eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders
Lumbar Degenerative Disk Disease
Updated: Jan 18, 2007
Introduction
Background
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 comprise the functional spinal unit, composed of 2 adjacent vertebral bodies and the intervertebral disk. The disk and 2 zygapophyseal joints at the same level function as a trijoint complex.
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).
Pathophysiology
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. 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. 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). 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.
Frequency
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.
Mortality/Morbidity
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 (Deyo, 1987). More recently, 44% of patients reported chronic symptoms (defined as back pain for >90 d in the previous 6 mo) over 2-year follow-up. 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 et al reported that 15-20% of primary care patients with LBP had moderate-to-severe limitations in activity during 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 (Von Korff, 1993).
- 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 (Frymoyer, 1996).More recently, Luo et al looked at statistics from 1998 and found total health care expenditures incurred by individuals with back pain in the United States to have reached $90.7 billion and total incremental expenditures attributable to back pain among these personswereapproximately$26.3billion. 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 (Luo, 2005).
Sex
LBP secondary to degenerative disk disease affects men and women equally.
Age
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.
Clinical
History
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.
- 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.
- 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
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.
Causes
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.
More on Lumbar Degenerative Disk Disease |
 Overview: Lumbar Degenerative Disk Disease |
| Differential Diagnoses & Workup: Lumbar Degenerative Disk Disease |
| Treatment & Medication: Lumbar Degenerative Disk Disease |
| Follow-up: Lumbar Degenerative Disk Disease |
| References |
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Further Reading
Keywords
lumbar degenerative disk disease, LDDD, lumbar degenerative disc disease, low back pain, LBP, lumbar spondylosis, annular tear, internal disc disruption syndrome, internal disk disruption syndrome, herniated disc, herniated disk, arthritis, lumbar strain, nucleus pulposus, annular delamination, annular lamellae, discogenic pain, diskogenic pain, disc degeneration, disk degeneration, lumbar arthrodesis, lumbar discectomy, lumbar laminectomy, spondylolisthesis, epidural steroid injection, ESI
