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Degenerative Lumbar Disc Disease in the Mature Athlete Clinical Presentation

  • Author: Gerard A Malanga, MD; Chief Editor: Sherwin SW Ho, MD  more...
 
Updated: Mar 06, 2014
 

History

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.
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Physical

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.

  • Inspection
    • 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.
  • Palpation
    • 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.
  • Flexibility
    • 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.[4]
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Causes

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.[5]
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Contributor Information and Disclosures
Author

Gerard A Malanga, MD Founder and Partner, New Jersey Sports Medicine, LLC and New Jersey Regenerative Institute; Director of Research, Atlantic Health; Clinical Professor, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey-New Jersey Medical School; Fellow, American College of Sports Medicine

Gerard A Malanga, MD is a member of the following medical societies: Alpha Omega Alpha, American Institute of Ultrasound in Medicine, North American Spine Society, International Spine Intervention Society, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine

Disclosure: Received honoraria from Cephalon for speaking and teaching; Received honoraria from Endo for speaking and teaching; Received honoraria from Genzyme for speaking and teaching; Received honoraria from Prostakan for speaking and teaching; Received consulting fee from Pfizer for speaking and teaching.

Coauthor(s)

Michal E Eisenberg, MD Staff Physician, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey, New Jersey Medical School

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.

Chief Editor

Sherwin SW Ho, MD Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, Arthroscopy Association of North America, Herodicus Society, American Orthopaedic Society for Sports Medicine

Disclosure: Received consulting fee from Biomet, Inc. for speaking and teaching; Received grant/research funds from Smith and Nephew for fellowship funding; Received grant/research funds from DJ Ortho for course funding; Received grant/research funds from Athletico Physical Therapy for course, research funding; Received royalty from Biomet, Inc. for consulting.

Additional Contributors

Joseph P Garry, MD, FACSM, FAAFP Associate Professor, Department of Family Medicine and Community Health, University of Minnesota Medical School

Joseph P Garry, MD, FACSM, FAAFP is a member of the following medical societies: American Academy of Family Physicians, American Medical Society for Sports Medicine, Minnesota Medical Association, American College of Sports Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor Stephen G Andrus, MD, to the development and writing of this article.

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Degenerative lumbar disc disease in the mature athlete. Degenerative changes of the lumbar spine, includingdecreased signal intensity and disc bulging at the L-3/4, L-4/5 and L-5/S-1 discs.
Degenerative lumbar disc disease in the mature athlete. The process of disc degeneration following internal discdisruption and herniation.
Degenerative lumbar disc disease in the mature athlete. The various forces placed upon the discs of the lumbarspine that can result in degenerative changes.
 
 
 
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