Symptoms
Rule out
Fever, malaise, unintentional weight loss
Infection
Fever, malaise, unintentional weight loss, night pain, history of cancer
Cancer
Neurologic deficits, bowel or bladder dysfunction
Cauda equina
Abnormal behavior, mood swings
Drug or steroid abuse
Obtaining a thorough and accurate history is essential in order to narrow the differential diagnosis and guide toward a correct diagnosis. The location of pain is an important distinguishing feature. LBP without radiating leg pain is often nonspecific and includes etiologies such as mechanical back pain, facet joint pain, muscle strain, and muscle spasm. LBP that localizes to a single midline point suggests an etiology involving a single motion segment, whereas diffuse LBP without leg pain more likely involves multiple motion segments and often suggests muscular pain. In contrast, LBP with radiating leg pain is indicative of nerve compression or irritation. The onset of pain is also indicative of the etiology of LBP. Sudden onset of LBP suggests an acute etiology, such as fracture or disc herniation. In contrast, an insidious onset is more suggestive of disc degeneration, spondylolysis, or stress fracture. Aggravating and alleviating factors also provide clues toward the correct diagnosis. Disc-related LBP is often aggravated by forward bending, whereas LBP arising from the posterior elements (e.g., facet joints, pars interarticularis) is worsened with lumbar extension and alleviated by forward flexion.
A positive family history can be suggestive of inflammatory rheumatologic disorders, such as ankylosing spondylitis and reactive spondyloarthropathies. Constitutional symptoms that are noted on review of systems may be indicative of systemic processes, such as connective tissue disorders (e.g., systemic lupus erythematosus) and endocrine disorders (e.g., hyperparathyroidism). The presence of red flag symptoms necessitates immediate further workup in order to evaluate for potentially serious problems such as cauda equina syndrome, infection (e.g., epidural abscess, vertebral osteomyelitis, discitis), and malignancy (e.g., multiple myeloma, lymphoma, metastases).
Physical Examination
The physical examination of an athlete with LBP begins with the inspection of static posture to assess for the presence of scoliosis, thoracic hyperkyphosis, or loss of lumbar lordosis. Posterior asymmetry in the shoulders, trunk, or pelvis should be noted with the athlete facing away from the clinician. Lateral inspection should then be performed to assess spinal curvature, including normal cervical lordosis, thoracic kyphosis, and lumbar lordosis. Next, palpation of the entire spine should be performed. The spinous processes and paraspinal muscles should be systematically palpated for tenderness. Point tenderness over a single spinous process suggests an etiology involving a single motion segment, whereas multilevel tenderness over the paraspinal muscles suggests muscle strain or spasm.
Range of motion in the lumbar spine should be evaluated. Flexion, extension, and rotation through the lumbar spine should be observed while ensuring that the pelvis remains in a fixed position in order to isolate lumbar spine motion. While assessing lumbar spine range of motion, it is important to distinguish between limited range of motion that is painless from limited range of motion that is painful. Painless limitation in range of motion suggests loss of spinal flexibility, whereas painful limitation in motion suggests that an underlying pain generator is being loaded. Painful forward bending is indicative of disc-related pain. Painful lumbar extension is more suggestive of pain arising from the posterior elements.
The flexion, adduction, internal rotation (FADIR) test to evaluate low back pain originating from hip pathology. (Reproduced with permission from Sierra et al. [18])
The Hoffmann reflex in which flipping the distal phalanx of the patient’s middle finger downward results in spontaneous flexion of the ipsilateral thumb and/or index finger. (Reproduced with permission from Emery [49])
The inverted radial reflex in which tapping the distal brachioradialis tendon results in abnormal finger flexion. (Reproduced with permission from Emery [49])
Laboratory Testing
Routine laboratory testing is typically not necessary in the initial evaluation of LBP in athletes. However, if the history and physical examination are concerning for infection or tumor, then laboratory testing should be performed, including a complete blood cell count, C-reactive protein, and erythrocyte sedimentation rate [19]. Further laboratory testing should be determined as clinically warranted on a case-by-case basis.
Imaging
In an athlete with LBP lasting more than a few weeks in the absence of red flag symptoms, plain radiographs of the lumbar spine should be performed. Although plain radiographs are often low yield with no remarkable findings, they can show spinal alignment abnormalities, such as thoracic hyperkyphosis, loss of lumbar lordosis, and spondylolisthesis. In addition, radiographs can also show evidence of acute or chronic fractures. Flexion and extension views are recommended and can demonstrate dynamic instability or spondylolysis that is not readily apparent on neutral standing radiographs. Oblique views may be helpful in visualizing the pars interarticularis and assessing for spondylolysis. However, recent studies have found no improvement in the sensitivity and specificity of diagnosing spondylolysis with oblique views [20]. Therefore, the additional cost and radiation exposure associated with oblique views may outweigh the lack of associated diagnostic benefit.
If LBP persists beyond 6 weeks without improvement after initial conservative treatment, advanced imaging should be obtained. The initial advanced imaging of choice is magnetic resonance imaging (MRI). MRI is useful in evaluating the intervertebral discs, neural elements, as well as soft tissues. MRI can also provide information regarding stress reactions, occult fractures, or spondylolysis. A CT scan can also be helpful in defining bony anatomy when plain radiographs do not provide sufficient detail. However, given the significant amount of radiation exposure associated with CT, it should be reserved for only those cases in which MRI is contraindicated or inconclusive in establishing a diagnosis.
In cases of spondylolysis, which will be discussed in more depth later in this chapter, CT has been considered the gold standard for detecting the bony defect. However, emerging evidence suggests that MRI is comparable to CT in terms of accuracy in detecting early stress reactions of the pars interarticularis without a fracture [21]. Single-photon emission computed tomography (SPECT) has been shown to be superior to plain radiographs and bone scan in detecting spondylolysis [21]. However, similar to CT , SPECT is limited by high radiation dose [21]. Furthermore, SPECT has been associated with high rates of false-positive and false-negative results [21].
Compared to spondylolysis, the detection of a stress reaction prior to fracture is more difficult. Stress reactions are not detectable on plain radiographs or standard CT. MRI or bone scan can be helpful in detecting stress reactions, but SPECT is the most sensitive test for diagnosing stress reactions [22, 23]. Early detection of a stress reaction is important in order to implement early treatment and prevent progression to a frank stress fracture.
An important consideration in the discussion of advanced imaging for LBP in athletes is that degenerative changes in the lumbar spine may be present in asymptomatic athletes. That is, the presence of both LBP and degenerative changes in the lumbar spine does not imply causality. For example, in a study of former national level athletes, the intensity of LBP symptoms was not significantly correlated with degenerative findings on MRI [24]. Multiple other studies have demonstrated a higher rate of degenerative changes on MRI in athletes compared to non-athletes, but no correlation between these MRI changes and the prevalence of LBP [25–27]. Therefore, care must be taken in establishing a causal relationship between clinical symptoms and imaging findings when evaluating athletes with LBP.
Differential Diagnosis
This section will focus on the most common etiologies of LBP with and without leg pain in athletes. Back pain is the most common reason for competitive athletes to lose playing time [28], and as such, a detailed knowledge of the causes of LBP is crucial for clinicians who take care of athletes. While the focus will remain on spinal conditions, it is important that the clinician also considers involvement of other systems and keeps their differential diagnosis broad initially. Among orthopedic etiologies of LBP, pain resulting from hip pathology may be referred to the back. The clinician must perform a thorough history and physical examination in order to rule out intra-articular hip issues (e.g., labral tears, femoroacetabular impingement) and extra-articular issues (e.g., trochanteric bursitis, muscle tears). Among non-orthopedic etiologies, the clinician should consider intra- and retropelvic conditions, such as those of the genitourinary system including renal and ovarian pathologies that may cause LBP with or without radiating leg pain. A full discussion of these conditions is out of the scope of this text; it is important for the clinician to keep a broad differential initially and consider further non-spine-related workup when indicated.
Muscle and Ligamentous Injury
Thoracolumbar musculo-ligamentous injuries are a common cause of LBP in athletes [28]. These occur most commonly in athletes participating in high speed and/or full contact sports when the trunk is exposed to significant rotational and flexion/extension forces. Athletes will typically not experience immediate symptoms. The onset of pain is often delayed 12–24 h, which has been attributed to the timing of the inflammatory cascade [17]. Patients typically complain of LBP that can be either diffuse or localized without radiation. On physical examination, there may be paravertebral spasm, diminished thoracolumbar range of motion, and pain with resisted rotation or flexion/extension. Since these injuries do not involve the spine itself, there should be no neurological deficits or associated radicular symptoms.
In general, musculo-ligamentous injury is a clinical diagnosis, and advanced imaging is not necessary. Radiographic findings are typically normal immediately after injury. If initial radiographs are normal and pain persists, flexion and extension views should be obtained after 2–3 weeks to rule out dynamic ligamentous instability that may not have been noticeable on static radiographs [17]. If there remains further concern, CT and/or MRI can be obtained to rule out occult fracture and ligamentous injury, respectively.
Treatment of musculo-ligamentous injury should focus on managing pain and inflammation. Modalities such as ice for inflammation reduction and heat for muscle relaxation may be effective initially. Nonsteroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants may be used as adjuncts as necessary for symptomatic management. Rehabilitation should begin when pain is tolerable and focus on range of motion and strengthening, with the goal of returning to pre-injury level of function. Bracing has been noted to possibly be helpful in the acute setting but should not be used as a long-term treatment. If pain persists beyond 3 weeks despite conservative treatment, advanced imaging as discussed above should be pursued [29].
Degenerative Disc Disease
Lumbar degenerative disc disease (DDD) refers to the process of disc space narrowing secondary to loss of disc hydration leading to facet arthropathy from abnormal loading of the facet joints. This has been described in a three-phase process [30]. In the initial phase, pain is produced from synovitis of the facet joints or annular tears of the intervertebral disc. This is followed by a second phase of segmental instability due to diminished functionality of the facet capsule and annulus. In the final phase, the facet and discovertebral joint restabilize [31].
Although historically, it was thought that increased loading such as that encountered by athletes was a predisposing factor for degenerative disc disease, several studies have also demonstrated a strong genetic component [32, 33]. However, there remains evidence that elite athletes have not only a higher incidence of early lumbar degenerative changes but also more severe changes when compared to the general population [34, 35].
The presentation of lumbar degenerative disc disease is nonspecific. In general, discogenic pain will occur with activities that load the intervertebral disc. Most typically, an athlete will complain of LBP that is worse with movements that stress the low back. On physical examination, increased pain with flexion and relief with extension of the lumbar spine is often seen.
Modic classification of signal changes on MRI in the vertebral body
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