Degenerative Lumbar Disc Disease in the Mature Athlete Clinical Presentation
- Author: Gerard A Malanga, MD; Chief Editor: Sherwin SW Ho, MD more...
Establishing a diagnosis in the mature athlete with lower back or leg complaints begins with obtaining a detailed history and performing a physical examination.
- The basic history should include a temporal account of the patient's symptoms and a complete description of complaints. Ask the patient whether their symptoms are associated with participation in a specific sport or activity. If the chief complaint is pain, the primary site, intensity, character, frequency, and radiation of the pain should be determined.
- Identify red flags by asking the patients questions regarding the following:
- Trauma, unexplained weight loss, fever, and chills: Answers to these questions may indicate a more serious medical condition that requires further workup.
- Prior episodes of similar symptoms: A history consisting of previous episodes may provide clues to the patient's present condition.
- Previous treatment: The examiner should ask what previous treatments have been tried (eg, use of ice or heat, use of any medications such as acetaminophen, aspirin, and nonsteroidal anti-inflammatory drugs [NSAIDs]). If lumbar injections of any type were a part of the patient's treatment, it is important to know which approach was used and whether fluoroscopic guidance was used because nonfluoroscopic injections have been noted to miss the epidural space in as many as 40% of patients.
- Previous physical therapy: Ask questions about previous participation in a physical therapy program, and attempt to understand the therapeutic exercises used. If, according to the patient, previous physical therapy failed, the physician should ask about the specific therapy approach used, modalities employed, and inclusion of and compliance with a home exercise program. Knowing this information is beneficial for the physician to appreciate the extent and comprehensiveness of previous treatment strategies.
- The clinical presentation that results from the underlying degenerative processes in the intervertebral discs of the mature athlete can take several different forms.
- As the intervertebral discs deteriorate, small tears can appear in the annulus, and these tears can coalesce to weaken the annulus. At this stage in degenerative disc disease (DDD), back pain is the most common symptom. Discogenic pain usually is worse with prolonged sitting and with flexion of the spine, and it is relieved with extension and moderation of activity.
- Increased pain with coughing, sneezing, or straining also may be consistent with a discogenic cause of back pain.
- If there is progression to frank herniation of the nucleus pulposus, then leg pain, with or without back pain, usually will be the predominant symptom. The distribution of the radiating pain in the extremities depends on which nerve root is compressed or inflamed. Associated motor and sensory deficits may occur, depending on the degree of nerve root involvement.
- This clinical picture usually is seen in persons aged 30-50 years, in whom degenerative changes are present in the disc but in whom the spine is still relatively mobile.
- As the spine ages, loss of disc height can lead to segmental instability and secondary spinal stenosis (ie, narrowing of the vertebral foramen).
- Symptoms of spinal stenosis are determined by the location of the compression on the neural elements. Typically, compression from central stenosis results in neurogenic claudication with unilateral or bilateral discomfort in the buttocks, thighs, or legs.
- Symptoms are produced by standing or walking, and they are relieved by adopting a lumbar flexed posture.
- Symptoms can include pain, numbness or paresthesias, weakness, or a combination of these symptoms.
- When the neural foramen is the site of stenosis, the clinical features are different from those of central canal stenosis. Patients can present with unilateral sciatic pain (usually L5 or S1 nerve root irritation) that is provoked by standing or walking and relieved by sitting or flexing the lumbar spine.
A comprehensive physical examination of the mature athlete with LBP should include an in-depth evaluation of the neurologic and musculoskeletal systems. Combining the findings of the history and physical examination increases the overall predictive value of the evaluation process.
- The examination begins with observation of the patient during the history portion of the evaluation. Note any paraspinal spasms, scoliosis, an increase or decrease in lordosis, muscle atrophies, or asymmetries.
- Observe the iliac crests for any difference in height that may indicate a functional leg length discrepancy.
- When acute disc herniation is present with nerve root involvement, the patient often will list to one side. With a disc herniation lateral to the nerve roots, the patient will list away from the side of the irritated nerve root in an attempt to draw the nerve root away from the disc. Likewise, when the herniation is medial to the nerve root, the patient will list toward the side of the lesion.
- Determine whether any tender or trigger points can be appreciated in the lumbar paraspinal musculature and whether muscle spasm is present. Tenderness also may be present along muscles in which symptoms are referred, such as in the gluteal region and in the lower extremity.
- Palpation of the lumbar spine in the midline sometimes can elicit pain at the level of a symptomatic intervertebral disc.
- Range of motion
- Determine range of motion (ROM) for flexion, extension, lateral bending, and rotation.
- On forward flexion, the lumbar spine should move from its normal lordotic curvature to a straight or slightly flexed posture. The Modified Schober test may be used to measure the amount of flexion occurring in the lumbar spine. A point is marked midway between the 2 posterior sacroiliac spines; then, points 5 cm below and 10 cm above that point are marked. The distance between the 3 points is measured. The patient then is asked to flex forward, and the distance is measured again. The distance between the 2 measurements is an indication of the amount of flexion occurring in the lumbar spine. Less than a 4-cm change between the 2 measurements suggests a loss of normal segmental motion in the lumbar spine.
- In addition to ROM of the spine, assess the other lower extremity joints because pain referral patterns may be confused with focal peripheral involvement. For example, a patient with anterior thigh pain and knee pain may actually have a degenerative hip condition, not an upper lumbar radiculopathy. Reproduction of the patient's pain with hip internal rotation, external rotation, or other provocative hip maneuvers may further distinguish hip pathology from spine involvement.
- Muscle strength
- Manual muscle testing is important to determine whether weakness is present and whether the distribution of weakness corresponds to a single root, to multiple roots, or to a peripheral nerve or plexus.
- Additionally, evaluate the dynamic stabilizers of the lumbar spine, including the abdominals and the muscles about the hip, to include the hip flexors, extensors, and abductors.
- Inflexibility of the musculature about the pelvis has a direct result on the mechanics of the lumbosacral spine.
- Increased tightness of the hamstrings or gluteus maximus muscles can cause a posterior tilt to the pelvis, reducing the lumbar lordosis. Tightness of the rectus femoris and iliopsoas muscles anteriorly can cause an anterior tilt to the pelvis, increasing the lumbar lordosis. Both of these effects can cause increased force to be distributed to the lumbar spine and can predispose individuals to LBP.
- Sensory examination
- On sensory examination, a dermatomal decrease or loss of sensation should be found in patients with clear-cut radiculopathy, whether caused by disc herniation or foraminal stenosis.
- Patients with radiculopathy also may have hyperesthesia to light touch and pinprick examination. However, the sensory examination can be quite subjective, since it requires patient response.
- Muscle stretch reflexes
- Muscle stretch reflexes are helpful in the evaluation of patients presenting with limb symptoms suggestive of a radiculopathy.
- Neither a decrease nor an increase of these reflexes can be interpreted as definitely abnormal. The asymmetry of reflexes is most significant; therefore, a patient's reflexes must be compared with the contralateral side.
- Straight leg raising test
- Provocative maneuvers, such as straight leg raising, may provide evidence of increased dural tension, indicating underlying nerve root pathology.
- Unilateral straight leg raising primarily tests the L5, S1, and S2 nerve roots, with symptoms further provoked by ankle dorsiflexion. Straight leg raising test is only considered positive if pain occurs when the leg is elevated 30-70° and when pain travels down below the knee. Minimal nerve root tension occurs below 30° of elevation, and pain elicited above 70° is most likely related to tightness within the hamstrings or gluteal muscles.
- Elevation of the asymptomatic lower extremity causing pain in the symptomatic side (crossed straight leg raising sign) is suggestive of a herniated disc.
- Peripheral vascular examination
- Examination of the peripheral circulation is important, especially when attempting to differentiate between the neurogenic claudication seen in spinal stenosis and the vascular claudication seen in peripheral vascular disease.
- Examination of the posterior tibial and dorsalis pedis arteries should be performed, as well as examination of the skin temperature and inspection for the presence of trophic changes seen with ischemic disease.
- Pain centralization maneuvers: Attempts at pain centralization through postural changes, such as lumbar extension, may suggest a discogenic cause for the back pain and may help in determining the success of future treatment strategies.
- The clinical features in many cases of radiculopathy are inadequately explained by anatomic abnormalities alone. High levels of an inflammatory enzyme, phospholipase A2, have been identified in lumbar herniated and degenerative discs. Saal et al and other authors support the concept that the clinical features of many patients with lumbar disc disease may be explained by inflammation caused by biochemical factors working alone or in combination with the mechanical deformations described above.
Deterioration of the spinal structures is a universal phenomenon with progression of age, occurring in both athletic and nonathletic populations. The intervertebral disc is part of a 3-joint complex; therefore, damage at the level of either the zygapophyseal joints or the disc affects the function of the entire unit.
- The deteriorative process most likely begins with the intervertebral disc. Tiny blood vessels enter and exit the disc in the early decades of life, but these vessels become obliterated, leaving the intervertebral disc an avascular structure. Thereafter, nutrition of the disc is supported only through extracellular fluid osmosis. Water is drawn into the disc, and, with motion, the water is partially expelled. This constant movement of water into and out of the disc is thought to allow the disc to remain healthy by bringing in needed nutrients. With the aging process, there is a loss of some of the connective tissue fibers within the disc and an alteration in the properties of the nucleus pulposus. This causes less water to be drawn into the disc and, ultimately, may lead to impairment of nutrition. The water content of a disc in young persons is 88%, but it is reduced to less that 70% in elderly persons.
- The deterioration process leads to a stiffening of the intervertebral disc and a change in its shape, causing the disc to lose its ability to distribute load uniformly.
- The fibers of the annulus run in different directions at different depths and allow the annulus to accommodate complex motions. Axial rotation of the spine or rotation of a flexed spine may isolate some of the annular fibers and cause small annular tears. These annular tears may or may not be symptomatic; however, in time, they may coalesce to weaken the annulus fibrosus. This can lead to disc bulging, disc space narrowing, or even frank herniation.
- In addition, the loss of disc space height may lead to segmental instability and increased forces on zygapophyseal joints, resulting in sclerosis and hypertrophy. The loss of disc height also causes bulging of the annulus into the spinal canal and buckling of the ligamentum flavum. Ultimately, this degenerative cascade can lead to a narrowing of the spinal canal and intervertebral foramen, producing an acquired spinal stenosis.
- These degenerative changes begin as early as the second to third decade of life and progress with advancing age. The clinical consequences of this deterioration vary with the age of the patient.
- In persons aged 30-50 years, degenerative changes and tears in the annulus of the disc may cause frank herniation of the disc material. This population usually has some compromise of the integrity of the disc, yet the nucleus is still pliable enough to be extrudable, and the spine is mobile enough to produce the required forces for herniation.
- With aging of the spine, the nucleus pulposus becomes firmer, spinal motion lessens, and bony overgrowth increases. The intervertebral discs do not herniate as frequently, and spinal stenosis becomes the prominent clinical picture.
- Athletes and nonathletes alike are subject to these progressive degenerative changes. However, it is not completely clear how the potentially beneficial effects of training interact with the potentially harmful effects of loading experienced by athletes. The greatest incidence of discogenic disease would be expected to be found in those athletes participating in sports with the greatest axial stresses.
- Hellstrom et al found that disc height reduction was much more common in athletes than nonathletes, and, specifically, it is most prevalent in wrestlers and male gymnasts.
- Horne et al found a high frequency of disc space narrowing in the thoracolumbar spines of water-ski jumpers.
- Other studies have failed to show a correlation between physical loading and increased spinal pathology or low back symptoms, and some evidence suggests that certain types of loading may slow down the degenerative process.
- Videman et al reported that former elite athletes overall reported less back pain than control groups in later adulthood. However, they did find an increase in the degenerative changes throughout the entire spine in former weight lifters and in the lower lumbar levels in soccer players when compared to controls. Despite these increased degenerative findings, the former weight lifters and soccer players still had less reported back pain than those in the control groups. This study and others provide some evidence that certain forceful athletic activities may accelerate the degenerative process, but that the degenerative changes seen on imaging studies do not correlate well with clinical symptoms.
Suratwala SJ, Pinto MR, Gilbert TJ, Winter RB, Wroblewski JM. Functional and radiological outcomes of 360 degrees fusion of three or more motion levels in the lumbar spine for degenerative disc disease. Spine (Phila Pa 1976). 2009 May 1. 34(10):E351-8. [Medline].
Arnold PM, Robbins S, Paullus W, Faust S, Holt R, McGuire R. Clinical outcomes of lumbar degenerative disc disease treated with posterior lumbar interbody fusion allograft spacer: a prospective, multicenter trial with 2-year follow-up. Am J Orthop (Belle Mead NJ). 2009 Jul. 38(7):E115-22. [Medline].
Hosea TM, Gatt CJ Jr. Back pain in golf. Clin Sports Med. 1996 Jan. 15(1):37-53. [Medline].
Saal JS, Saal JA. Management of chronic discogenic low back pain with a thermal intradiscal catheter. A preliminary report. Spine. 2000 Feb 1. 25(3):382-8. [Medline].
Videman T, Sarna S, Battié MC, Koskinen S, Gill K, Paananen H, et al. The long-term effects of physical loading and exercise lifestyles on back-related symptoms, disability, and spinal pathology among men. Spine. 1995 Mar 15. 20(6):699-709. [Medline].
Carragee EJ, Tanner CM, Khurana S, Hayward C, Welsh J, Date E, et al. The rates of false-positive lumbar discography in select patients without low back symptoms. Spine. 2000 Jun 1. 25(11):1373-80; discussion 1381. [Medline].
Khot A, Bowditch M, Powell J, Sharp D. The use of intradiscal steroid therapy for lumbar spinal discogenic pain: a randomized controlled trial. Spine. 2004 Apr 15. 29(8):833-6; discussion 837. [Medline].
Buttermann GR. The effect of spinal steroid injections for degenerative disc disease. Spine J. 2004 Sep-Oct. 4(5):495-505. [Medline].
Buttermann GR. Treatment of lumbar disc herniation: epidural steroid injection compared with discectomy. A prospective, randomized study. J Bone Joint Surg Am. 2004 Apr. 86-A(4):670-9. [Medline].
Gibson JN, Waddell G. Surgery for degenerative lumbar spondylosis: updated Cochrane Review. Spine. 2005 Oct 15. 30(20):2312-20. [Medline].
Fritzell P, Hägg O, Wessberg P, Nordwall A,. 2001 Volvo Award Winner in Clinical Studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine. 2001 Dec 1. 26(23):2521-32; discussion 2532-4. [Medline].
Brox JI, Sørensen R, Friis A, Nygaard Ø, Indahl A, Keller A, et al. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. Spine. 2003 Sep 1. 28(17):1913-21.
Keller A, Brox JI, Gunderson R, Holm I, Friis A, Reikerås O. Trunk muscle strength, cross-sectional area, and density in patients with chronic low back pain randomized to lumbar fusion or cognitive intervention and exercises. Spine. 2004 Jan 1. 29(1):3-8. [Medline].
Barendse GA, van Den Berg SG, Kessels AH, Weber WE, van Kleef M. Randomized controlled trial of percutaneous intradiscal radiofrequency thermocoagulation for chronic discogenic back pain: lack of effect from a 90-second 70 C lesion. Spine. 2001 Feb 1. 26(3):287-92. [Medline].
Freeman BJ, Fraser RD, Cain CM, Hall DJ, Chapple DC. A randomized, double-blind, controlled trial: intradiscal electrothermal therapy versus placebo for the treatment of chronic discogenic low back pain. Spine. 2005 Nov 1. 30(21):2369-77; discussion 2378. [Medline].
Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K, Bogduk N. A randomized, placebo-controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine J. 2004 Jan-Feb. 4(1):27-35. [Medline].
Park SY, Moon SH, Park MS, Kim HS, Choi YJ, Lee HM. Intradiscal electrothermal treatment for chronic lower back pain patients with internal disc disruption. Yonsei Med J. 2005 Aug 31. 46(4):539-45. [Medline].
Boden SD, Swanson AL. An assessment of the early management of spine problems and appropriateness of diagnostic imaging utilization. Phys Med Rehabil Clin N Am. 1998 May. 9(2):411-7, viii. [Medline].
Bogduk N, Modic MT. Lumbar discography. Spine. 1996 Feb 1. 21(3):402-4. [Medline].
Buschbacher R. The aging athlete's spine. J Back Musculoskel Rehabil. 1995. 5:55-74.
Dawson E, Bernbeck J. The surgical treatment of low back pain. Phys Med Rehabil Clin N Am. 1998 May. 9(2):489-95, x. [Medline].
Dreisinger TE, Nelson B. Management of back pain in athletes. Sports Med. 1996 Apr. 21(4):313-20. [Medline].
Gamradt SC, Wang JC. Lumbar disc arthroplasty. Spine J. 2005 Jan-Feb. 5(1):95-103. [Medline].
German JW, Foley KT. Disc arthroplasty in the management of the painful lumbar motion segment. Spine. 2005 Aug 15. 30(16 Suppl):S60-7. [Medline].
Goins ML, Wimberley DW, Yuan PS, Fitzhenry LN, Vaccaro AR. Nucleus pulposus replacement: an emerging technology. Spine J. 2005 Nov-Dec. 5(6 Suppl):317S-324S. [Medline].
Greenan TJ. Diagnostic imaging of sports-related spinal disorders. Clin Sports Med. 1993 Jul. 12(3):487-505. [Medline].
Hackley DR, Wiesel SW. The lumbar spine in the aging athlete. Clin Sports Med. 1993 Jul. 12(3):465-8. [Medline].
Hession WG, Stanczak JD, Davis KW, Choi JJ. Epidural steroid injections. Semin Roentgenol. 2004 Jan. 39(1):7-23. [Medline].
Hickey DS, Hukins DW. Relation between the structure of the annulus fibrosus and the function and failure of the intervertebral disc. Spine. 1980 Mar-Apr. 5(2):106-16. [Medline].
Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994 Jul 14. 331(2):69-73. [Medline].
Kahler DM. Low back pain in athletes. J Sport Rehabil. 1993. 2:63-78.
Kaul MP, Herring SA. Rehabilitation of lumbar spine injuries in sports. Phys Med Rehabil Clin N Am. 1994. 5(1):133-56.
Malanga GA, Nadler SF. Nonoperative treatment of low back pain. Mayo Clin Proc. 1999 Nov. 74(11):1135-48. [Medline].
Mayer HM. Total lumbar disc replacement. J Bone Joint Surg Br. 2005 Aug. 87(8):1029-37.
Modic MT. Degenerative disc disease and back pain. Magn Reson Imaging Clin N Am. 1999 Aug. 7(3):481-91, viii. [Medline].
Nachemson A, Zdeblick TA, O'Brien JP. Lumbar disc disease with discogenic pain. What surgical treatment is most effective?. Spine. 1996 Aug 1. 21(15):1835-8. [Medline].
Nadler SF, Malanga GA, DePrince M, Stitik TP, Feinberg JH. The relationship between lower extremity injury, low back pain, and hip muscle strength in male and female collegiate athletes. Clin J Sport Med. 2000 Apr. 10(2):89-97. [Medline].
Nadler SF, Wu KD, Galski T, Feinberg JH. Low back pain in college athletes. A prospective study correlating lower extremity overuse or acquired ligamentous laxity with low back pain. Spine. 1998 Apr 1. 23(7):828-33. [Medline].
Rothman RH. The clinical syndrome of lumbar disc disease. Orthop Clin North Am. 1971 Jul. 2(2):463-75. [Medline].
Sinaki M, Mokri B. Low Back Pain and Disorders of the Lumbar Spine. Braddom RL. Physical Medicine & Rehabilitation. 2nd. Philadelphia, Pa: WB Saunders; 1996. 813-50.
Tall RL, DeVault W. Spinal injury in sport: epidemiologic considerations. Clin Sports Med. 1993 Jul. 12(3):441-8. [Medline].