Management of Lumbar Conditions in the Elite Athlete

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

Disclosures

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

In This Article

Lumbar Degenerative Disk Disease

Lumbar 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 IV disk and/or facet anatomic areas.

Historically, a physical loading model was thought to be the predominant risk factor for lumbar DDD, but this theory has not been substantiated in the literature.[15] High-level evidence supports the notion that the most important risk factor for lumbar DDD is genetic predisposition, although aging, occupational hazards, and smoking also have been associated with its development.[16] In a cross-sectional study, Patel et al[16] demonstrated that patients with a first or third-degree relative with DDD have a markedly elevated risk for DDD. Similarly, in a cohort study of twins, Battié et al[15] 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.[15]

Despite limited evidence of physical loading as a risk factor for DDD in the general population, differences in the level of physical activity in the elite athlete must be considered. 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.[17] Hangai et al[17] 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.[18]

The initial radiographic assessment for DDD consists of standard lumbar radiographs to 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.[19] 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.[20] Conversely, in more severe cases, Modic changes that affect the bone marrow of the vertebral body have been described[21] (Table 1 and Figure 2). These radiographic signs recently have been shown to correlate positively to the presence of symptomatic LBP.[21]

Figure 2.

Sagittal lumbar MRI showing degenerative disk disease at L4-L5 and type II Modic changes in a 37-year-old athlete. A, T1-weighted MRI showing increased signal in the L4-L5 vertebral bodies. B, T2-weighted MRI showing increased signal in the L4-L5 vertebral bodies.

Management

Nonsurgical. Nonsurgical management is the standard of care for lumbar DDD in the elite athlete. Physical therapy combined with anti-inflammatory medications are prescribed routinely. Many physical therapy protocols exist for long-term treatment of LBP in athletes, but the combination of core strengthening, lumbar mobilization, and biopsychosocial support yields good outcomes.[22] A staged rehabilitation protocol involving early protected mobilization, stabilization exercise, and a maintenance program is used to aid in the return to play. The duration of rehabilitation is patient and symptom-specific.

Evidence is lacking to support epidural spinal injections and facet joint injections as therapeutic interventions for lumbar DDD.[23] A Cochrane review of 18 trials involving 1,179 patients found insufficient evidence to support using injection therapy to manage subacute and chronic LBP.[23] Alternative methods of treatment, including acupuncture, chiropractic care, massage therapy, traction, and behavioral therapy, can be trialed, but little evidence exists to support the efficacy of such modalities.

Surgical. Surgical management of lumbar DDD should be used only in select patients in whom nonsurgical management has failed and in those who cannot return to sport. Strict surgical indications include mechanical LBP with evidence of a single-level degenerative disk on imaging studies, failure of at least 6 months of nonsurgical treatment, and localized midline spinal tenderness that corresponds to the radiographic level of disease. Narcotic abuse, smoking, and unrealistic patient expectations are relative contraindications to surgical treatment. Even when using selective indications, the clinical success of surgical management of DDD is unpredictable. Provocative diskography, which previously has been used widely to enhance surgical decision making for DDD, can lead to considerably faster progression of degenerative findings than that seen in control subjects.[24] Therefore, the American Pain Society recently published guidelines recommending against using provocative diskography.[25]

Surgical management of DDD involves removal of the diseased disk and subsequent fusion or arthroplasty. Lumbar fusion is the standard treatment, but concerns over adjacent segment disease led to an increased interest in total disk arthroplasty (TDA). Symptomatic adjacent segment disease, possibly caused by increased stresses next to the fused segment, is estimated to occur in as many as 36% of patients at 10 years postfusion.[26] Consequently, TDA treatments have been studied and compared directly with fusion.[27] However, no reduction in the incidence of adjacent segment disease in short-term and midterm follow-up after TDA versus fusion for the management of lumbar DDD was found. Lumbar fusion outcomes can be affected by workers' compensation claims, chronic narcotic abuse, smoking, and the number of levels fused, which are negative predictors for the successful surgical management of lumbar DDD.[28]

Few studies have investigated the outcomes following the surgical treatment of athletes with DDD. Siepe et al[29] reported that, of 39 athletes who underwent TDA to treat LBP, 37 (95%) resumed their sporting activity, and 33 (85%) were completely satisfied with the surgery, based on patient surveys. After surgery, 69% of patients returned to play within the first 3 months, and the average time to peak fitness was 5.2 months, based on patient surveys. Minor subsidence was observed in 13 patients (33%) within the first 3 months, with no further implant migration observed in 12 of these patients. Of note, only two patients were involved in contact sports (karate, wrestling) and neither was able to return to play. Tumialán et al[30] compared the outcomes of lumbar fusion with those of TDA for LDH or DDD in military personnel. Ten of 12 patients treated with TDA (83%) returned to unrestricted full duty compared with 8 of 12 patients treated with lumbar fusion (67%), leading to the conclusion that TDA is comparable to fusion for treatment of active patients. In a study of eight professional hockey players who underwent single-level fusion, all the players returned to play and remained active after 4 years.[12] The study also showed no substantial differences in the number of games played or performance scores before or after the procedure, but definitive conclusions were limited by the small sample size. Similarly, Schroeder et al[31] reported productive careers in two NFL players after undergoing lumbar fusion; one player had a two-level fusion and had a 7-year NFL career postoperatively. Further studies are needed to identify the appropriate indications for and long-term outcomes of surgically treated DDD in elite athletes, but the current literature does show that lumbar fusion does not necessarily contraindicate a return to play.

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