Lumbar Disk Herniation in Immature and Adult Athletes

Tyler J. Jenkins, MD

Wellington Hsu, MD

Dr. Hsu or an immediate family member has received royalties from Stryker; is a member of a speakers’ bureau or has made paid presentations on behalf of AONA; serves as a paid consultant to AONA, Bacterin, Bioventus, CeramTec, Globus, Graftys, Lifenet, Medtronic Sofamor Danek, Relievant, Rti, SI Bone, and Stryker; has received research or institutional support from Medtronic; and serves as a board member, owner, officer, or committee member of the AAOS, the Cervical Spine Research Society, the Journal of Spinal Disorders and Techniques, the Lumbar Spine Research Society, and the North American Spine Society. Neither Dr. Jenkins nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this article.

Introduction

The prevalence of back pain can be as high as 30% in competitive athletes.¹^,² Lumbar disk herniation (LDH) should be considered when an athlete is presenting for evaluation of radiating leg or back pain.³ Athletes may be predisposed to a higher incidence of LDH than the general population because of the rigorous demands of their sports.⁴ Although extensively studied in the general population, the evaluation and management of LDH in this patient population is still evolving. This chapter highlights the pathoanatomy, clinical evaluation, and management of LDH in athletes using the best literature available to date.

Pathoanatomy

Lumbar disk herniations occur when the gel-like nucleus pulposus ruptures through the fibrous outer annulus, causing a displacement of disk contents beyond the circumferential border of the intervertebral disk. Because of the relative weakness of the posterior longitudinal ligament (PLL) at the posterolateral disk space, herniations occur most commonly at this location.⁵^,⁶ The disk herniation then leads to irritation of an adjacent nerve root.

Disk herniations vary considerably, and the terminology associated with LDH has also evolved over time. Disk bulges are ubiquitous throughout the population and are commonly seen in MRIs of asymptomatic patients.⁷^,⁸ Asymptomatic herniations discovered with the increased use of advanced imaging have led to a paradigm shift in the nomenclature associated with LDH. LDH today primarily describes symptomatic pathology and not the common disk bulge.⁵

After childhood development, intervertebral disks receive a limited nutrient supply via diffusion through vertebral vasculature.⁵^,⁶ The inherent avascularity allows the accumulation of irreparable disk degeneration over time.⁵^,⁶ Recurrent torsional strain causes fissure development in the outer annulus, combined with increased intradiscal pressure from axial loading and forward flexion, can culminate in the herniation of the nucleus pulposus.⁵^,⁶ The lumbosacral spine is particularly susceptible to herniation because of its mobility in flexion, extension, and torsion.⁹

The most clinically relevant LDH classifications describe the location and anatomic characteristics of the fragment. The anatomic location describes the disk fragment relationship to the thecal sac and includes central, posterolateral (paracentral), foraminal, and extraforaminal (i.e., far lateral) (Figure 18-1).⁵ Anatomic descriptions of LDH can include protrusions, extrusions, and sequestrations. Another important factor to consider when describing a LDH is the size of the annular defect. A larger annular defect is associated with a higher risk of recurrent LDH after lumbar discectomy.¹⁰

Symptoms associated with LDH occur secondary to nerve root irritation. The nerve root irritation is initiated
by two intertwined pathways: chemical inflammation and mechanical compression. Many studies have looked at which pathway is the predominate factor in symptomatology, but they are inconclusive to date.¹¹^,¹²^,¹³^,¹⁴^,¹⁵ Nucleus pulposus extracts have been shown to set off an inflammatory cascade when exposed to nerve roots, causing the release of several cytokines.¹¹^,¹²^,¹³^,¹⁴ This inflammatory cascade leads to priming of the nerve root and secondary hypersensitivity from mechanical compression, which in turn cases local ischemia and irritation, further propagating the cascade.⁵^,¹¹^,¹²^,¹³^,¹⁴^,¹⁵ The cytokines most prevalent in this inflammation cycle include tumor necrosis factor alpha, osteoprotegerin, interleukin-6, prostaglandin E₂, and phospholipase A2.

FIGURE 18-1 L4 to L5 lumbar disk herniation. A, Axial T2-weighted MRI illustrating a common posterolateral L4 to L5 herniation. The patient presented with a L5 radiculopathy caused by irritation of the traversing L5 nerve root. B, Axial T1-weighted MRI illustrating a far-lateral L4 to L5 herniation. The patient presented with L4 radiculopathy caused by irritation of the exiting L4 nerve root. (Reprinted from Hsu WK: Lumbar degenerative disease, in: Orthopaedic Knowledge Update, Update 10. Rosemont, IL: American Academy of Orthopaedic Surgeons, 2011.)

Clinical Presentation

Lumbar disk herniations classically result in dermatomal radicular pain with patients complaining of pain, paresthesias, and weakness of the lower extremities. The unique pattern of pain experienced by the patient depends on the level and location of the herniation. Up to 95% of LDHs occur at the L4 to L5 and L5 to S1 levels.¹⁶^,¹⁷ Axial back pain and sclerotomal pain are also commonly present. These symptoms of low back, buttock, and posterior thigh pain occur secondary to irritation of local mesodermal tissue (i.e., muscle and ligaments) and can also indicate dorsal rami involvement.

Evaluation of the athlete presenting with a combination of leg and back pain should include a broad differential diagnosis. Evaluation of common lower extremity sports injuries should be excluded, including primary hip pathology, knee pathology, muscle sprains, and ligament tears. Common back injuries that athletes present with include muscle strains, aggravation of degenerative disk disease, and spondylolysis.¹⁸ The predominance of leg pain over back pain, dermatomal distribution of pain, and pain that increases with Valsalva maneuver and forward flexion are more specific signs for LDH.¹⁹^,²⁰

Complete neurologic evaluation should be performed on all patients, including sensation, muscle strength, and reflex testing. Abnormal sensation in a dermatomal pattern, muscle weakness, and decreased reflexes are all associated with LDH (Table 18-1). A positive ipsilateral straight-leg raise (SLR) result is sensitive but not specific for LDH; a positive contralateral SLR test result is more specific but less sensitive.¹⁹^,²⁰ For herniations affecting the L1 to L4 nerve roots, the femoral-nerve stretch test may alternatively be used. A reproduction of anterior thigh radiculopathy is a positive test result.

Evaluation should also exclude the two surgical urgencies associated with LDH: cauda equina and conus medullaris syndrome. Both conditions cause saddle anesthesia, autonomic nervous system dysfunction (i.e., overflow incontinence, impotence), and leg pain. Concern for either diagnosis should lead to prompt advanced imaging. The urgency of these two conditions is largely justified by the poor outcomes seen with delays in surgical decompression.²¹

Case Presentation 1 (Figure 18-2)

Imaging

Plain radiographs of the lumbosacral spine can rule out associated pathology in athletes presenting with radicular pain.²² Nonspecific findings such as loss of disk height, loss of lumbar lordosis, and vacuum phenomena can identify preexisting conditions.⁵^,²² A noncontrast MRI scan allows for unparalleled evaluation of nerve roots and soft tissues.²³ The high rate of asymptomatic LDH illustrates the importance of correlating presenting symptoms and physical examination findings to the pathology observed on MRI.⁷^,²⁴ If MRI is contraindicated, then a CT myelogram may be performed to visualize neural element compression.⁵^,²³

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