Lumbar Degenerative Disk Disease and Spinal Stenosis in Athletes

Heath P. Gould, BS

Colin M. Haines, MD

William J. Kemp, MD

Timothy T. Roberts, MD

Thomas Mroz, MD

Dr. Mroz 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 AO Spine; serves as a paid consultant to Ceramtec and Stryker; has stock or stock options held in Pearl Diver; and serves as a board member, owner, officer, or committee member of the AO Spine North America Education, NASS, and SpineLine. Dr. Roberts or an immediate family member has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research–related funding (such as paid travel) from McGraw-Hill Education. None of the following authors or 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: Mr. Gould, Dr. Haines, and Dr. Kemp.

Epidemiology

Participation in sports is an independent risk factor for the development of lumbar disk degeneration at an early age.¹ Multiple studies have demonstrated that degenerative changes of the spine are more common in athletes than in nonathletes.²^,³^,⁴^,⁵^,⁶ Furthermore, disk degeneration in athletes tends to be more severe than in nonathletes, with 58% of all degenerative disks in athletes being categorized as severely degenerated.⁷ Much of the increased risk for lumbar disk degeneration in athletes can be attributed to the repetitive stress placed on their lumbar spines over extended periods. Athletes are routinely subject to supraphysiologic loads in positions not routinely experienced by the general population. Thus, these individuals are uniquely susceptible to lumbar disk degeneration, with L4 to L5 and L5 to S1 being the most commonly affected levels.⁸^,⁹ Still, the epidemiologic data comparing athletes with nonathletes must be cautiously interpreted. Whereas the general population may overreport pain and injury for various reasons, athletes have been shown to underreport symptoms.¹⁰^,¹¹ Prevalence statistics in athletes may also be skewed by the “healthy worker effect,” which is the phenomenon in which epidemiologic investigations typically study only the active athletes while neglecting to capture individuals who have ended participation because of injury.¹²

Both injury type and severity vary based on age in athletes.¹³ Whereas the majority of lumbar injuries in adult athletes are related to muscle strain and diskogenic disease, 70% of lumbar injuries in adolescent athletes occur in the posterior elements. Micheli and Wood examined several possible causes of low back pain in 100 young athletes and 100 nonathlete adults.¹³ Only 11 adolescent participants had low back pain attributable to degenerative disk disease compared with 48 adult participants. In the same study, no adolescents had low back pain attributable to spinal stenosis compared with 6 adults. Orchard et al later corroborated this finding when they reported a correlation between lumbosacral impingement of the L5 and S1 nerves and increasing athlete age.¹⁴

Sports involving repetitive hyperextension, axial loading or jumping, twisting, or direct contact are associated with a higher incidence of lumbar disk degeneration.¹⁵^,¹⁶ Gymnastics, in particular, has been strongly associated with degenerative changes of the lumbar spine. A landmark MRI study by Swärd et al showed a 75% prevalence of disk degeneration in male gymnasts compared with 31% in control participants.¹⁷ Goldstein et al conducted a subsequent MRI study that further
stratified gymnasts into pre-elite, elite, and Olympic-level groups.¹⁸ The study reported prevalence rates of lumbar spine abnormality as 9%, 43%, and 63%, respectively, suggesting that an increased level of competition may be associated with an increased risk of lumbar spine abnormality.

In addition to gymnastics, elite weight lifting has also been strongly associated with lumbar disk degeneration. MRI evidence of disk degeneration presents early in weight lifters, typically in the first decade in men and the second decade in women. By age 40 years, degenerative changes are present in 80% of male weight lifters and 65% of female weight lifters.¹⁹ Weight lifters also claim the highest prevalence of degenerative disk changes from L1 to L3; soccer players have the highest prevalence of disk pathology from L4 to S1.²⁰

FIGURE 19-1 T2-weighted MRI showing mild degeneration of the L5 to S1 disk. A dark disk is also present at T12 to L1.

FIGURE 19-2 T2-weighted MRI showing moderate degeneration of the L5 to S1 disk.

Several groups have examined the effect of American football on the lumbar spine. Semon and Spengler reported axial back pain in 27% of American football players, including 50% of interior lineman.²¹ In a biomechanical investigation, Gatt et al concluded that average loads to the lumbar spine during American football blocking maneuvers exceed the minimum threshold necessary to cause pathologic changes in the intervertebral disk.²² With these studies in mind, Gerbino and d’Hemecourt conducted a review of the literature and definitively concluded that playing American football increases an athlete’s risk of developing degenerative changes in the lumbar spine.²³

In addition, other sports associated with increased prevalence of lumbar disk degeneration include waterski jumping, golf, tennis, and diving.²^,²⁴^,²⁵^,²⁶ In contrast, dancing and distance running have been associated with a lower prevalence of lumbar disk degeneration compared with control participants.¹²^,²⁷

Disk Pathology

Mechanism of Disk Degeneration

The process of intervertebral disk degeneration occurs gradually and varies widely in severity (Figures 19-1 to 19-3). Initially, the inner layers of the disk begin to weaken and separate. This can produce a concentric annular tear that places increased stress on the outer layers. Under this increased stress, the outer layers may separate and create a radial tear of the intervertebral disk. When the outer layers tear, the nerve endings in these layers may convert nociceptive input into discogenic back pain. The inner layers then separate with portions of the nucleus pulposus. Subsequent axial loads displace the nucleus to the weakest area of the annulus with the least resistance.²⁵ If this sequence is completed, the disk will herniate at this weakest location. This can initiate an inflammatory response that
can irritate the dura, posterior longitudinal ligament, and nerve roots.²⁸ In most cases, the annular tear will heal with time. Despite healing, the disk will not regain the same biomechanical functionality. Discogenic pain may persist secondary to the formation of intradiscal granulation tissue.

FIGURE 19-3 T2-weighted MRI showing severe degeneration of the L5 to S1 disk.

It is also pertinent to understand the biomechanics behind disk degeneration. Three predominant forces act on the spine: compression, shear, and torque. The combination of compression and shear forces produces tensile stress on the annulus fibrosus and shear stress on the neural arch. During athletic activity, the vertical compressive force on the L3 to L4 disk can reach 7500 N in golf²⁹ and 6100 N in rowing.³⁰ On the L4 to L5 disk, the vertical compressive force can reach 8600 N during football blocking²² and 17000 N while lifting weights.³¹ Because the body’s center of gravity lies anterior to the vertebral column, the spine is also subjected to torque.²⁵ The torque (τ) can be calculated by the equation τ = rFsinθ, where F is the body weight, r is the distance from the body’s center of gravity to the spine, and θ is the angle of axial force with respect to the spine (typically 90°). The erector spinae muscles and the lumbodorsal fascia normally resist this torque. With abnormal stresses added to the equation, annular tears of the intervertebral disk are more likely to occur.

Disk Degeneration in Aging Athletes

As the intervertebral disk ages, it undergoes a series of compositional changes. With increasing age, the nucleus pulposus loses water; the water content begins at 90% in infancy and diminishes to 70% by age 70 years.³² This parallels the age-related loss of proteoglycans and an increase in density of type 2 collagen fibers, leading to decreased tensile strength and a corresponding inability to distribute loads uniformly. After age 12 years, the disk becomes avascular, and nutrition occurs via diffusion from the end plates.³³ As the cartilaginous end plates calcify with aging, diffusion to the nucleus center becomes increasingly difficult. Additionally, the oxygen content of the disk is lower in older individuals. This leads to increased lactate formation and a corresponding decrease in intradiscal pH.³⁴

Changes in disk composition such as loss of hydration, decreased proteoglycans, and increased type 2 collagen are characteristic of normal aging.³⁵^,³⁶^,³⁷ Normal aging is distinct from the degenerative process (Table 19-1), which may be described as a spectrum that ranges from degenerative disk disease to facet joint arthritis and spinal stenosis. This degenerative process is the most common source of low back pain and leg pain in the aging population and is often accelerated in athletes.³⁸

The intervertebral disk is part of a three-joint complex that comprises the motion segment of the spine. Damage to the intervertebral disk, in the form of annular tears that occur in degenerative disk disease, leads to alterations in the mechanics of the motion segment. This results in increased force distribution to the facets, rendering the joints vulnerable to the onset of osteoarthritis.³⁴ In an MRI study examining 41 vertebral levels with facet degeneration, Butler et al found evidence of disk degeneration in all but one, suggesting that degenerative disk disease precedes facet joint osteoarthritis in older athletes.³⁹

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