Lumbar disk herniation is the most common surgical condition of the spine. High-level athletes participate in activities that place extreme loads on the intervertebral disks. These repetitive loads may lead to an elevated risk for degenerative disk disease, which in turn predisposes to disk herniations. Treatment algorithms for athletes with disk herniations are similar to those in the nonathletic population; however, success in the athletic population is often measured in the ability to return to play. Both nonoperative and operative treatment show a high success rate in return to play in athletes treated for disk herniations.
Lumbar disk herniation (LDH) is a common cause of morbidity in athletes with low back pain.
Underlying degenerative disk disease is prevalent in athletes and is a risk factor for the development of LDH.
Given the pressures regarding return to play, athletes are more likely to undergo surgical intervention earlier in their treatment course.
Return to play after LDH is favorable; however, career duration and return to preinjury performance level may be affected.
Lumbar disk herniation (LDH) is a common cause of morbidity and health care cost in the United States. It is estimated 2% of the population will suffer from a symptomatic LDH in their lifetime. Given the physical demands placed across the lumbar spine in various sports, athletes are known to have a higher lifetime incidence of low back pain (LBP) compared with the general public. Although the main causes of LBP in athletes are musculoligamentous strain, degenerative disk disease (DDD), and spondylolysis, it is has been reported that up to 11% of acute cases of LBP are a result of LDH. ,
To alleviate symptomatology and facilitate return to sport, a thorough understanding of the pathoanatomy, clinical presentation, diagnosis, and treatment of LDH is paramount.
The intervertebral disk is composed of a central nucleus pulposus (NP) and an outer fibrous ring known as the annulus fibrosus (AF). The central NP is composed of type II collagen and contains proteoglycans that bind water molecules. The high water content of the NP and resultant hydrostatic pressure functions to resist axial compression of the spine. In comparison, the AF is composed of primarily type I collagen and contains far fewer proteoglycans and thus fewer water molecules. The AF serves as a tensile ring that contains the NP and serves as an attachment to the corresponding vertebral body endplates. When the intervertebral disk is placed under axial load, the NP flattens and generates a tensile hoop stress. The AF functions to resist this generated force. Formation of an LDH occurs when this generated force disrupts a portion or the entire thickness of the AF and it no longer appropriately contains the NP.
Force generation across a healthy intervertebral disk is well established in the literature. When standing upright, an individual generates 440 Newtons (N) across a lumbar motion segment. This force increases to 1190 N when one remains upright and forward flexes at the waist. Sitting in a relaxed position generates 380 N, whereas bending forward increases the force to 1130 N. A previous cadaveric study demonstrated failure of the AF and formation of a disk protrusion when an average force of 5448 N was applied with a flexion angle of 12.8° across the lumbar intervertebral disk (IVD).
Although athletes are typically better conditioned than the general public, the demands of sport often place the lumbar spine under significant loads. Gatt and colleagues investigated the forces generated across the L4-5 disk in Division I-A college football linemen. They reported an average force generation of 8679 N during a typical blocking sequence. An analysis of professional and amateur golfers concluded that 7500 N and 6100 N of force are generated across the L3-4 motion segment, respectively. Cholewicki and colleagues studied world-class power lifters and noted an average compressive load of 17,192 N acting across the L4-5 motion segment during dead lifts. The work of Hosea and Hannafin with elite rowers documented an average cyclical load of 6100 N. The demands athletes place across their lumbar spines is likely a predisposing factor in the development of lumbar pathology.
The natural aging process leads to biochemical and biomechanical changes within the intervertebral disk. Loss of proteoglycans within the NP leads to decreased water content and disk desiccation. In addition, degradation of the extracellular matrix and changes in local pH further contribute to this process. Progressive loss of NP size, pressurization, and disk height alter the normal load-bearing characteristics of the IVD. The altered NP can no longer handle compressive forces as effectively, leading to increased force transmission across the AF and the propensity for disruption.
Various genetic factors have been studied and linked to DDD and early desiccation. It is believed that up to 75% of early DDD is a result of genetic predisposition. Genes regulating collagen formation, matrix metalloproteinases, structural proteins, and various growth factors, as well as apoptosis-regulating genes have all been implicated in this phenomenon.
Preexisting DDD has been linked to an increased incidence of LDH. A high prevalence of DDD has been reported in various sports. In 1991, Swärd and colleagues reported DDD in 75% of elite male gymnasts with an average age of 18, versus 31% in age-matched controls. A study conducted at the 2016 Olympic Summer Games in Rio de Janeiro found 39% of screened athletes had preexisting lumbar DDD. The investigators concluded that in comparison with previously reported age-matched controls, these athletes had higher rates of moderate to severe degenerative changes. Multiple studies have reported a high prevalence of DDD in football linemen. Rajeswaran and colleagues evaluated 98 asymptomatic junior elite tennis players and found that 62% had underlying DDD. A study of 75 elite alpine skiers, age range 16 to 20 years, found a prevalence of DDD in 56% of those studied versus 30% in age-matched controls. The high prevalence of DDD among athletes may place them at increased risk for development of LDH.
Signs, symptoms, physical examination, and diagnostic guidelines
Symptoms associated with LDH include axial LBP, radicular pain, and possible sensorimotor deficits. Symptoms vary depending on the size, location, and inflammatory response of the LDH. After the inciting event, it is not uncommon for the patient to experience a prodrome of LBP followed by dysesthesias, paresthesias, and/or numbness. Patients may exhibit motor dysfunction in a specific lumbosacral nerve root. Central LDHs typically present with axial back pain without radicular features, whereas paracentral LDHs are more likely to have radicular features, given their proximity to the traversing nerve root. Severe cases of LDH can present as cauda equina syndrome (CES). CES represents a constellation of motor and sensory disturbances of the lower extremities coupled with saddle anesthesia, and potential bladder, bowel, and/or sexual dysfunction.
Symptoms of LDH may be exacerbated by straining, coughing, and sneezing, as these actions lead to increased intrathecal pressure. Forward flexion at the waist and sitting load the anterior column and increase the intradiskal pressure by up to 40%. Clinical signs associated with LDH include the straight leg raise, contralateral straight leg raise, and the femoral stretch test. These examinations stretch an already irritated nerve root and may lead to increase in radicular complaints.
The sensory and motor findings vary based on the level and location of the disk herniation. Ninety-five percent of LDHs occur at L4/5 and L5/S1. Between 95% and 98% of LDHs are described as central or paracentral in nature. Paracentral is the most common location, as it is just lateral to the lateral boundaries of the posterior longitudinal ligament. Paracentral LDHs occur near the traversing nerve root ( Fig. 1 ). As a result, a paracentral LDH at L4/5 often manifests with L5 radicular symptoms. In comparison, a far-lateral LDH ( Fig. 2 ), which is much less common, will affect the exiting nerve root (L4 root at the L4/5 level). ,
The North American Spine Society’s Evidence-Based Guideline Development Committee recommends manual muscle testing, sensory testing, and classic and crossed straight leg raise as the gold standard for clinical diagnosis of LDH (grade of recommendation: A). Rabin and colleagues found that there is a statistical difference in favor of the supine straight leg raise over the seated straight leg raise with the sensitivity of 0.67 versus 0.41, respectively. They found insufficient evidence to make a recommendation for or against the use of the cough impulse test, Bell test, hyperextension test, femoral nerve stretch test, slump test, lumbar range of motion, or absence of reflexes in diagnosing LDH with radiculopathy (grade of recommendation: I).
Lumbar radiographs are the first-line imaging modality used in evaluating LBP with or without radiculopathy. In the absence of red flags, radiographs are indicated after completing 6 weeks of conservative care. Weight-bearing anteroposterior and lateral radiographs assess overall alignment, presence of transitional anatomy, DDD, spondylosis, spondylolisthesis, and fracture. It is the authors’ recommendation to include flexion and extension radiographs to evaluate for underlying instability. Potential radiographic findings of LDH include compensatory scoliosis and endplate avulsion fracture.
MRI is the gold standard for confirmation of a suspected LDH. MRI has the highest sensitivity and specificity among imaging modalities for the confirmation of LDH. When recurrent LDH is suspected, intravenous gadolinium contrast can be used to delineate LDH from epidural fibrosis.
Given the diagnostic accuracy of MRI, the role of computed tomography (CT) is limited to individuals who have a contraindication to MRI. Previous studies have compared CT alone versus CT myelogram in the diagnosis of LDH. Myelogram increases the sensitivity and specificity of CT. If MRI is contraindicated, a post myelogram CT is recommended.
Although the general treatment algorithm of athletes with LDH is similar to nonathletes, sport-specific factors are often considered. The timing of one’s injury with respect to the season, the demands of the sport, and contractual and monetary factors influence the decision-making process. Although the mainstay of treatment of symptomatic LDH is multimodal conservative care, elite athletes are more likely to undergo surgical intervention.
Nonsurgical care, including pain management and functional restoration, is the mainstay of initial treatment. As in the nonathletic population, nonsurgical care is associated with a high chance of success and return to play in the athletic population. Previous literature has documented that 90% of patients with a known symptomatic LDH have favorable outcomes with conservative care. Initial care consists of a short period of rest to last no more than 1 week followed by early mobilization and the initiation of formal physical therapy. Physical therapy focuses on core stability and strengthening, lower extremity flexibility, and maintaining truncal and lower extremity mobility. Given the high level of physical conditioning in athletes before their injury state, earlier and more rigorous therapy is often initiated. In addition, elite athletes have access to state-of-the-art training facilities and providers to guide and tailor their therapy protocols.
Oral pharmacologic therapy is also considered a first-line treatment for symptomatic LDH. Nonsteroidal anti-inflammatory drugs (NSAIDs) decrease inflammatory cytokine mediator production by inhibiting cyclooxygenase enzyme function. NSAIDs have shown a small treatment effect in symptomatic LDH. Corticosteroids also decrease inflammatory cytokine production by downregulating gene expression associated with cytokine production. A randomized clinical trial examining the use of corticosteroids in symptomatic LDH showed a modest improvement in function, but no reduction in pain at 3 weeks. Gabapentinoids (gabapentin, pregabalin), which bind voltage-dependent calcium channels, are frequently used in neuropathic pain. Although these medications are commonly used for lumbar radicular pain resulting from LDH, studies have shown them to be ineffective. Muscle relaxants, a diverse group of medications that can be classified into antispasmodics and antispastics, work by altering central nervous system conduction or directly improving muscle tonicity and spasm directly through the spinal cord or skeletal muscle, respectively. Limited data are available on the use of muscle relaxants and their efficacy in treating LDH.
Lumbar epidural steroid injections (ESIs), including interlaminar and transforaminal, are commonly used as second-line agents in the treatment of symptomatic LDH. The literature is contradictory regarding the efficacy of injection therapy. ESIs have been shown to be effective in reducing pain and radicular symptoms in 20% to 85% of those with a symptomatic acute LDH. , Their mechanism of action is to decrease the local inflammatory cascade and stabilization of the nerve cell membrane. Thus, the role of ESI is best suited in the inflammatory stage and for the reduction of acute pain and dysfunction. Multiple studies have shown that ESIs do not reduce the potential need for surgery.
Evaluating conservative care versus surgical intervention in athletes, Iwamoto and colleagues compared 1 prospective and 6 retrospective studies of symptomatic LDH. The investigators found no difference in return to play in athletes treated operatively versus nonoperatively. Of those treated conservatively, they reported a return to play of 78.9% at an average of 4.7 months.
In the absence of red flags (acute/progressive motor deficit, loss of bowel or bladder function), surgical candidates for LDH are those who have failed nonoperative management over a course of at least 6 weeks. In the elite athlete, relative indications for surgery include inability to perform their sport after a course of conservative care. The timeline of conservative care may be different in the athlete population given the multitude of variables associated with their return to play and their level of conditioning. Typically, surgery is considered earlier with elite athletes than the general population.
The standard operative treatment for LDH is a laminotomy with diskectomy. Multiple surgical techniques have been described, including traditional open laminotomy with diskectomy, minimally invasive tubular microdiskectomy ( Fig. 3 ), and endoscopic microdiskectomy. Multiple large studies have shown that operative management of LDH improves short-term outcomes; however, the difference is controversial at mid-range and long-range outcomes when compared with conservative care. ,