Management of Lumbar Conditions in the Elite Athlete

Wellington K. Hsu, MD; Tyler James Jenkins, MD


J Am Acad Orthop Surg. 2017;25(7):489-498. 

In This Article

Lumbar Disk Herniation

An LDH occurs when the nucleus pulposus ruptures through the outer annulus of the intervertebral (IV) disk. The rigorous demands of elite sports may predispose athletes to LDH.[2] After adolescence, IV disks receive a limited nutrient supply by diffusion through the vertebral vasculature. The inherent avascularity of the disk contributes to the accumulation of irreparable damage. The damaged disk ultimately can herniate with repetitive athletic maneuvers, such as torsion and axial loading. These repetitive maneuvers are required for elite athletic performance and underscore the risk for LDH in athletes.

After herniation, the nucleus pulposus can irritate an adjacent nerve root, producing the symptoms associated with LDH. Two intertwined pathways drive nerve root irritation: chemical inflammation and mechanical compression. The inflammatory cascade leads to a priming of the nerve root and secondary hypersensitivity from mechanical compression, which causes local ischemia and inflammation, further propagating the cascade. LDH should be considered in any athlete presenting for the evaluation of radiating leg and/or back pain.

Clinical Presentation

LDH results in dermatomal radicular pain associated with paresthesia and weakness of the lower extremities. The 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-L5 and L5-S1 levels.[4] Commonly, axial back pain and sclerotomal pain also are present. These symptoms of low back, buttock, and posterior thigh pain occur secondary to the irritation of local mesodermal tissue, such as muscle and ligaments. Age can provide a clue for diagnosis because athletes aged 20 to 35 years have the highest risk of symptomatic LDH.[5]

More specific signs for LDH include the predominance of leg pain over back pain, dermatomal distribution, reduced reflexes, and pain that increases with the Valsalva maneuver. A positive ipsilateral straight leg raise is sensitive but not specific for LDH, whereas a positive contralateral straight leg raise test is more specific but less sensitive. For herniations affecting the L1-L4 nerve roots, the femoral nerve stretch test alternatively may be used. A reproduction of anterior thigh radiculopathy is considered a positive test.

LDH evaluation also should exclude two surgical urgencies: cauda equina syndrome and conus medullaris syndrome. Both conditions cause saddle anesthesia; autonomic nervous system dysfunction, such as overflow incontinence and impotence; and leg pain. Concern for either diagnosis warrants prompt advanced imaging. The urgency of these two conditions is justified largely by the poor outcomes associated with delays in surgical decompression.

Plain lumbar radiographs can be used to rule out any associated pathology and may show nonspecific findings for LDH, including loss of disk height, loss of lordosis, or vacuum phenomena. Noncontrast MRI is the imaging study of choice for an LDH diagnosis. The high rate of asymptomatic LDH illustrates the importance of correlating presenting symptoms and physical examination findings to the pathology observed on MRI. If MRI is contraindicated, then a CT myelogram may be performed to visualize neural element compression.


Nonsurgical. In the general population, >90% of patients with LDH improve within 6 weeks of symptom onset after nonsurgical treatment.[2] Similarly, in a study of 342 professional basketball, American football, baseball, and hockey players diagnosed with LDH, 82% were able to return to their sport after treatment.[2] Nonsurgical treatment options do not alter the natural history of LDH symptoms but provide symptomatic relief while the radiculopathy resolves naturally.

Anti-inflammatory medications reduce the production of inflammatory cytokines. Oral corticosteroids long have been advocated to treat acute radiculopathy, but a recent randomized clinical trial showed that they provided no benefit over placebo.[6] Psychological support is used to establish an expectation for recovery and to reaffirm the rehabilitation process. Short-term management with narcotics is reserved for patients with severe pain that limits rehabilitation. The treating physician must weigh the potential for abuse and complications associated with these drugs.

Commonly, physical therapy also is prescribed during the nonsurgical management of LDH. Therapy regimens mainly focus on core and back muscle strengthening and flexibility. A phased rehabilitation protocol for athletes with LDH that correlates with the natural history of disk herniation resolution has been described[7] (Figure 1). Specifically, movements that increase intradiskal pressure, such as rotation and flexion, are incorporated into the routine gradually.[7]

Figure 1.

Chart showing the phased rehabilitation protocol for athletes with a lumbar disk herniation.

Epidural steroid injections provide an alternative to surgical treatment in patients with severe symptoms. Temporary symptom improvement may enable surgery to be avoided in up to 50% of patients.[8] A study of 17 National Football League (NFL) athletes with LDH treated with epidural steroid injections showed a return-to-play rate of 89% and an average loss of only 0.6 games played.[8]

Surgical. Surgical management of LDH typically is considered after failure of a 6-week course of nonsurgical management. The surgical treatment of choice for LDH is laminotomy with diskectomy. High-level evidence to support specific treatment options for LDH in elite athletes is currently lacking because numerous external variables make performance of a well-designed clinical trial challenging. In this review, we present the highest level of evidence currently available. In a systematic review of elite athletes undergoing lumbar diskectomy, Nair et al[5] reported that 75% to 100% of elite athletes successfully return to play 2.8 to 8.7 months after surgery. Athletes who successfully returned to play had a career longevity that ranged from 2.6 to 4.8 years. Similarly, the authors of a multidisciplinary study concluded that no differences in return to play, career games, and years played were observed after surgical or nonsurgical management for LDH in professional athletes.[2] Certain subgroups, such as players who were younger and had more game experience, had better performance-based outcomes after treatment.[2]

Inherent differences in specific sports and sport positions should be considered when treating elite athletes. For example, linemen in American football are considered to have a higher risk of LDH than that of players in other sports because of the flexion and axial loads experienced by the spine during position-specific movements. A cohort study of NFL linemen demonstrated that surgical treatment yielded a significantly higher rate of return-to-play than nonsurgical treatment (81% and 29%, respectively; P < 0.05).[9] Of note, 7 of 52 of the surgically treated linemen required revision decompression (13%); however, 6 of the 7 patients successfully returned to play (86%).[9] Conversely, professional baseball players with LDH treated surgically have considerably longer recovery times than those players treated nonsurgically (8.7 and 3.6 months, respectively).[10] Furthermore, career length in patients treated surgically was shorter than in those treated nonsurgically (233 games versus 342 games, respectively; P = 0.08).[10] One potential explanation for these differences is the daily rotational torque demands of throwing and hitting that are unique to baseball.[11] In National Hockey League athletes, 82% returned to play after treatment for LDH; no differences were seen between the surgical and nonsurgical cohorts with regard to games played or statistical performance.[12]

A pediatric athlete presenting with LDH is rare, and the literature on LDH in this subpopulation is limited. In children, LDH has a different natural history than that of LDH in adults with regard to the time to diagnosis and the potential success of nonsurgical treatment.[13] A delay in diagnosis is common in children because the incidence of LDH is far lower than in adults. Although the evidence is limited, one study has suggested that nonsurgical treatment may be less successful in relieving symptomatic LDH in the pediatric population.[13] Despite this assertion, a trial of nonsurgical treatment should be attempted. Laminotomy and sequestrectomy produce excellent outcomes in patients in whom nonsurgical treatment has failed, and 90% of pediatric patients experience minimal pain or no pain 1 year postoperatively.[13] However, a survivorship analysis performed as part of a long-term study of 72 pediatric patients treated with lumbar diskectomy predicted that only 80% of surgically treated pediatric patients will be able to avoid additional spinal surgery at 10 years postoperatively.[14]