Degenerative Disc Disease
Lumbar disc degeneration is a complicated condition that is characterized by the degeneration of the intervertebral disc over time and the associated pain, generally in the lower lumbar and cervical spine. Lumbar disc degeneration may involve the narrowing of the disc space and the presence of anterior vertebral osteophytes1. There is currently no consensus on what “disc degeneration” is or really means2. It is hard to differentiate degenerative disc disease from natural growth, aging, healing, and remodeling processes. It is also difficult to distinguish from being a possible form of spinal osteoarthritis.
The human spine comprises 23 intervertebral discs, which change in shape and size throughout the spine3. The disc is made up of a tough outer layer (the annulus fibrosus) and a softer inner layer (the nucleus pulposus). The annulus is comprised mainly of type 1 collagen, with fibers that run in multiple directions to help dissipate forces. The nucleus pulposus is made up of water, proteoglycans, and type 2 collagen fibers4. Normal IV discs are avascular, and disc cells exchange nutrients by passive diffusion. The outermost layers of the annulus are innervated by sinuvertebral nerves, while the inner layer and nucleus are not innervated.
DDD generally affects the lower lumbar spine but can affect the upper lumbar and cervical spine. Can be assymptomatic in up to 1/3 of those affected. Tends to get worse after heavy physical labor or prolonged positioning1, sitting, bending, lifting, or twisting. May initially ease with rest from labor.
- Low back pain
- Gradual onset of increasingly severe midline lower back pain
- May last a few days, or be intermittent
- Pain may increase with further episodes
- May last longer in duration
- Radicular Symptoms into the buttocks and thighs or into the shoulders (cervical)
- Aching of the buttocks and thighs during ambulation
Changes in the integrity of the IV disc may be due natural aging, genetic factors, inadequate metabolic transport, and history of significant repetitive loading1. Nutritional deficiency of the disc cells is accelerated by smoking, end-plate calcification, and the overall nutritional status of the individual. This nutritional deficient and oxygen transport can lead to an increase in lactic acid build up in the disc, disrupting the ability of the disc to re-synthesize and maintain its extracellular matrix4. As the disc degenerates, more pressure is placed on the contents of the disc and, and the vertebral bodies above and below. This structural failure however of the disc does not always correspond to pain.
Process of Degeneration
- Nucleus loses the ability to absorb water
- disc becomes dehydrated
- nucleus becomes thicker and more fibrous
- Nucleus loses ability to absorb shock
- routine stress and strain take a greater toll
- Tears may form around the annulus
- Disc weakens, may collapse
- bones of the spine compress on each other
- compression on nerve roots may illicit radicular symptoms
- Compression of vertebral bodies
- spinal stenosis may occur
- spondylolisthesis may occur (generally in adults older than 65 yrs)
- OA of the facet
- Osteophytes around the margins of the vertebral bodies may form
Lumbar intervertebral disks (midsagittal section; anterior on the left).
A, Young disk in a male, 35 years old. B, Mature disk in a male, 47 years old. C, Disrupted disk in a male, 31 years old. Note the endplate and inward collapse of the inner anulus. (From Adams MA: The biomechanics of back pain, Edinburgh, 2002, Churchill Livingstone. - Science Direct)
- Low back pain is the most frequently reported musculoskeletal problem and the third most frequently reported symptom of any kind. Nearly 20% of all visits to physicians for low back pain involved individuals over age 657.
- It is estimated that about 18% of the population is having low back pain at any time5.
- Although degenerative disc disease can occur before age 20, it tends to peak in the fourth and fifth decades of life and declines after that1.
- It is thought that discogenic pain from internal disc disruption accounts for the largest proportion of chronic low-back pain3
- Medicare data from 1991-2002 shows a 132% increase in low back pain patients and a 387% increase in related charges for low back pain6.
- Its lifetime prevalence is 58-84% in the labor force, and is a leading cause in number of working days lost per year in the US (exceeds 100 million)3.
Genetics is viewed as being the greatest risk factor for disc degeneration, which accounts for approximately 50-70% of the variability in disk degeneration between identical twins1.
These have also been thought to be risk factors, though the research is still somewhat conflicting2.
-History of back pain
-heavy physical activity
Research has also shown that there may be progression rates as high asf 3% per year in terms of disc space narrowing, and 4% per year for osteophyte occurence with disc degeneration and that these rates are related to risk factors such as age, history of back pain, and radiographic findings of associated hip and knee osteoarthritis2.
Radiograph of a lumbar spine (anterior on left) with severe disc narrowing, vertebral osteophytes, sclerosis of the endplates, and selective loss of horizontal trabeculae from the vertebral body.
Diagnosis of DDD requires a thorough subjective examination, objective physical examination, and imaging when available.
- Imaging methods:
- Provacative Discography: dye is injected into disc and may reveal annular tears; this can reveal information about the health of the discs
- X-rays: can help measure disc space narrowing, which may be indicative of DDD. Can also help reveal osteophyte formation, spondylolysis or spondyloisthesis.
- MRI: can help reveal if discs are able to absorb water, if they have radial fissures, and if nerves are affected. MRI, however, is poorly correlated with clinical signs and symptoms1. It has poor predictive validity for pain in older adults between the ages of 53 and 706. They can generally find IV disc degeneration in adults over 50 years old. But cannot differentiate between painful disc and aging discs5.
- CT Discography: Can show the formation of vascularized granulation tissue and innervation patterns in the annulus and nucleus with torn fissures. This has been shown in at least one study to be a possible distinct pathological characteristic of discogenic based low back pain5.
- Active movements
- Combined/Repetitive Movements
- Quick Tests: Squat, Hop
- Clear possible referral joints: Shoulder, Thoracic, SIJ, Hip, knee and ankle (if radicular symptoms are present)
- Special Tests:
- Straight Leg Raise (may indicate nerve root compression or be the result of inflammatory irriation from chemicals released by the damaged disc1).
- SIJ asymmetry
- Traction (relief of symptoms may indicate compression)
- Mckenzie Back Extension Exercises
- Nuero Tests (if radicular symptoms are present)
- Tension Tests
- Prone Knee Bend
- Neck Flexion
- Slump Test
The goal of conservative treatment is to manage pain and introduce the patient to normal exercises as soon as possible. Long term studies show that conservative care and surgical management have the same outcomes after 10 years if the patient does not have neurological symptoms at the initial incident1.
- Mild Analgesics
- Lifestyle changes (weight loss, initiate fitness program)
- Aerobic conditioning
- Back extension exercises
- Postural training
- Hamstring and Core strengthening exercises
- Modalities for pain management: heat/cold, E-Stim
- Biological treatments to promote matrix repair and physiological function
- protein growth factors
- gene delivery
- tissue engineering
Modality Based Treatments
Interventions used to treat DDD commonly include heat/cold, electrical therapy (TENS or IFC), ultrasound, cold laser, mechanical traction, manual therapy, and alternative medicines such as acupuncture. Research has shown that more than half of primary care doctors routinely recommend or prescribe these treatments when managing back pain7
AHCPR (Agency for Health Care Policy and Research) guidelines for treatment of back pain encourage the teaching of self application of heat or cold for pain control and discourage the use of modalities such as TENS, ultrasound, and biofeedback, which have an uncertain effectiveness8
A joint Clinical Practice Guideline from the American College of Physicians and the American Pain Society in 2007 indicated that TENS and intermittent or continous traction have not been proven effective for chronic low back pain and that there is also insufficient evidence to recommend the use to interferential (IFC) therapy, or low level laser therapy, shortwave diathermy, or ultrasonography9.
A 2010 Systematic Review and Meta-Analysis on the use of IFC for all musculoskeletal pain problems including acute and chronic low back pain provided little evidence towards a superior effectiveness of the IFC in treatment alone over other modalities, though it was found to be superior to placebo treatments. Its preferred use would be in conjunction with a wide array of treatment modalities; however, in this setting it is difficult to tell if or how much the IFC is actually contributing to the pain management10.
In spite of the insufficient evidence, physical therapists continue to use these treatments as they see fit. In a 2001 survey of 569 physical therapists in Canada on their treatment of individuals with low back pain, information was gathered about their typical physical examination, their treatment and recommendations, and their beliefs regarding management of these patients. Only data from 274 physical therapists whose weekly workload included more than 10% of people with lumbar impairment were included. Results from this study included:
—-Patient Education, exercise, and electrotherapeutic and thermal modalities were the preferred interventions for acute lumbar impairments (with and without sciatica), and exercise and work modification were preferred for subacute lumbar impairment (>5 weeks from symptom onset).
81.9% and 65.7% agreed that ice and heat were effective from acute lumbar impairment
61.4% agreed that ultrasound was effective, and 53% agreed that TENS was effective treatment for lumbar impairments
30% indicated use of mechanical spinal traction for acute sciatica
0.1% indicated bed rest, and 97.7% indicated physical activity was crucial to recovery
67% indicated that back education programs were effective in reducing recurrences
And 84.9% of the therapists indicated that they were comfortable managing patients with lumbar impairment8.
Surgery to remove the disc or portions of the irritable disc may be performed if conservative treatment approaches fail to significantly manage painful symptoms or neurological signs are present. Minimally invasive procedures include discectomy, laminectomy, and spinal fusion. These approaches have limited and inconsistent clinical results, and may lead to restricted range of motion3. One to three injections of epidural steroids combined with numbing agents into the space surrounding the nerve roots can be performed and has shown some popularity1. Disc decompression is also an option.
In 2004, the FDA approved of artificial disc replacement (ADR) as a treatment approach. The ADR device is inserted into the space between two vertebral bodies where the damaged disc once was. This treatment approach attempts to create better disc height, spinal alignment, and spinal movement, but carries some risk in possible infection, implant failure, or fracture. Where a total artificial disc replacement may be unnecessary, but pain is present, use of a prosthetic disc nucleus (PDN) has been shown to promote significant pain relief, mobility, and function in the long term11.
Links to Webpages about DDD
1. Goodman, Catherine C.. Pathology: Implications for the Physical Therapist, 3rd Edition. W.B. Saunders Company, 112008. 27.10.5
2. Hassett G, Hart DJ, Manek NJ, Doyle DV, Spector TD. Risk Factors for Progression of Lumbar Spine Disc Degeneration. The Chingford Study. Arthritis & Rheumatism. 2003:48:11:3112–3117.
3. Zhang Y, An HS, Tannoury C, Thonar EJ-MA, Freedman MK, Anderson DG: Biological treatment for degenerative disc disease: implications for the field of physical medicine and rehabilitation. Am J Phys Med Rehabil. 2008;87:694–702.
4. Yong-Soo Choi. Pathophysiology of Degenerative Disc Disease. Asian Spine Journal. 2009:3:1:39-44
5. Peng B, Hao J, Hou S, Wu W, Jiang D, Fu X, Yang Yi. Possible Pathogenesis of Painful Intervertebral Disc Degeneration. Spine. 2006: 31:5;560–566
6. Hicks G, Morone N, Weiner D. Degenerative Lumbar Disc and Facet Disease in Older Adults: Prevalence and Clinical Correlates. Spine. 2009: 34:12:1301-1306
7. Cohen S, Argoff C, Carragee E. Management of Low Back Pain. BMJ, 2008: 337:a7718
8. Li L, Bombardier C. Physical Therapy Management of Low Back Pain: An Exploratory Survey of Therapist Approaches. Physical Therapy. 2001, 81:4 (1018-1028)
9. Chou R, Qaseem A, Snow V, Casey D, Cross Jr T, Shekelle P, Owens, D. Diagnosis and Treatment of Low Back Pain: A Joint Clinical Practice Guideline from the American College of Physicians and the American Pain Society. Ann Intern Med, 2007: 147(478-491)
10. Fuentes J, Olivo S, Magee D, Gross D. Effectiveness of Interferential Current Therapy in the Management of Musculoskeletal Pain: A Systematic Review and Meta-Analysis. Physical Therapy. 2010, 90:9, 1219-1238
11. Selviaridis P, Foroglou N, Tsitlakidis A, Hatzisotiriou A, Magras I, Patsalas I. Long-term outcome after implantation of prosthetic disc nucleus device (PDN) in lumbar disc disease. Hippokratia. 2010:14,3: 176-184