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Lumbar Degenerative Disk Disease Workup

  • Author: Rajeev K Patel, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
Updated: Apr 26, 2016

Laboratory Studies

See the list below:

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

Imaging Studies

See the list below:

  • Radiography
    • 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 [16, 17]
    • CT can be used to identify symmetric uniform 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[18] 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.
    • CT also may demonstrate endplate degenerative changes, including sclerosis and cortical irregularity with erosions. CT 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 [16]
    • MRI is currently the criterion standard imaging modality for detecting disk pathology. MRI has demonstrated degenerative changes in 3 times as many motion segments as contrast-enhanced CT scan. 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.[2]
    • 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.[19] 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.[20] 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).[21, 22]
    • In vitro, MRI can demonstrate radial tears of the disk annulus.[23] 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.[24] 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.[25, 26]
    • 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

See the list below:

  • 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. [27]
  • Both April and Schellhaus have suggested that HIZL observed on MRI may be a marker of a painful disk. [22, 28] However, findings from 4 independent studies of the clinical usefulness of HIZL as an indicator of a symptomatic disk are not supportive of this conclusion.
  • 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. [29]
  • 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. [30] 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.


See the list below:

  • 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. [31] 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. [32]
  • In 1972, Winnie and colleagues emphasized the importance of placing medication as close to the site of pathology as possible to maximize the outcome. [33] 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.[34]
      • 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.[35] 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.[36] 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.[37] 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.[38] 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.[39] 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 affect in the outcome of that surgery due to the temporal delay caused by the trial of transforaminal ESIs.[40]
    • 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.[41]
      • Lutz and colleagues reported 69 patients, with an average of 22 weeks of symptoms, who had MRI evidence of a HNP and radicular pain.[42] 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.[43]
  • 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.

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.[44]

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.[45] 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.

Contributor Information and Disclosures

Rajeev K Patel, MD Assistant Professor, Department of Orthopedics, University of Rochester; Consulting Surgeon, Strong Health Spine Center, Strong Memorial Health System

Rajeev K Patel, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, North American Spine Society

Disclosure: Nothing to disclose.


Curtis W Slipman, MD Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center

Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, North American Spine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Patrick M Foye, MD Director of Coccyx Pain Center, Professor and Interim Chair of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School; Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Additional Contributors

J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR Senior Associate Dean, Associate Dean of Clinical Medicine, Consultant in Sports Medicine, Assistant Vice President of Program Development, Division of Health Sciences, DeBusk College of Osteopathic Medicine; Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Manipulative Medicine, Lincoln Memorial University-DeBusk College of Osteopathic Medicine

J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, American Osteopathic Academy of Sports Medicine

Disclosure: Nothing to disclose.

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