Disk Herniation and Degenerative Disk Disease in the Athlete

Level

Nerve root/dermatome

Motor weakness

Sensory distortion

Reflex loss

L1–L2, L2–L3

L2,L3

Hip flexors

Anterior thigh

None

L3–L4

Quadriceps

Medial calf

Patellar

Tibialis anterior

Medial foot

L4–L5

Extensor hallucis longus

Lateral calf

None

Peroneals

Dorsum of foot

L5-S1

Posterior calf

Gastrocnemius

Ankle

Plantar foot

S2–S4

S2, S3, S4

Bowel/bladder dysfunction

Perianal

Cremasteric

More specific signs for LDH include dermatomal distribution of symptoms, the predominance of leg pain over back pain, 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. Alternatively, the femoral nerve stretch test may be used for herniations affecting the L1–L4 nerve roots. 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, (i.e., overflow incontinence and impotence), and leg pain. Concern for either diagnosis should lead to 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 lordosis, loss of disk height, or vacuum phenomena. Non-contrast MRI is the imaging study of choice for LDH diagnosis. Asymptomatic LDH occurs at a high rate and 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.

Management

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]. The natural history of LDH is not altered by nonsurgical treatment options; however they 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 complication 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 has been described by Watkins and is discussed in the rehabilitation chapter in this book [7].

In patients with severe symptoms, epidural steroid injections provide an alternative to surgical treatment. Improvement in symptoms may enable surgery to be avoided in up to 50% of patients [8]. A study of 17 National Football League 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 (Fig. 15.1). 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 chapter, 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 75–100% of elite athletes successfully return to play 2.8–8.7 months after surgery. Athletes who successfully returned to play had a career longevity that ranged from 2.6 to 4.8 years [5]. Similarly, Hsu et al. 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. Certain subgroups, such as players who were younger and had more game experience, had better performance-based outcomes after treatment [2].

../images/468535_1_En_15_Chapter/468535_1_En_15_Fig1_HTML.jpg — Fig. 15.1

This is a 21-year-old division 1 defensive lineman presenting with 5 days of severe left buttock pain and numbness extending into the top of his foot. He had 4/5 strength and is left EHL and peroneals. Imaging in the left and top right panel are a T2 sagittal and axial MRI showing a large L4–L5 left paracentral disk herniation. The timing of the injury was 2 months prior to the start of his season. One epidural steroid injection was attempted with some relief of pain for a day, but his strength had not improved 1 week after the injection. Continued nonoperative treatment was offered, but the player wanted to have a chance to return for the upcoming season, and the motor deficit was concerning to the patient. A microdiscectomy was performed and the removed disk herniation is shown in the bottom right panel. The 2 weeks’ postoperative visit showed a healed wound, improvement in motor strength, and no pain. Functional rehabilitation was performed, and in this motivated patient he was back to practice at the 2 months’ postoperative timepoint. He was able to return to play later that same season

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 (81%) than that of the nonsurgical cohort (29%) [9]. Of note, 7 of 52 of the surgically treated linemen (13%) required revision decompression; however, 6 of the 7 patients (86%) successfully returned to play [9]. Conversely, professional baseball players with LDH treated surgically have considerably longer recovery times (8.7 months) than those players treated nonsurgically (3.6 months) [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].

Lumbar Degenerative Disk Disease

Lumbar degenerative disk disease (DDD) refers to the progressive degenerative changes seen in the IV disk. Lumbar DDD is characterized by the loss of disk hydration, disk space narrowing, and annular tears, ultimately culminating in ankylosis of the lumbar segment. Altered biomechanics underlie the observed pathologic changes. The loss of nucleus pulposus hydration causes the disk to become fibrotic, leading to abnormal loading of the facet joints. This process in turn facilitates the development of facet arthropathy and a further deterioration of normal biomechanics. The etiology of pain associated with lumbar spondylosis has been associated with nerve root irritation, claudication, or IV disk and/or facet pain.

A physical loading model was thought to be the predominant risk factor for lumbar DDD, but this theory has not been substantiated for the general population [13]. High-level evidence supports the notion that the most important risk factor for lumbar DDD is genetic predisposition [14], although aging, occupational hazards, and smoking also have been associated with its development [14]. In a cross-sectional study, Patel et al. [14] demonstrated that patients with a first-degree or third-degree relative with DDD have a markedly elevated risk for DDD. Similarly, in a cohort study of twins, Battié et al. [13] reported that, despite substantial differences in adult physical loading activities, no differences were observed in the incidence or severity of DDD. Smoking did predispose patients to DDD across all spinal levels, but the effect appeared to be minimal. The authors concluded that DDD is influenced largely by genetics, with minor contributions from environmental factors [13].

Despite limited evidence of physical loading as a risk factor for DDD in the general population, elite athletes are subjected to a higher level of physical activity. Intense training regimens begun at early ages may leave the adolescent spine at risk. In these patients, the spine experiences daily repetitive loads greater than those of most manual laborers [15]. Hangai et al. [15] compared 308 university athletes with 71 nonathlete university students and noted a considerably higher incidence of early lumbar degenerative changes in the athletes. These findings suggest that the physical demands of elite athletes may play an additive role in the development of DDD, especially in the adolescent spine.

Clinical Presentation

The history and physical examination of patients with isolated lumbar DDD is often nonspecific. The typical description is a deep, aching LBP. Discogenic pain is exacerbated by movements that load the disk and is relieved with rest and supine positioning. Age can once again provide a clue for diagnosis; in a study of 100 adolescent athletes and 100 adult athletes with LBP, only 11% of the adolescent athletes had disk pathology, compared with 48% of adult athletes [16].

Standard lumbar radiographs are the initial radiographic assessment for DDD and evaluate for disk space narrowing, subchondral cysts, facet degeneration, and osteophytes. Flexion and extension radiographs can be obtained to assess mobility, but they provide little information in cases of isolated lumbar DDD. MRI has a much higher sensitivity for detecting disk pathology and degenerative changes. MRI findings consistent with DDD include a loss of signal intensity on T2-weighted images, annular tears, and associated bone marrow/vertebral end plate changes. These findings do not necessarily correlate with the incidence of LBP, however, because one study showed that they can be seen in more than one third of asymptomatic patients [17]. A 7-year follow-up to this study showed that degenerative changes also did not predict the development of LBP, confirming that the correlation between imaging and symptoms is crucial in the management of DDD [18]. Conversely, in more severe cases, Modic changes that affect the bone marrow of the vertebral body have been described (Table 15.2, Fig. 15.2) [19]. These radiographic signs recently have been shown to correlate positively to the presence of symptomatic LBP [19].

Table 15.2

Modic classification of signal changes on MRI in the vertebral body

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