If the aforementioned measures are appropriate and completed, an active, dynamic rehabilitation program to stabilize the lumbar spine may be started on an outpatient basis.

Dynamic lumbar-spine stabilization programs are aimed at maintaining a neutral spine position throughout various daily activities. An extension bias commonly is used to help reduce intradiskal pressure.

Surgical intervention

Available surgical approaches in LDDD include anterior, posterior, and combined procedures; interbody fusion with allograft autologous bone or threaded titanium cage; and intertransverse process in situ fusion with or without instrumentation.


Posterior elements of the lumbar spinal functional unit typically bear less weight than anterior elements in all positions. Anterior elements bear over 90% of forces transmitted through the lumbar spine in sitting; during standing, this portion decreases to approximately 80%. As the degenerative process progresses, relative anterior-to-posterior force transmission approaches parity. The spine functions best within a realm of static and dynamic stability. Bony architecture and associated specialized soft tissue structures, especially the intervertebral disk, provide static stability. Dynamic stability, however, is accomplished through a system of muscular and ligamentous supports acting in concert during various functional, occupational, and avocational activities.

The overall mechanical effect of these structures maintains the histologic integrity of the trijoint complex. Net shear and compressive forces must be maintained below respective critical minima to maintain trijoint articulation integrity. Persistent, recurrent, nonmechanical, and/or excessive forces to the motion segment beyond minimal thresholds lead to microtrauma of the disk and facet joints, triggering and continuing the degenerative process.[3] Degenerative cascade, described by Kirkaldy-Willis, is the widely accepted pathophysiologic model describing the degenerative process as it affects the lumbar spine and individual motion segments.[4] This process occurs in 3 phases that comprise a continuum with gradual transition, rather than 3 clearly definable stages.

Phase I

The dysfunctional phase, or phase I, is characterized histologically by circumferential tears or fissures in the outer annulus. Tears can be accompanied by endplate separation or failure, interrupting blood supply to the disk and impairing nutritional supply and waste removal. Such changes may be the result of repetitive microtrauma. Since the outer one third of the annular wall is innervated, tears or fissures in this area may be painful. Strong experimental evidence suggests that most episodes of LBP are a consequence of disk injury, rather than musculotendinous or ligamentous strain. Circumferential tears may coalesce to form radial tears. The nucleus pulposus may lose its normal water-imbibing abilities as a result of biochemical changes in aggregating proteoglycans.

Studies suggest proteoglycan destruction may result from an imbalance between the matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1).[5, 6, 7] This imbalance results in diminished capacity for imbibing water, causing loss of nuclear hydrostatic pressure and leading to buckling of the annular lamellae. This phenomenon leads to increased focal segmental mobility and shear stress to the annular wall. Delamination and fissuring within the annulus can result. Annular delamination has been shown to occur as a separate and distinct event from annular fissures.

Microfractures of collagen fibrils in the annulus have been demonstrated with electron microscopy. MRI at this stage may reveal desiccation, disk bulging without herniation, or a high-intensity zone (HIZ) in the annulus. Structural alteration of the facet joint following disk degeneration is acknowledged widely, but this expected pathologic alteration does not necessarily follow. Changes associated with zygapophyseal joints during the dysfunctional phase may include synovitis and hypomobility. The facet joint may serve as a pain generator.

Phase II

The unstable phase, or phase II, may result from progressive loss of mechanical integrity of the trijoint complex. Disk-related changes include multiple annular tears (eg, radial, circumferential), internal disk disruption (IDD) and resorption, or loss of disk-space height. Concurrent changes in the zygapophyseal joints include cartilage degeneration, capsular laxity, and subluxation. The biomechanical result of these alterations leads to segmental instability. Clinical syndromes of segmental instability, IDD syndrome, and herniated disk seem to fit in this phase.

Phase III

The third and final phase, stabilization, is characterized by further disk resorption, disk-space narrowing, endplate destruction, disk fibrosis, and osteophyte formation. Diskogenic pain from such disks may have a higher incidence than that of the pain from the disks in phases I and II; however, great variation of phases can be expected in different disks in any given individual and individuals of similar ages vary greatly.



United States

Lifetime incidence of LBP is reported to be 60-90% with annual incidence of 5%. Each year, 14.3% of new patient visits to primary care physicians are for LBP, and nearly 13 million physician visits are related to complaints of chronic LBP, according to the National Center for Health Statistics.[8, 9]


The natural history has been reported to be favorable in some studies and is frequently quoted to patients. Reports indicate that 40-50% of patients are symptom-free within 1 week and up to 90% of symptoms resolve without medical attention in 6-12 weeks.

  • Deyo and Tsui-Wu reported that 33.2% of patients with LBP reported symptoms for less than 1 month, 33% reported pain for 1-5 months, and 32.7% reported pain for longer than 6 months.[10] Later, over a 2-year follow-up, 44% of patients reported chronic symptoms (defined as back pain for >90 d in the previous 6 mo). Most patients had low levels of back pain, with 20% rating their pain at 4 or greater on a scale of 0-10 (where 0 indicates no pain), 13% rated their pain as 5 or greater, and 8% reporting pain of 6 or greater.

    • Von Korff and colleagues reported that 15-20% of primary care patients with LBP had moderate-to-severe limitations in activity during a 1-year follow-up after their initial episode resolved. Recurrence rates of 60-85% have been reported in the first 2 years after an acute episode of LBP.[11]

  • Although incidence of LBP has remained relatively static, disability from LBP has increased 14 times the rate of population growth. Back pain results in more lost productivity than any other medical condition and is second only to upper respiratory complaints as cause of time lost from work. Back pain accounts for approximately 175.8 million days of restricted activity each year in the United States. At any given time, 2.4 million Americans are disabled because of LBP, with 1.2 million on a chronic basis. As of 2005, lower back pain ranks as the number one cause of disability in individuals under the age of 45.

  • In 1990, 400,000 industrial low back injuries resulted in disability in the United States. This number represents approximately 21% of injuries in the workplace but accounted for 31% of compensation payments. After a patient receiving worker's compensation is out of work for more than 6 months, the likelihood of his or her returning to work is only 50%. After 1 year, the likelihood is only 25%, and after 2 years, the individual will likely never return to productive work. In 1990, direct medical cost of spinal disorders was estimated to than $23 billion in the United States. Furthermore, plausible estimates of total costs of low back disorders ranged from $25 billion to almost $85 billion in 1990.[12]

  • Looking at 1998 statistics, Luo and colleagues found total health care expenditures incurred by individuals with back pain in the United States to have reached $90.7 billion; total incremental expenditures attributable to back pain among these persons were approximately $26.3 billion. On average, individuals with back pain incurred health care expenditures that were approximately 60% higher than individuals without back pain ($3498 vs $2178). Of service expenditures, 75% were attributed to those individuals within the top 25% of expenditure. Disk disorders were also found to be associated with higher medical costs.[13]


LBP secondary to degenerative disk disease affects men and women equally. Gautschi et al found in a cohort of 214 patients with lumbar degenerative disk disease that preoperatively, females scored worse than males on measurement of subject functional impairment but that males and females scored similarly in terms of objective functional impairment. The investigators also found that postoperative results did not differ between the sexes at 6-week, 6-month, and 1-year follow-up.[14]


LBP secondary to degenerative disk disease is a condition that affects young to middle-aged persons with peak incidence at approximately 40 years. With respect to radiologic evidence of LDDD, the prevalence of disk degeneration increases with age, but degenerated disks are not necessarily painful.




The patient's history is an extremely valuable tool for identifying the intervertebral disk as the nociceptive source. Classic historic features are associated with a diskogenic etiology of mechanical low lumbar complaints. The clinician must ask several key questions to elicit the information necessary for correct diagnosis. These questions address events that cause the symptoms, the location and nature of the symptoms, any exacerbating and mitigating factors or positions, and the patients' medical and surgical history. Often, a nociceptive source of back pain is not found.[15]

  • Patients with diskogenic pain typically describe an inciting traumatic event resulting in sudden forced flexion and/or rotational moment; however, some patients describe a spontaneous onset of symptoms.

  • Symptoms, usually isolated in the low lumbar region and buttocks, can vary, with referral to the lower thoracic and/or upper lumbar region, abdomen, flanks, groin, genitals, thighs, knees, calves, ankles, feet, and toes.

  • Classic diskogenic pain is exacerbated by activities that load the disk, such as sitting, arising from a seated position, awaking in the morning, lumbar flexion with and without rotation/twisting, lifting, vibration (eg, riding in a car), coughing, sneezing, laughing, and the Valsalva maneuver.

  • Symptoms are mitigated by lying on the side with hips and knees flexed (fetal position), by changing positions frequently, and/or by engaging in activity.

  • Diskogenic pain is usually described as aching; however, a wide spectrum of adjectives can be reported, from soreness to stabbing pain.

  • Patients with a surgical history of lumbar arthrodesis, lumbar diskectomy, or lumbar laminectomy have changes in lumbar spine biomechanics resulting in susceptibility to diskogenic disease.[16]

  • The patient's medical history should be investigated with specific inquiry directed toward a personal history of cancer, arthritis, or infection or systemic disease that could increase risk of infection.

  • The review of systems should include assessments for fever, incontinence, symptoms suggestive of metastasis or metabolic disease, and psychological issues including depression and drug use or abuse.


Physical examination is an important adjunct to history in determining diskogenic etiology of symptoms, beginning with the first view of the patient in the examination room. The patient may prefer to stand, pace, or sit in a reclining position since these positions usually alleviate symptoms of diskogenic etiology.

  • Note the patient's height and weight, as obesity may produce excess load to the low lumbar intervertebral disks.

  • Inspection of the low lumbar region is important since this part of the examination may offer a clue to history of lumbar surgery if a scar exists. Inspection while the patient is standing and during forward flexion and extension may reveal a kyphotic or scoliotic deformity. Inspection and palpatory examination should be performed in flexion with the patient standing and seated to determine whether the pain source is in the pelvis or sacral area.

  • Palpation of the lumbar paraspinals and spine stabilizers may elicit tenderness, as these muscles may be tight, have active or latent trigger or tender points, or be in reactive muscle spasm.

  • A step deformity, in which the spinous process of the segment involved protrudes ventrally, may exist as a consequence of spondylolisthesis.

  • Measure the lower extremity circumference at mid thigh and mid calf at the same time of day so comparable results are obtained; they should be symmetric. Hips, knees, and ankles should have full range of motion (ROM), without crepitus or effusions.

  • Diskogenic stress maneuvers usually reproduce the patient's low lumbar and buttock symptoms. These maneuvers include pelvic rocking and sustained hip flexion.

    • Perform pelvic rocking with the patient in a supine position. Flex the patient's hips until the flexed knees approximate to the chest; then, rotate the lower extremities from one side to the other.

    • Perform sustained hip flexion with the patient supine; raise the patient's extended lower extremities to approximately 60° in relation to the examination table. Then ask the patient to hold the lower extremities in that position and release. Query the patient regarding reproduction of low lumbar and/or buttock pain. Then lower the extremities successively approximately 15°, and, at each point, note the reproduction and intensity of pain. The test is positive if the patient complains of low lumbar and/or buttock pain of increasing intensity as the extremities are lowered at successive angles. Sacroiliac joint stress maneuvers do not provoke pain. Root tension signs are negative.

  • Orientation, mood, and affect usually are within normal limits, and excessive emotional lability may be a sign of nonorganic pathology. These provocative maneuvers should not be accompanied by exorbitant demonstrations of perceived pain. Such overt pain behavior should alert the clinician to important psychosocial issues.

  • Normal neurologic examination, with intact pinprick sensation throughout all dermatomes, full muscle strength throughout all myotomes, and symmetric muscle stretch reflexes, are associated with diskogenic disease. Two muscles should be tested with reflexes elicited representing each lumbar root; this test helps determine whether the problem is root pathology or a focal neuropathy; the straight leg test also should be performed in supine and seated positions.

  • Gait usually is normal.

  • Lumbar ROM usually is limited and painful, chiefly into flexion; however, extension also can be restricted and painful. Lumbar ROM should be assessed in flexion, extension, lateral bending, and rotation. A careful, systematic, and thorough structural examination should be performed to assess for subtle abnormal findings that may be amenable to manual therapy or manipulation.


The cause of LDDD is unknown. Several theories cite traumatically induced acute annular tear as the inciting pathologic event. Other theories suggest that degeneration of the lumbar disk is a natural part of aging; however, these theories do not explain spontaneously occurring annular tears and disk degeneration in the young. Therefore, the cause of LDDD is most likely multifactorial. Various genetic, environmental, autoimmune, inflammatory, traumatic, infectious, toxin-induced, and other factors, alone or in various combinations, may result in initiation and progression of degeneration of the lumbar disks in a way that has not been elucidated.



Diagnostic Considerations

These include the following:

  • Muscle strain

  • Ligament/tendon injury

  • Sacroiliac joint syndrome

  • Lower lumbar zygapophyseal joint syndrome

  • Hip joint pain

  • Compression fracture

  • Stress reaction

  • Stress fracture

  • Spondylolysis

  • Spondyloarthropathy

  • Myofascial pain syndrome

  • Neoplastic disease

Differential Diagnoses



Laboratory Studies

No clinically relevant laboratory studies associated with LDDD have been found.

Imaging Studies


Plain radiographs can be helpful in visualizing gross anatomic intervertebral disk changes. Obtain standing anteroposterior (AP) and lateral views. Intervertebral disks are visualized best on lateral views. Plain images are often not helpful unless evidence suggests a more dangerous etiology for LBP.

Signs of degeneration include loss of disk height, sclerosis of the endplates, or osteophytic ridging. In addition, spondylolisthesis can be diagnosed and the degree of slippage visualized easily on lateral images. Oblique views may be helpful if spondylolysis is suggested.

Coned-down lateral view provides a detailed look at the L5-S1 interspace. Flexion/extension images may help determine whether excess motion occurs between 2 vertebral bodies.

Nuclear imaging

Nuclear imaging assesses tissue metabolism by using radionuclide labeled technetium-99m that emits radiation in proportion to its attachment to targeted structures. These studies have not been helpful in identifying disk pathology.

Myelography may help in assessing neural compression, but it is not helpful in evaluating intervertebral disks unless it is combined with CT scanning.

CT scanning

CT scanning can be used to identify uniform, symmetrical degenerative changes of the disk that result in a diffuse annular disk bulge, seen as diffuse peripheral extension of disk material. The margin of the annular bulge is usually smooth in contour[17] but may be asymmetric. Overlapping 3- to 5-mm axial sections in 3-mm increments with multiplanar reformations is the optimal protocol. Sagittal reformations or CT scans may demonstrate loss of disk height. An intradisk vacuum phenomenon is seen commonly as focal or linear areas of markedly diminished density within the intervertebral disk.[18, 19]

CT scanning also may demonstrate endplate degenerative changes, including sclerosis and cortical irregularity with erosions. CT scanning allows for visualization of disk degeneration, bulging, and herniations but not with the detail of MRI. Degeneration of the intervertebral disk and endplate commonly is observed at autopsy and in imaging studies in asymptomatic patients. In the lumbar spine, CT scans are abnormal in 35% of asymptomatic volunteers of all ages and in 50% of persons aged 40 years or older.

Magnetic resonance imaging

MRI is currently the criterion standard imaging modality for detecting disk pathology. MRI has demonstrated degenerative changes in three times as many motion segments as contrast-enhanced CT scanning. MRI uses a magnetic field to obtain direct multiplanar images with excellent soft-tissue contrast, and MRI provides superb resolution and precise localization of intervertebral disks.[3]

On MRI, degeneration of the intervertebral disk results in diminished signal intensity on T1- and T2-weighted images. These signal intensity changes are due to diminished water and glycosaminoglycan content and increased collagen content of the intervertebral disk.[20] Sagittal images provide the best depiction of the loss of intervertebral disk height. Bulging of the disk annulus can be demonstrated on axial and sagittal images.[21] Posterior extension of the disk annulus by >1.5 mm is invariably correlated with radial tears of the disk annulus. Furthermore, tears of the annulus fibrosus can be visualized as HIZ lesions (HIZL).[22, 23]

In vitro, MRI can demonstrate radial tears of the disk annulus.[24] The sensitivity of MRI is 67% compared with diskography in detecting radial annular tears. Focal enhancement of radial tears may be seen on gadolinium-enhanced T1-weighted MRIs. This enhancement has been attributed to granulation tissue in the tear. A vacuum phenomenon is demonstrated as an area without signal intensity in the intervertebral disk; this is best appreciated on sagittal T1-weighted images.[18, 25] MRI shows notable abnormalities in approximately 30% of asymptomatic people of all ages, and in 57% of those aged 60 years or older. Disk degeneration or a bulging intervertebral disk is observed in 35% of subjects aged 20-39 years and in nearly 100% of those aged 60-80 years.

An important component of the degenerative process of the lumbar intervertebral disk is degeneration of the cartilaginous endplate. The cartilaginous endplate cannot be discretely identified on MRI because of its thinness and the chemical-shift artifacts at the endplate; however, MRI demonstrates reactive changes in the bone marrow due to the degenerative process in the diskovertebral joint associated with chronic repetitive stress. Disruption and fissuring of the endplate with granulation tissue and reactive woven bone result in endplate changes where vascularized fibrous tissue replaces adjacent marrow.[26, 27]

Type 1 endplate changes are characterized by decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. Disruption of the endplate with replacement of the hematopoietic elements in the adjacent marrow by fat result in type 2 changes. Consequently, type 2 endplate changes are nearly isointense with fat, have hyperintensity on T1-weighted images and isointensity or slight hypointensity on T2-weighted images. Type 1 changes appear to convert to type 2 changes over time. Extensive bony sclerosis with thickening of subchondral trabeculae results in type 2 endplate changes. Type 3 changes have decreased signal intensity on both T1- and T2-weighted images.

MRI and CT scanning have considerable false-positive rates and less frequent false-negative results.

Other Tests

Plain radiographs, myelography (of value only in patients with nerve impingement on moving or standing), enhanced or nonenhanced CT, and nuclear imaging cannot depict painful disks. MRI is helpful in showing changes in signal intensity generated by the nucleus pulposus and, occasionally, in adjacent vertebral bodies; however, the same types of MRI changes can be seen in lifelong asymptomatic individuals.[28]

Both April and Schellhaus have suggested that HIZL observed on MRI may be a marker of a painful disk.[23, 29] However, findings from four independent studies of the clinical usefulness of HIZL as an indicator of a symptomatic disk are not supportive of this conclusion.

A retrospective study by Son et al indicated that in patients with early to middle-stage lumbar disk degeneration, discrepancy of the disk height between the standing and supine positions can aid in screening for disk degeneration–related LBP. The investigators found that in persons with intractable diskogenic pain, the disk height discrepancy ratio was significantly higher than that for individuals with mild LBP (14.55 vs 1.47, respectively), even though the disk degeneration level was similar between both groups.[30]

Provocation of concordant pain with lumbar diskography has been well demonstrated. The key feature of diskography is the patient's response to disk stimulation and not the appearance of the disk.

Results of physiologic testing explicitly determine whether a disk is painful. Specificity of diskography in this regard has been well established by the work of Walsh and colleagues.[31]

Because the only available diagnostic intervention that identifies a symptomatic disk is provocative diskography, consider ordering this diagnostic tool before surgery. Diskography remains controversial; some spinal physicians do not acknowledge its reliability or validity.[32] Their contention primarily rests in a desire to prevent inappropriate surgery because of a potential to abuse diskography combined with the view, albeit unsubstantiated, that IDD represents a constellation of symptoms rather than a specific diagnosis. The value of diskography is debatable. Actual demonstration of disk disruption has been shown to be no more important than pain reproduction.

After diskographic assessment, refer patients for surgery, nonoperative treatment, or psychological care. The best candidates for surgery should have involvement of only 1 disk, possibly the 2 most caudal lumbar disk segments, or the 2 most cephalic disks. Refer patients with any other combination of disk involvement for nonsurgical pain modulation.

Electrodiagnostic testing (nerve conduction studies and electromyography) is warranted when their results may change the patient's therapy. In particular, electrodiagnostic testing is indicated (1) if patients have symptoms suggestive of cauda equina syndrome and their imaging studies are not diagnostic; (2) if imaging studies show an abnormality not consistent with the symptoms; (3) if such studies appear to be normal despite clinical suspicions; (4) if the clinician suspects focal nerve entrapment, polyneuropathy, or myopathic condition; and (5) if the clinician needs to identify which of several anatomic lesions in the spine is the cause of radicular symptoms.

If a malignancy is suggested, laboratory studies, including determination of the complete blood count, erythrocyte sedimentation rate, and alkaline phosphatase levels and serum protein electrophoresis, may be helpful. Conversely, if a rheumatologic etiology is considered, tests for antinuclear antibody, rheumatoid factor, uric acid, and HLA-B27 levels may be beneficial.

Histologic Findings

The lumbar intervertebral disk is composed of the nucleus pulposus and annulus fibrosis. The disk is intimately related as a functional unit to the cartilaginous endplate. The intervertebral disk contains water, collagen, and proteoglycans. The nucleus pulposus normally is well hydrated, containing approximately 85-90% water in children aged 0-10 years and 70-80% water in adults. Elongated fibrocytes are organized loosely, forming a gelatinous matrix. The nucleus has a higher content of proteoglycans than the disk annulus.

The annulus fibrosis contains 75% water in children aged 0-010 years and 70-80% water in adults. The peripheral annulus is primarily composed of type I collagen, lending tensile strength to the intervertebral disk. The inner annulus is primarily composed of type 2 collagen, which, in conjunction with the nucleus pulposus, provides compressive strength. Type 2 collagen may contain more water than type 1 collagen.

The collagenous lamellae are fewer, thinner, and more tightly packed posteriorly than anteriorly. The central depression of the vertebral endplate is covered by hyaline cartilage.

With age-related degeneration, the volume of the nucleus pulposus diminishes with decreasing hydration and increasing fibrosis. Changes in water content are from alteration in the relative composition of proteoglycan, as well as decrease in the extent of aggregating proteoglycans. By age 30 years, in-growth of fibrous tissue into the nucleus results in an intranuclear cleft. Fibrocartilage, derived from cells in the annulus and endplate, gradually replaces mucoid material within the nucleus. Gradual loss of definition between nucleus and inner annular fibers occurs.

In the final stages of degeneration, the nucleus is replaced completely by fibrocartilage indistinguishable from the fibrotic disk annulus. Specifically, the type 1 collagen content of the disk annulus increases, especially posteriorly, and type 2 collagen content diminishes. Cartilaginous metaplasia begins in the inner annular fibers with changes in the overall fiber direction from vertical to horizontal. Infolding of fibers of the outer annulus occurs early with myxoid degeneration of the outer annular fibers.

Concentric and/or transverse tears in the annulus fibrosis are frequent findings. Peripheral tears are more frequent posterior or posterolateral where the annular lamellae are fewer. The development of a radial tear, particularly a tear extending to the disk nucleus, is a major hallmarks of disk degeneration. The degenerated intervertebral disk loses height and overall volume. Herniation of both nuclear material and annulus fibrosis may occur through the tear. With aging, the cartilage endplate may become thin and eventually calcified. In advanced disk degeneration, the cartilage endplate is calcified, with fissuring and microfractures. At autopsy, 97% of adults aged 49 years or older have degenerative changes.

For a structure to be considered a pain generator, it must have a nerve supply, it must be susceptible to disease or injuries known to be painful, and it must be capable of causing pain similar to that observed clinically. The superficial layers of the annulus fibrosis contain nerve fibers in the posterior portion of the annulus, which are branches from the sinuvertebral nerves. The sinuvertebral nerves are branches of the ventral rami. They also contain fibers derived from the grey ramus. Small branches from the grey ramus communicans or sympathetic fibers innervate the anterior longitudinal ligament and lateral and anterior annulus. The grey ramus communicans joins the sinuvertebral nerve that reenters the intervertebral foramen and spinal canal to innervate the posterior annulus and the posterior longitudinal ligament.

A dense nerve network on the posterior portion of the lumbar intervertebral disk has been demonstrated in rats. This network disappears almost completely after total resection of bilateral sympathetic trunks at L2-L6. In rats, sympathetic nerves bilaterally and multisegmentally innervate the posterior portion of the lumbar intervertebral disk and posterior longitudinal ligament. A variety of free and complex nerve endings have been demonstrated in the outer one third to one half of the annulus. Coppes and colleagues observed that disk innervation was more extensive in severely degenerated lumbar disks than in compared normal disks.[33]

Substance P immunoreactivity suggest nociceptive properties of at least some of these nerves, which provides further evidence for a morphologic substrate of diskogenic pain. Nerve fibers were restricted to the outer or middle third of the annulus in control samples.

In the patient population undergoing spinal fusion for chronic LBP, nerves extended into the inner third of the annulus fibrosis in 46% and into nucleus pulposus in 22%. The findings that isolated nerve fibers express substance P deep within diseased intervertebral disks and the association with pain suggests an important role for nerve ingrowth into the intervertebral disk in the pathogenesis of chronic LBP.

Weinstein and colleagues identified substance P, calcitonin gene-related peptide (CGRP), and vasoactive intestinal polypeptides (VIP) in the outer annular fibers of the disk in rats.[34] These chemicals are all related to pain perception. Substance P–, dopamine-, and choline acetyltransferase–immunoreactive nerve fibers are found in human longitudinal ligaments that have been removed surgically. These findings not only provide evidence to support the first criterion but also reveal changes associated with painful disks.



Rehabilitation Program

Physical Therapy

Physical rehabilitation with active patient participation is a key approach to treatment of patients with diskogenic pain. Physical therapy programs prescribed specifically to address the primary site of injury and secondary sites of dysfunction can provide a means of treatment, with or without adjunct medications, therapeutic procedures, or surgical intervention.

Relative rest, which restricts all occupational and avocational activities, for up to the first 2 days after an acute episode, may be indicated to help calm initial pain. Rest for longer periods has not been shown to be beneficial and can cause deconditioning, loss of bone density, decreased intradiskal nutrition, loss of muscle strength and flexibility, and increased segmental stiffness. Passive modalities are valuable during the initial 48 hours of relative rest to aid in pain relief, but protracted courses of passive treatments become counterproductive, as they place patient in a dependent role instead of an active one.

Education is one of the most important components of any back-care program and should include an explanation of the natural history of acute, subacute, and chronic disk injury. The physical rehabilitation program should also include training in proper body mechanics and lumber ergonomics during various functional, occupational, and avocational activities. Manual techniques may be applied to increase soft tissue pliability when secondary myofascial tightness is present. If the aforementioned measures are appropriate and completed, an active, dynamic rehabilitation program to stabilize the lumbar spine may be started on an outpatient basis. In addition, rehabilitation of other associated components of the functional kinetic chain may be appropriate, as these structures may also be affected.

Dynamic lumbar-spine stabilization programs are aimed at maintaining a neutral spine position throughout various daily activities. An extension bias commonly is used to help reduce intradiskal pressure. This position allows for balanced segmental force distribution between the disk and zygapophyseal joints, it provides functional stability with axial loading to help minimize the chance for acute dynamic overload upon the disks, it minimizes tension on ligaments and fascia planes, and it decreases symptoms. Repetition is key to increasing flexibility, building endurance, and developing the required muscle motor engrams that subconsciously activate a series of key multimuscular contractions to maintain the lumbar spine in a neutral position throughout static and dynamic activities.

For athletes, the aforementioned program can be progressively combined with sport-specific plyometrics to help the lumbar spine maintain neutral position during high-intensity, unpredictable, reaction-intensive sports. Rehabilitation of athletes should also train them to maintain a neutral spine position in sport-specific motions. These component motions should then be grouped into a new, safe spine-stable movement. Cardiovascular training is an important adjunct to comprehensive rehabilitation programs because it provides endurance necessary to prevent fatigue of the muscles that stabilize the spine.

Occupational Therapy

Occupational therapy can be an important adjunct in the rehabilitation process when generalized muscular deconditioning has created adverse effects on strength, endurance, and flexibility of the upper extremities and/or impairment in activities of daily living (ADLs).

An occupational therapist often provides this portion of the rehabilitation program. Essential elements consist of ensuring proper ergonomics at the work site, which may involve simply reconfiguring a desktop and/or workstation, or it may require complex solutions. Another aspect involves rehabilitation before the patient resumes full-time duties. After the offending source of pain is resolved, the patient typically has deconditioning and may require activity-specific reconditioning to prevent new or recurring injury.

Recreational Therapy

Recreation therapy may have a role in assisting the patient to resume avocational activities, possibly with adaptations in technique or with the use of adaptive equipment.

Medical Issues/Complications

Medical causes of LBP include the spondyloarthropathies (eg, enteric arthropathy, Reiter syndrome, ankylosing spondylitis, psoriatic arthritis), Marfan syndrome, fibromyalgia, myofascial pain syndrome, diskitis, and neoplastic disease.

Surgical Intervention

Available surgical approaches include anterior, posterior, and combined procedures; interbody fusion with allograft autologous bone or threaded titanium cage; and intertransverse process in situ fusion with or without instrumentation. The introduction of disk arthroplasty has been proposed as a possible surgical option in those patients who would like to maintain as much segmental motion as possible.

The rate of surgical treatment for LDDD in the United States more than doubled during the first decade of the 21st century, according to a study by Yoshihara and Yoneoka. Using Nationwide Inpatient Sample data from patients aged 18 years or older with lumbar/lumbosacral DDD, the investigators found that between 2000 and 2009, the population-adjusted incidence of LDDD surgery increased 2.4-fold. More specifically, the incidence of combined anterior and posterior lumbar fusion (APLF) rose three-fold, while that for posterior lumbar interbody fusion/posterolateral lumbar fusion (PLIF/PLF) increased 2.8-fold. In contrast, the incidence of total disk replacement (TDR) did not significantly rise.[35]

Of the more than 380,000 patients who underwent LDDD surgery between 2000 and 2009, according to the study, the majority (67.9%) were treated with PLIF/PLF, while 16.8% underwent anterior lumbar interbody fusion (ALIF), 13.6% were treated with APLF, and 1.8% underwent TDR. While TDR was more commonly performed in younger patients than in older ones, the opposite was true for PLIF/PLF. Regionally, it was found that LDDD surgery was more frequently performed in the Midwestern and Southern United States than it was in the Northeast.[35]

Effectiveness of surgery

To date, no prospective, randomized, blind study has demonstrated the superiority of any surgical approach or technique. One retrospective study was performed to compare posterolateral fusion with iliac-crest allografting and translaminar facet-screw augmentation, anterior interbody fusion with fibula allografting, posterolateral fusion with pedicle screw-rod fixation, and anterior interbody threaded cage fusion combined with facet-joint fusion and posterolateral fusion. The results suggested that the last procedure may provide superior outcomes.

Other investigators report outcome rates ranging from 39% to 82-93% for various procedures. With respect to disk arthroplasty, the literature is not clear on its definitive role, if any, in the treatment of symptomatic LDDD.

In a study of 59 patients suffering from low back pain and 1- or 2-level LDDD, Freudenberger et al compared the effectiveness of ALIF with anterior tension band plating (ALIF-ATB) with that of PLIF with pedicle screw instrumentation.[36] The investigators found that both techniques had similar fusion rates, but that patients who underwent PLIF had greater estimated blood loss and required more surgical time than did patients who were treated with ALIF-ATB.

Similarly, a study by Bozzio et al reported some advantages to ALIF in comparison with anteroposterior fusion and transforaminal lumbar interbody fusion (TLIF) performed in association with posterior fusion. The investigators cited a shorter surgical time in patients who underwent ALIF, as well as less blood loss and a decreased hospital stay. They also found that ALIF and anteroposterior fusion had better results than TLIF with regard to disk angle, disk height, and pelvic tilt. However, fusion rates did not differ between the three techniques.[37]


Consultation of the primary care physician with a nonsurgical spine specialist is appropriate for patients with symptoms lasting longer than 6 weeks secondary to LDDD. Consultation with a spinal surgeon may be appropriate for patients with intractable severe function-limiting symptoms secondary to IDD, at 1 or 2 contiguous levels, for those with symptoms lasting longer than 6 months who have had no relief from nonsurgical approaches, and for persons with abnormal neurologic findings.

Other Treatment

Steroid injections

Initial reports of epidural injections almost a century ago described the instillation of cocaine into the epidural space to treat lumbago and sciatica. In the early 1900s, epidural injection of local anesthetic was used to treat intractable sciatica. In 1952, Robecchi and Capra reported success with the first epidural steroid instillation in treating lumbar and associated sciatic pain.[38] Instillation of steroid into the epidural space has become a common modality in treating lumbar and lower-extremity pain due to a suspected inflammatory etiology.

Patient characteristics that may suggest an unfavorable or suboptimal response to possible epidural steroid injection (ESI) are a long duration of symptoms, a nonradicular diagnosis, unemployment because of pain, smoking, increasing use of pain medication, increasing number of treatments for pain, pain not relieved by medication, and pain not increased by activity.

Optimal timing for the administration of epidural steroids has not been elucidated. Patients generally undergo conservative palliative measures (eg, NSAID therapy, lumbar-spine stabilization therapy) before they are considered for ESIs. However, do not delay epidural injections when conservative treatments do not seem to be helping. Delaying aggressive treatment may allow the ongoing inflammatory process to result in fibrosis and possibly permanent damage.

How often ESIs can be administered is unknown. Practitioners often wait as long as 2 weeks before reassessing the patient for a response to the injection and for possible reinjection. This practice became popular after Swerdlow and Sayle-Creer suggested that steroid injected into the epidural space may remain in situ for up to 2 weeks.[39]

In 1972, Winnie and colleagues emphasized the importance of placing medication as close to the site of pathology as possible to maximize the outcome.[40] They reported improvement in 80% of patients in whom steroids were injected at the site of pathology. The best route for injection of steroids into the epidural space in patients with a diskogenic source is transforaminal. This route allows the clinician to drive the injected steroid ventrally with approximately 5 mL of local anesthetic to bathe the suspected diskogenic inflammatory source. The efficacy of this approach has been demonstrated in various prospective studies in lumbar axial pain syndromes and in those associated with corroborative radicular pain.

Only 2 nonrandomized, retrospective studies have address the outcome of transforaminal ESIs on spinally mediated lumbar axial pain due to diskogenic pathology without imaging evidence of nerve-root involvement.

Rosenberg and colleagues reported greater than 50% pain reduction after 1 year in 59% of patients.[41]

Manchikanti and colleagues examined patients with spinally mediated lumbar axial pain treated with blind interlaminar ESI, fluoroscopically guided caudal injection, or fluoroscopically guided transforaminal injection. The authors reported superior short- and long-term pain relief with the transforaminal route.[42] This conclusion makes anatomic sense because transforaminal ESIs likely distribute the injectate more focally to the ventral epidural space than do the interlaminar and caudal routes. Therefore, is may be most target specific when one attempts to deliver medication to the focus of a posterior diskogenic inflammatory response.

The optimal route for injection of corticosteroids into the epidural space at the site of pathology in patients with diskogenic mediated lumbar axial pain syndromes with corroborative radicular involvement is the transforaminal route. This approach allows the clinician to deliver the injectate, composed of a betamethasone 6-12 mg and 1% lidocaine 0.5-1 mL. The goal is to precisely eradicate the known inflammatory response emanating from the potentially inflammagenic herniated nucleus pulposus (HNP) focally on the corroborative inflamed nerve root sleeve.

The efficacy of the aforementioned approach has been demonstrated in 4 randomized prospective, double-blind controlled clinical trials.

Riew and colleagues reported the results of fluoroscopically guided lumbar transforaminal injections in 55 patients with imaging evidence of nerve-root compression and corroborative radicular symptoms.[43] Twenty-eight patients received bupivacaine and betamethasone, and 27 received bupivacaine. At 13- to 26-month follow-up, 33.3% of patients in the bupivacaine group decided not to have surgery, compared with 71.4% of the bupivacaine-and-betamethasone group. The difference in surgical rates was statistically significant (P< .004). This study demonstrated the beneficial effect of precisely delivered corticosteroids in obviating operative treatment in patients with HNP and/or spinal stenosis.

Kraemer and colleagues reported long-term pain relief with transforaminal ESI.[44] In their study, 49 patients with lumbar radicular pain were randomly assigned to into a corticosteroid group and control group.

Karppinen and colleagues reported 160 consecutive patients with symptomatic herniated disks with no history of lumbar-spine surgery.[45] Patients were randomly selected for a corticosteroid group or a normal-saline group. Outcome measures obtained at 2 weeks, 3 months and 6 months included pain relief, sick leave, medical costs, findings on the Nottingham Health Profile, and future requirements for surgical intervention. Transforaminal ESI provided significant short- and long-term improvement in all of the outcome measures.

Thomas and colleagues reported the relative effectiveness of fluoroscopically guided lumbar transforaminal ESIs versus blind interlaminar ESIs in patients with radicular pain.[46] Transforaminal ESIs were superior a variety of outcome measures, including finger-to-floor lumbar flexion, daily activity (including work and vocational function), and Dallas pain scores. Findings from this direct comparison underscore the importance of fluoroscopic guidance and of delivering medication accurately and precisely to the site of a potential ongoing inflammatory response.

In a prospective nonblinded randomized study by Buttermann, transforaminal ESIs provided efficacy measured by reduced symptoms and disability and obviation of surgery at a follow-up of up to 3 years. Patients had large (>25% of the cross-sectional area of the spinal canal) symptomatic lumbar herniated disks. Buttermann also reported that patients who had short-term improvement or ineffectiveness of transforaminal ESIs and who require surgical diskectomy had no adverse effect in the outcome of that surgery, due to the temporal delay caused by the trial of transforaminal ESIs.[47]

Findings from several prospective nonrandomized clinical trials of the efficacy of transforaminal ESI strongly suggest the beneficial effects of transforaminal ESIs for HNP that causes lumbar axial pain with corroborative radicular pain.

Weiner and colleagues reported that 21 of 28 patients with a CT-documented HNP and corroborative lower-extremity pain had moderate or complete pain relief after receiving a single transforaminal infusion of betamethasone and 1% Xylocaine; patients did not require surgery at an average of 3.4 years during follow-up.[48]

Lutz and colleagues reported 69 patients, with an average of 22 weeks of symptoms, who had MRI evidence of a HNP and radicular pain.[49] Patients underwent an average of 1.8 transforaminal injections of betamethasone and 1% Xylocaine followed by a 6- 12-week course of lumbar-spine stabilization therapy. At an average of 80 weeks of follow-up, 75% of patients had a success outcome (defined as pain reduction by 50% or more and return to previous or near-previous level of function).

In a retrospective evaluation, Wang and colleagues demonstrated significant short- and long-term symptomatic improvement and the avoidance of diskectomy in 77% of patients with lumbar disk herniations who were treated with 1-6 transforaminal ESIs.[50]

The literature discussed above strongly suggests that transforaminal ESI should be the standard of care for index interventional spinal procedure in patients with spinally mediated lumbar axial pain syndromes associated with radicular involvement due to diskogenic disease and/or HNP when more conservative measures fail. Furthermore, in most cases of HNP, the known phagocytic immunologic response and consequent benign anatomic natural history contributes to the relatively high long-term success rates of transforaminal ESIs.

Contraindications to steroid instillations in the epidural space are pregnancy (because of the adverse effects of fluoroscopy on the fetus), hypersensitivity to any component of the injected steroid, bacteremia, full anticoagulation, and bleeding diathesis. Other concerns are elevation of serum glucose levels in patients with diabetes, elevation of blood pressure in hypertensive patients, and fluid retention in patients with congestive heart failure. Use of aspirin and other NSAIDs has not been demonstrated to predispose patients to clinically significant bleeding when they are receiving epidural injections.

Other therapies

New intradiskal techniques are being investigated to ascertain whether they can obviate fusion procedures. With intradiskal electrothermal therapy, a navigable intradiskal catheter is used to heat the posterior annular wall at the nuclear interface corresponding to the 4- to 8-o'clock zone.[51, 52] Temperatures produced in the outer annulus (46-48°C) are sufficient for thermal coagulation of nervous tissue. Temperatures in the nucleus and the annulus (65-75°C) are sufficient for collagen contraction or shrinkage.

Saal and colleagues observed 20% focal nuclear shrinkage (by volume) and 7% total nuclear shrinkage after treatment.[53] Therefore, some authorities postulate that this intervention may cause thermocoagulation of annular nerve fibers. In addition, by means of collagen shrinkage, it may also result in tightening of the fibrous structure of annular tissue that then may enhance structural integrity of a degenerated or damaged disk and possibly stabilize annular fissures. Intradiskal electrothermal therapy showed great promise in initial studies and was touted as being effective at controlling diskogenic axial lumbar back pain. However, a later investigation, a double-blinded, controlled study conducted by Freeman and colleagues, established safety with limited efficacy.[54]

  • Saal and Saal reported their results in 36 patients who were followed up for 6-13 months.[53] Improvement in function, lowering of pain scores, and improvement in sitting tolerance times were observed in 75%.

  • In a clinical trial of 20 patients, Derby reported a mean 2-point decrease on a 10-point visual analog scale (P< .05) at 6 months.[55] In addition, 73% reported satisfaction with outcome and indicated that they would repeat the procedure for the same outcome. Although early results are promising with this exciting novel technique, no definitive judgments can be made because only preliminary outcomes with short-term follow-up have been reported to date.

  • The idea of intradiskal injections and procedures is becoming exciting with new trials of OB1 and other biological therapies being developed in the hopes of being able to regenerate diskal materials and reverse the degenerative cascade underway.

  • Since their discovery by Marshall Urist, MD at UCLA, bone morphogenetic proteins have been categorized as either growth or differentiation factors and consist of a family of proteins with important regulatory and developmental effects on bone growth and the development of musculoskeletal tissue. These proteins are clinically used by spine surgeons to facilitate bony fusion and obviate the need for autografting.

    • Studies have shown that these proteins are capable of controlling the mRNA transcription of cells within human and animal disk models. At the 2002 North American Spine Society (NASS) annual meeting, studies were presented that showed great promise with regard to the development of treatments for degenerative disk disease using bone morphogenic proteins 2 and 7, with augmentation of diseased disks employed at an early stage to offset the degenerative cascade.[56, 57]

    • Miyamoto and colleagues showed restoration of disk viscoelastic properties in a rabbit model of degenerative disk disease after injection of osteogenic protein 1 (OP-1). It is hoped that disk regenerative therapy using intradiskal injections of biological pharmaceuticals will become an effective treatment for degenerative disk disease.[58]



Medication Summary

Medications are an integral part of treatment of LDDD. A myriad of medications of various subtypes has been prescribed by a wide array of medical specialties to help patients with sequelae of LDDD. Several types of medications may be helpful in treatment of diskogenic pain (eg, analgesics [peripheral and centrally acting], muscle relaxants, sedatives, glucocorticoids, anticonvulsants, antidepressants, antihistamines, stimulants). Mainstays of oral treatment of LDDD, peripherally acting analgesics, are discussed here. The following information was collected from the Physician's Desk Reference.

Analgesics act either peripherally or centrally. Peripherally acting analgesics include nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. NSAIDs are the drugs of choice (DOCs) in initial pharmacologic treatment of acute episodes of diskogenic pain or with acute exacerbation of chronic diskogenic pain. NSAIDs have mild-to-moderate analgesic, antipyretic, and anti-inflammatory properties. NSAIDs have multiple mechanisms of action, including inhibition of cyclo-oxygenase, competition with prostaglandin at receptor sites, and inhibition of WBC migration and of lysosomal enzymes from WBCs.

Analgesic effect appears earlier and at lower doses than anti-inflammatory effects. Increasing dosage usually increases analgesic effect, with a ceiling effect after which increasing dosages do not increase therapeutic efficacy but do increase toxicity. Use of these medications on a long-term basis is not advised. For reasons not well understood, some patients respond to some NSAIDs and not to others despite their apparently similar mechanisms of action.

This response does not correlate with the class of NSAIDs. Therefore, 7- to 14-day trials of up to 3 different NSAIDs should be performed before one deems NSAIDs ineffective for an individual patient. NSAIDs can be divided into categories based on the cyclo-oxygenase (COX-2) specificity and short, intermediate, or long half-lives. COX-2 specific NSAIDs are primarily beneficial because they do not inhibit the COX-1 isoenzyme. This property dramatically decreases risk of GI and renal adverse effects. NSAIDs with a short half-life (4-6 h) include aspirin, ibuprofen, ketoprofen, and flurbiprofen. Of these medications, aspirin and ibuprofen are the DOCs. NSAIDS with an intermediate half-life (8-12 h) include naproxen, etodolac, diclofenac, sulindac, and diflunisal. Of these, naproxen

Ketoralac requires special consideration because it is the NSAID best known for its analgesic effect at the opioid level. However, it should be used for a maximum of 5 days (in any form). Acetaminophen is effective for mild to moderate pain. It has analgesic and antipyretic properties but no anti-inflammatory action.

Nonsteroidal anti-inflammatory drugs

Class Summary

These drugs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. They may have other mechanisms as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Aspirin (Anacin, Bayer Aspirin, Ascriptin)

Best-known NSAID; widely available; cardioprotective, cerebroprotective, and anticoagulation properties. Treats mild to moderate pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Ibuprofen (Ibuprin, Motrin)

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

Naproxen (Naprelan, Naprosyn, Aleve)

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

Nabumetone (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclooxygenase enzyme, which inhibits pain and inflammation.

Meloxicam (Mobic)

Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Ketorolac (Toradol)

Inhibits prostaglandin synthesis by decreasing activity enzyme, cyclo-oxygenase, decreasing formation of prostaglandin precursors.

Celecoxib (Celebrex)

Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek lowest dose for each patient.

Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).

Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.


Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain. The FDA has cleared duloxetine to treat chronic musculoskeletal pain.

Acetaminophen (Tylenol, Aspirin Free Anacin, Feverall)

Ensures patient comfort, promotes pulmonary toilet, and has sedating properties.

Duloxetine (Cymbalta)

Potent inhibitor of neuronal serotonin and norepinephrine reuptake. Indicated for chronic musculoskeletal pain, including discomfort from osteoarthritis and chronic lower back pain.

Skeletal muscle relaxants

Class Summary

These drugs are effective in reducing morbidity. Their mechanism of action not clearly understood.

Orphenadrine (Norflex)

Although the exact mode of action not well understood, has clinical effectiveness in muscular injury. Effectiveness may be related to analgesic properties. May have atropinelike effects and analgesic properties.

Cyclobenzaprine (Flexeril)

Acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons. Structurally related to tricyclic antidepressants.

Skeletal muscle relaxants have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle strains and, used intermittently, for diffuse and certain regional chronic pain syndromes. Long-term improvement over placebo has not been established. Often produces a "hangover" effect, which can be minimized by taking the nighttime dose 2-3 h before going to sleep.




Back schools and other training programs that are not job specific have not been shown to be effective statistically; however, programs that integrate job requirements into training programs show statistically significant results.


IDD, or incompetent disk disease, may account for 39% of all cases of chronic LBP. Alterations in the internal structure and metabolic functions of the disk account for associated symptoms.

  • IDD most commonly occurs after significant trauma (eg, sudden or unexpected lifting, forces transmitted through the disk secondary to high-speed accidents, substantial axial load). Some individuals develop IDD in the absence of a known inciting event. For inexplicable reasons, a small number of individuals with insidiously progressing degenerative disk disease develop IDD.

  • The major clinical characteristic is a deep-seated spinal ache. IDD typically worsens over several months after onset and is aggravated by activities that increase compressive forces on the spine. No explanation of why such activities cause pain is accepted widely, though several theories exist. One is possible leakage of disk catabolites, which may create adverse reactions in the regional nerves around the disk and spinal canal and/or produce constitutional disturbances mediated by the immune system.

Adams and colleagues have proposed an appealing biomechanical model, suggesting that creep leads to concentrated areas of stress in the annulus.

  • Results from in vivo stress profilometry led to the postulation that biomechanical changes due to degeneration may transmit excess force to the vertebral endplate and that shear stress develops in the disk because of anisotropic force concentration. The result is that the annulus functions as a mechanical support rather than a retaining membrane.

  • Combining these postulates with results of previous intradiskal pressure studies leads to a potential explanation of why patients with IDD frequently have predictable symptoms and examination findings. That is, patients often indicate that their symptoms do not improve rapidly with rest but that unloading the spine may ameliorate them.

  • Partial pain relief is achieved by resting in the lateral decubitus position, that is, the supine position with knees and hips flexed, and changing from unsupported to supported sitting. Symptom exacerbation occurs with positions or maneuvers that load the spine.

Patients frequently describe increased symptoms during prolonged sitting and lumbar flexion, and lumbar flexion, especially with rotation. Aerobic and anaerobic deconditioning, resulting from prolonged inactivity, leads to complaints of frequent fatigue, weight gain, and soft tissue tightness.

  • Some patients experience weight loss, but, in clinical experience, this tends to be the exception.

  • Some patients describe extremity or perineal pain.

  • An insidious history is typical and peripheral symptoms fluctuate directly with intensity of back pain.

  • Radicular complaints are rarely confused with these somatically referred symptoms.

  • A deep aching pain, a sense of weakness without corroborative objective evidence, and a feeling of heaviness are experienced commonly.

  • Lower-extremity symptoms may involve the thigh, lower leg, and/or foot.

Some depression is common. When one assesses patients with IDD, make a critical assessment of psychological factors, particularly when surgical intervention is considered.

  • Physical findings consistent with IDD syndrome, which are not found in every case, include provocation of back pain with pelvic rocking, straight leg raise, partial forward flexion in the standing position with the knees extended, pressure application over the intervertebral disk space, and sustained hip flexion.

  • These provocative maneuvers should not be accompanied by exorbitant demonstrations of perceived pain. Such overt pain behavior should alert the clinician to possible psychosocial issues.

Partial pain relief is achieved by reducing axially transmitted forces. Although the patient is sitting at the edge of the bed, ask him or her to shift his or her weight to the hands by lifting the buttock slightly off the bed. ROM testing of the lumbar spine leads to commonly observed findings.

Performing standing forward flexion with or without simultaneous trunk rotation with the knees fully extended is painful, whereas extension may provide symptom reduction.

  • In some instances, peak pain intensity is described during the return to the neutral position from the terminally flexed position. When this occurs, patients commonly use their hands to apply force to the anterior thigh, reducing the intensity of the pain associated with this task. Such symptom and examination findings are generally accepted but not proven by scientific study.

  • In 1 study of the components of history or physical examination that were predictive of IDD, none could be identified. Results of another study suggest that using a McKenzie approach can reliably differentiate diskogenic from nondiskogenic pain.

Patient Education

An education-based paradigm for the patient with LBP can be inexpensive, beginning with providing reassuring information to patients.

  • Seeds of the educational approach exist in back schools, functional restorative programs, and innovative prevention and rehabilitation strategies.

  • LaCroix found that 94% of patients with a good understanding of their condition returned to work, whereas only 33% of patients with poor understanding of their condition returned to employment.

  • Reassurance that activity is helpful promotes return to function.

For excellent patient education resources, see eMedicineHealth's patient education articles, Low Back Pain, Lumbar Laminectomy, and Chronic Pain.