Frank Fumich MD
Adam C. Crowl MD
James D. Kang MD
Cervical Spine Injuries in Athletes
Anatomy
The anatomy of the cervical spine must be understood to appreciate its susceptibility to injury in athletics. Mobility of the head is afforded at the cost of stability. The cervical spine is made up of seven vertebrae relying on bone and ligamentous and muscular attachments to confer stability to axial loads, rotational movements, and bending movements.
The architecture of the cervical spine protects the spinal cord circumferentially by the vertebral body and the paired lamina that make up the protective roof of the spinal canal. Each vertebral body articulates with the adjacent vertebra with an interposed intervertebral disk. The uncovertebral joints of Luschka form the anteromedial boundary of the neuroforamen, which is bordered posteriorly by the facet joint. Through this neuroforamen the nerve root exits (Figure 7-1). Anterior to the spine and covering the vertebral bodies and intervertebral disks the anterior longitudinal ligament (ALL) spans the length of the entire vertebral column. The posterior longitudinal ligament spans the posterior aspect of the vertebral bodies in a similar fashion. These osseous and ligamentous structures make up the anterior spinal column, provide axial support to load imparted to the head, provide protection to the neural structures, and allow mobility in rotation and bending movements. The posterior cervical spine is made up of the lamina, facet articulations, lateral masses, and spinous processes that give the posterior spinal column the ability to share axial loads and provide sites of attachment for muscles that control head and neck movement. Each vertebra has a paired set of facets that articulates superiorly and inferiorly with the adjacent vertebra.
Approximately one-half of the flexion and extension arc occurs through the atlantooccipital articulation and approximately one-half of neck rotation occurs between the atlas and axis. Each segment below the axis allows coupled rotation and lateral bending due to the unique shape of the uncovertebral articulation and facet joints, which further increases the functional range of cervical motion.
Static and dynamic restraints are of great importance due to the lack of intrinsic stability in the neck. The osseous anatomy of the cervical spine is connected by several ligaments that provide restraint to the extremes of neck motion. The primary static stabilizers of the cervical spine include the anterior longitudinal ligament, intervertebral disk, posterior longitudinal ligament, ligamentum flavum, facet capsules, and interspinous and supraspinous ligaments. These ligamentous structures function only as a checkrein at the end point of neck movements. The dynamic stabilization, which is the muscular support of the neck, includes the sternocleidomastoid, trapezius, and strap muscles and paraspinal musculature. The protective function of the neck musculature functions throughout the range of motion. Both the static and dynamic stabilizers of the neck are vulnerable to injury during sporting events that involve high-energy impact of the head or neck.
Differential Diagnosis
Most injuries to the cervical spine are minor. The most commonly diagnosed injuries are soft-tissue trauma including ligament sprains, muscle strains, and contusions of soft tissue. The magnitude and direction of force applied to the neck determine the type and severity of injury. Cervical strains are injuries to the musculotendinous portions of the neck and cervical sprains are injuries to the ligaments of the neck. Cervical strains are the most common neck injury of athletes. Differentiating these two injuries may be very difficult in the clinical setting. The most common mechanism of injury involves high-velocity contact sports. Two other common mechanisms include sudden deceleration of the body involving a whiplash of the head and overuse syndromes. Sporting accidents are second only to motor vehicle accidents as the leading cause of emergency department visits involving neck injuries.
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Figure 7-1. Anterior view of cervical spine skeletal structure displaying uncovertebral joints and facet articulations. |
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Cervical Strain
Essentials of Diagnosis
Prevention
The prevention of neck injury such as a strain or sprain is best done through muscular conditioning and development. This includes isometric exercises to strengthen the paraspinal musculature. Other measures include proper education of the athlete concerning techniques of play and avoidance of spearing and facemask holding, for example.
Clinical Findings
Muscle strains in the neck occur as a result of a blow to the head or neck during muscle contraction producing eccentric muscle loading. The complaint of pain following the described mechanism suggests injury to the musculotendinous junction of the involved muscle. These complaints may be preceded by amnesia to the event depending on the severity of impact or deceleration.
Painful limited cervical range of motion and tenderness over the involved neck muscles are the cardinal signs of cervical strain injury.
Radiographic imaging of the cervical spine is necessary to rule out fractures and dislocations that make the cervical spine unstable. At a minimum, two orthogonal views with visualization from the occiput to the C7 to T1 junction are necessary. Instability may be suspected with findings of interspinous widening, vertebral subluxation, compression fracture, or loss of cervical lordosis. Other studies looking at the stability afforded by the ligaments of the spine have identified horizontal displacement of 3.5 mm or angular displacement of 11° or more as signs of instability (Figures 7-2 and 7-3).
In the acute setting lateral flexion and extension views may be of less benefit in patients experiencing
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significant pain. Subacute instability describes patients who present with normal radiographs initially but demonstrate instability later. Paraspinal muscle spasm can mask instability acutely because it prevents adequate excursion on flexion and extension radiographs. Therefore the flexion and extension radiographs should be repeated when the muscle spasm has improved after a period of cervical immobilization with a collar.
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Figure 7-2. The method of measuring translatory displacement. A distance of 3.5 mm or greater is considered to be clinically unstable. (Reproduced, with permission, from White AA et al: Biomechanical analysis of clinical stability in the cervical space, Clin Orthop Relat Res 1975;120(109):85. ) |
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Figure 7-3. A difference of 11° or greater than that of either adjacent interspace is considered clinically unstable. (From White AA 3rd et al: Spinal stability: evaluation and treatment. Instr Course Lect 1981;30:457. ) |
The use of MRI has been reserved for situations involving cervical instability and neurologic compromise. For cervical spine trauma the rate of detection of cervical ligamentous injury and spinal cord injury with MRI is 100%.
A thorough examination to find areas of cervical spine tenderness and the assessment of the fullest amount of pain-free range of motion of the neck are the foundation of an examination for a cervical muscular strain injury. As in all spinal injuries, assessment of mental status and neurologic examination of the extremities are of paramount importance in making decisions concerning the athlete's care and possible return to play. Otherwise, no other special examinations or tests are necessary to diagnose a muscle strain injury.
Treatment
Treatment is generally conservative requiring initial immobilization with a cervical collar. The collar is worn until muscle spasm is relieved. This usually takes 7–10 days, at which time follow-up flexion and extension radiographs may be obtained to rule out instability. During the period of immobilization antiinflammatory medications may be of benefit. With the resolution of spasm and determination from follow-up radiographs that serious injury has been ruled out a physical therapy program is instituted. The collar is weaned as gentle range of motion exercises and isometric strengthening are done. Prolonged immobilization results in muscular atrophy and deconditioning of healthy muscle fibers. Physical therapy prevents muscular deconditioning and postinjury stiffness. Advancement of activities is allowed with clinical improvement.
Surgery is necessary only after severe injury that has resulted in instability. Ligamentous disruption may have been initially masked through muscular spasm. Surgical options in most cases involve arthrodesis of the destabilized segment, but this is quite rare.
Return to Play
Late complications of cervical strains include continued pain or discomfort. The prognosis is good and most athletes, upon resolution of symptoms and regaining of full and pain-free neck range of motion, return to play within weeks of the injury. For return to play in football the use of cervical orthoses has been shown to limit hyperextension of the cervical spine yet allow enough extension to prevent axial loading injuries.
Holmes JF et al: Variability in CT and magnetic resonance imaging in patients with cervical spine injuries. J Trauma 2002;53:524.
Jarvinen TA et al: Muscle strain injuries. Curr Opin Rheumatol 2000;12:155.
Kelley LA: In neck to neck competition are women more fragile? Clin Orthop 2000;(372):123.
Versteegen GJ et al: Neck sprain not arising from car accidents: a retrospective study covering 25 years. Eur Spine J 1998;7:201.
Common Fractures
Cervical fractures are much less common than fractures of the thoracolumbar spine. Anatomic differences in the shape of the vertebra and the increased range of motion of the neck account for this difference. The three most common minor fractures of the cervical spine due to athletic participation are compression fractures, spinous-process fractures, and isolated lamina fractures. Hyperflexion is believed to be the cause of cervical spine
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compression fractures. The amount of posterior ligamentous injury is directly proportional to the amount of force imparted to the neck at the time of fracture. Posterior ligamentous disruption present in combination with a fracture significantly increases the amount of instability of the neck and requires a careful work-up to determine its presence.
Spinous process fractures may occur in isolation, but as with compression fractures a thorough work-up must be completed to rule out ligamentous injury. The upper and lower cervical spinal segments are the most commonly involved levels of spinous process fracture. The most common mechanism of injury for spinous process fracture is contraction of the trapezius and rhomboid muscles causing an avulsion of the spinous process. Extreme hyperflexion and hyperextension as seen in the high-energy trauma of a collision may also produce a spinous process fracture by avulsion of the spinous process when pulled by the supraspinous and interspinous ligaments. Much less commonly a direct blow may cause a spinous process fracture.
An isolated lamina fracture is rare and is usually associated with a more complex mechanism of injury such as a burst fracture or a fracture dislocation of the cervical spine. Axial loads with or without rotation produce vertical lamina fractures and are usually associated with fracture of the vertebral body. Transverse fractures of the lamina are due to avulsion as the ligamentum flavum pulls during extreme hyperflexion. These transverse lamina fractures may be associated with instability.
Essentials of Diagnosis
Clinical Findings
The primary complaint associated with fracture of the cervical spine is pain. The onset of pain from fracture in the cervical spine correlates with time of injury and the magnitude of load imparted to the neck.
Resistance to movement of the neck is seen. Neurologic injury may be present depending on the nature of the fracture, the presence of a facet fracture and/or associated dislocation, and the presence of disk or bone fragments impinging on the spinal cord or nerve roots.
As with any trauma to the cervical spine a complete radiographic evaluation of the athlete injured during play is mandatory. Imaging of the cervical spine begins with anteroposterior and lateral views of the cervical spine, which allow visualization of the atlantooccipital articulation and the C7–T1 junction. If the cervicothoracic junction cannot be visualized with plain radiographs a computed tomography (CT) scan of this area may be done. Common cervical fractures associated with sporting accidents include compression, spinous process, and isolated lamina fractures.
There are no special tests other than a standard history and physical examination assessing the mechanism of injury, energy imparted to the head or neck at the time of injury, and a thorough skeletal and neurologic examination to diagnose a cervical spine fracture.
Complications
The possible complications of a cervical fracture sustained during athletic participation depend on the nature of the fracture, the presence of neurologic compromise, the overall stability of the neck after injury, and the presence of other injuries sustained at the same time. Most fractures that occur in the neck from sports participation are minor in comparison to the entire scope of cervical fractures and heal uneventfully, especially in a young and motivated patient population. When fractures or ligamentous disruption have occurred that have gone unrecognized the athlete is at risk for future neurologic injury or posttraumatic deformity.
Treatment
Isolated compression fractures are usually treated with a semirigid collar for 8–10 weeks. Spinous-process fractures are benign and usually heal without any significant problem. Immobilization in a cervical collar for 4–6 weeks relieves pain. For both types of fractures flexion and extension radiographs should be taken at the end of the immobilization period to rule out a more serious ligamentous disruption.
Lamina fracture treatment is dictated by the stability of the cervical spine. When lamina fractures occur in isolation without any other ligamentous injury or fracture the neck may be immobilized in a cervical collar for 8–10 weeks. This is followed by lateral flexion and extension radiographs to rule out instability.
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Surgery is necessary to stabilize the cervical spine when bony or ligamentous injury has occurred that cannot be treated with immobilization alone or to perform decompression when either bone or soft tissue such as disk material causes neurologic deficits. These are rare instances in athletes but surgery is necessary when the stability of the cervical spine has been compromised.
The procedures used to confer stability to the neck after a destabilizing injury in almost all circumstances involve performing an arthrodesis of the destabilized segments. Anterior and posterior approaches are available to accomplish this goal. The direction taken is influenced by the site of destabilization and the presence of neurologic compromise that may require decompression.
Return to Play
The athlete may be allowed to return to play after healing of the fracture and determining by lateral flexion and extension radiographs that instability is not present. In addition, a full rehabilitation course aimed at achieving full neck strength and range of motion will reduce discomfort and the possibility of recurrence when returning to full contact sports.
Laporte C et al: Severe hyperflexion sprains of the lower cervical spine in adults. Clin Orthop 1999;363:126.
Makan P: Neurologic compromise after an isolated laminar fracture of the spine. Spine 1999;24:1144.
Neck Pain & Paresthesias
A “burner” or “stinger” is a transient neurologic event characterized by pain or paresthesias in one upper extremity following an impact to the neck or shoulder.
Essentials of Diagnosis
Prevention
An athlete who has sustained a previous stinger is at risk for sustaining a second occurrence. Protective equipment to restrain excessive movements in side bending and extension of the neck for play in football is recommended. The use of a strap that connects the helmet to the shoulder pads to limit cervical extension is not recommended.
Proper tackling technique and not dropping the shoulder also help to prevent injury by limiting the amount of neck extension. Maintaining eye contact with the opposing player results in a more upright position during tackling and thereby decreases the risk of sustaining a stinger.
Clinical Findings
Athletes experience sensations of tingling, burning, or numbness in a circumferential distribution with an inability to move the involved extremity. The athlete is often seen either holding the affected arm with the other arm or trying to shake off the feeling of pain and numbness. The symptoms may localize to the neck or radiate to the hand on the affected side. A stinger differs from a radiculopathy, which involves symptoms in a single dermatomal pattern.
The injurious event usually involves the downward displacement of the shoulder with concomitant lateral neck flexion toward the contralateral shoulder applying stretch to the brachial plexus. Head rotation may also play a part in the etiology of stingers. Head rotation to the affected side narrows the neuroforamen causing compression of the exiting nerve root. Direct blunt trauma to Erb's point may also result in a stinger.
A patient who has sustained a stinger requires a thorough examination of the cervical spine with a complete neurologic assessment. The integrity of the neck's ligamentous and bony anatomy is determined by palpation for areas of tenderness and testing the active range of motion of the neck. Palpation is done to find tenderness, localized swelling, and deformity. Range of motion testing includes active rotation, lateral bending, forward flexion, and extension. The neurologic examination includes strength testing of all muscle groups, sensory examination over all dermatomes, deep tendon reflex and testing, and performing an upper motor neuron assessment with either the Hoffmann reflex test or the radial reflex test. The shoulder examination includes assessment of the clavicle, acromioclavicular joint, supraclavicular region, and glenohumeral joint. Percussion of Erb's point may elicit radiation of pain into the upper extremity when injury to the brachial plexus has occurred.
The player typically presents with an inability to move the involved upper extremity following a high-energy collision with another player. The on-field evaluation of the injured player shows arm weakness and a burning pain present in the involved extremity. Shoulder abductor,
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external rotation, and arm flexion are reliable indicators that the player has sustained a stinger. Weakness in the upper trunk of the brachial plexus including the deltoid, biceps, supraspinatus, and infraspinatus muscles is commonly seen. In most cases these symptoms resolve within minutes. Motor weakness may develop hours to days after the injury, therefore repeat examinations are necessary. When nerve-root injuries have occurred the athlete may maintain a slightly flexed posture of the neck to alleviate pressure from the affected nerve roots.
The lateral cervical spine radiograph is most useful to determine if cervical stenosis is present. Encroachment of the facet articulations on the spinolaminar line is a positive indicator. The Torg ratio is determined by measuring the space available for the spinal cord from the posterior aspect of the vertebral body to the spinolaminar line and then dividing this distance by the anteroposterior width of the vertebral body at the same level (Figure 7-4). In most people this ratio is one. College athletes with a Torg ratio less than 0.8 have a three-fold increased risk of sustaining a stinger with cervical spine extension–compression injuries. In a group of high school athletes in which Torg ratios and foramen/vertebral body ratios were used to assess foraminal stenosis, athletes with cervical spinal canal or foraminal stenosis were demonstrated to be at an increased risk of sustaining a stinger.
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Figure 7-4. The Torg ratio is determined from the distance from the mid-point of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line (a) divided by the anteroposterior width (b) of the vertebral body. (From Torg JS et al: Neuropraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 1986;68A:1354. ) |
Electrodiagnostic testing is rarely necessary as stingers are usually temporary. The abnormal spontaneous activity seen on electromyographic (EMG) testing is not evident for at least 2 weeks following injury and maximizes at 3–5 weeks. EMG testing is most useful for the evaluation of persistent weakness at 2–3 weeks. Evidence of nerve injury shows fibrillation potentials in the involved muscles. When nerve root injury is suspected an MRI is the study of choice. The MRI will show shifting of the cord away from an avulsed cervical nerve root when present.
Studies of electrodiagnostic testing for stinger syndrome have found that even though the patient's strength improved over time up to 80% of athletes continued to have abnormal EMG studies at 5 years postinjury. It therefore can be concluded that only in rare instances is EMG testing necessary following stingers and the most reliable criteria for return to play remain the physical examination and appropriate imaging studies.
The Spurling's maneuver may be used to assess foraminal narrowing and has been shown to reproduce arm symptoms in 70% of those who have experienced stingers. By laterally bending the neck with concomitant application of axial load a compressive load is produced on the neural foramen. When arm pain is reproduced the test is considered positive as this indicates that nerve root irritation has occurred.
Stingers involving the upper extremity are always unilateral and have not been reported to occur in the lower extremity. When bilateral symptoms and or deficits occur the possibility of a spinal cord injury must be ruled out. This clinical situation requires an assessment of motion and areas of tenderness. Reluctance to move the neck and severe tenderness are signs of a potentially serious injury. This requires immobilization of the patient and transport on a backboard to a nearby trauma center for a full work-up and radiologic testing.
Treatment
Isolated stingers are considered to be benign injuries. By definition stingers are transient injuries and usually do not require formal treatment other than observation and supportive care. The athlete should not be allowed to return to play until the symptoms completely resolve. For severe injuries, a sling should be worn while clinicians await the resolution of symptoms. Modalities in a physical therapy center and medications can be used as necessary to control pain. Rehabilitation should then ensue to strengthen all of the upper extremity muscles including those not involved in the injury.
Rehabilitation of the cervical spine after a stinger involves conditioning of the neck and shoulder musculature. Attaining full neck range of motion essentially
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clears the patient of nerve root irritation as an irritable nerve root will limit the ability to move the neck due to pain. The strengthening program should include isometrics with progression to isotonic exercises with inclusion of the shoulder and trapezius musculature.
Prognosis
A player should not be allowed to return to play when the risk of play outweighs the benefits for the player. The relative risk of a player sustaining a second stinger increases when compared to the risk of a player sustaining an initial stinger. Players should be excluded from further participation in contact sports when they remain symptomatic after a stinger or have persistently abnormal diagnostic studies.
Long-term muscle weakness with persistent paresthesias may result from severe or repeated stingers. Repeated stingers in athletes may result from a combination of cervical stenosis and degenerative disk disease.
Return to Play
Vaccaro and co-workers' return to play criteria for cervical spine injury in the athlete provide one of the most complete guidelines for managing players who have sustained a stinger. For a first time stinger an athlete may return to play only if neck range of motion is full and painless and the upper extremity strength is full. An athlete who has sustained three or fewer episodes of stingers in the past each of which has lasted fewer than 24 hours may also return to play on the day of injury. An athlete whose symptoms do not resolve on the sideline may not be allowed to return to play until either the symptoms resolve or further imaging studies are performed to determine the cause of the stinger.
The relative contraindications to return to play include a prolonged symptomatic burner lasting for more than 24 hours or more than three stingers that have occurred in the past. Absolute containdications to return to play include (1) more than two episodes of transient quadriparesis, (2) a clinical history, examination findings, or an imaging study that confirm cervical myelopathy, and (3) any continued neck discomfort, decreased range of motion, or any neurologic deficit sustained from any prior cervical spine injury.
Aldrige JW et al: Nerve entrapment in athletes. Clinics Sports Med 2001;20:95.
Bergeld JA et al: Brachial plexus injury in sports: a five year follow-up. Orthop Trans 1998;12:743.
Feinberg JH: Burners and stingers. Phys Med Rehab Clin North Am 2000;11:771.
Proctor MR, Cantu RC: Head and neck injuries in young athletes. Clinics Sports Med 2000;4:693.
Slipman CW et al: Symptom provocation of fluoroscopically guided cervical root stimulation: are dynamic maps identical to dermatomal maps? Spine 1998;23(20):2235.
Vaccaro AR et al: Cervical spine injuries in athletes: current return-to-play criteria. Orthopedics 2001;24:699.
Weinstein S: Assessment and rehabilitation of the athlete with a “stinger”: a model for the management of noncatastrophic athletic cervical spine injury. Clinics Sports Med 1998; 17:127.
Spinal Cord Neuropraxia & Transient Tetraplegia
Essentials of Diagnosis
Temporary paralysis after a sports-related collision followed by the resolution of symptoms and a normal physical examination has been named spinal cord neuropraxia (SCN) or transient tetraplegia. Cervical spine radiographs of athletes show congenital spinal stenosis, believed to be the most significant contributing factor to the development of this entity. Hyperextension of the neck is believed to cause an infolding of the ligamentum flavum leading to a 30% reduction in the anteroposterior diameter of the spinal canal. As the neck extends the spine shortens, resulting in the infolding of the dura mater, thickening of the spinal cord, buckling of the ligamentum flavum, and narrowing of the subarachnoid space, known as the “pincher mechanism.” Any one or a combination of these events effectively increases the pressure on the cervical spinal cord and decreases its blood flow contributing to an SCN episode. Congenital narrowing of the spinal canal increases the risk of injury as a lower functional reserve is available for the spinal cord to adapt during significant blows to the head or neck.
Episodes of SCN are described in terms of neurologic deficit, duration of symptoms, and anatomic distribution. The terms paresthesias, paresis, and plegia describe a continuum of neurologic deficits that ranges from sensory involvement alone, to sensory involvement with motor weakness, to episodes of complete paralysis. There are three grades of SCN injury. Grade I injury involves symptoms lasting fewer than 15 minutes. Grade II injuries last from 15 minutes to 24 hours. Grade III injuries persist longer than 24 hours. When all four extremities are involved the term “quad” is used to describe the pattern. The term “upper” indicates that
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both arms are affected and “lower” that both legs are affected. Involvement of one leg and arm on the same side constitutes a “hemi” pattern.
Prevention
The prevention of SCN begins with the education of athletes participating in contact sports emphasizing proper technique to avoid injury. The spearing of other helmeted players has been prohibited since 1976 when the National Federation of State High School Associations and the National Collegiate Athletic Association banned this style of play in football. These rules were implemented because cinematographic and epidemiologic data revealed that the majority of cervical spine injuries were caused by axial loading. As players have learned how to play without making contact with the crown of the helmet the incidence of catastrophic and permanent quadriplegia has significantly decreased.
Clinical Findings
Symptoms include sensory changes of burning pain, numbness, tingling, and loss of sensation with motor changes ranging from weakness to complete paralysis. These episodes are transient and complete recovery usually occurs in 10–15 minutes, although some patients may not recover until 36–48 hours after injury. Neck pain is usually not present at the time of injury except for burning paresthesias.
The basic principles of advanced trauma life support (ATLS) and immobilization of the spine may make the difference between an uneventful recovery and permanent deficit or injury when initiating the work-up and treatment of the athlete. Patients who are transiently paralyzed may require respiratory support if a high cervical cord injury has occurred. Respiratory support requires removal of the helmet and shoulder pads, which must be done while maintaining full immobilization of the spine. In the event of airway obstruction or need for immediate intubation the facemask may be removed with a screwdriver or clippers either on the field or in the hospital setting when control of the airway is imperative. The principals of ATLS are always maintained. A thorough neurologic examination of both the upper and lower motor neurons is the foundation of the assessment of an athlete who has sustained an SCN. This involves full assessment of both upper and lower extremity strength, sensation, and lower and upper motor neuron reflexes.
A complete set of cervical spine radiographs is the first priority in the radiographic work-up of a patient who has sustained a spinal cord neuropraxia. The lateral radiograph allows the dimension of the sagittal canal to be determined. A 15-mm anteroposterior cervical canal diameter is considered normal but a canal of less than 13 mm is considered stenotic. Differences may occur due to the radiographic technique, thereby making measurements of the canal diameter inconsistent. The Torg ratio, described in the section on burners and stingers, has also been used to diagnose developmental stenosis. In the collegiate and professional football leagues it has been found that the Torg ratio has a low positive predictive value due to the relatively larger vertebral bodies in this group of athletes.
An MRI of the cervical spine is mandatory following an episode of SCN. The space available for the spinal cord may be more accurately assessed with an MRI scan. Results of MRI have led to the concept of functional stenosis, as assessment of focal cord deformation and blockage of cerebrospinal fluid flow are made possible. Athletes who have experienced an episode of transient SCN and who also show functional stenosis on MRI should perhaps not be allowed to return to play. Signal changes in the spinal cord shown on MRI that suggest actual injury indicate that the athlete should be prohibited from returning to high-risk athletic participation.
There are no special tests necessary to diagnose an SCN such as EMG. Plain radiographs and MRI, in addition to the physical examination, are the only tests routinely necessary. Only in very rare instances, such as when patient size, severe claustrophobia, or metallic implants prohibit obtaining an MRI, is it necessary to obtain a CT myelogram of the cervical spine to evaluate the spinal canal.
No special examinations other than a thorough musculoskeletal, spinal, and neurologic examination are required to diagnose an SCN.
Complications
The most serious complication of an SCN, aside from its recurrence, is the possibility of a devastating and permanent neurologic injury resulting in quadriplegia. The patient is predisposed to such injury with any significant blow to the head that results in a fracture at the area of stenosis. This may occur as a result of a fall, motor vehicle accident, or even return to play, depending on the energy imparted to the head and neck at the time of collision.
Treatment
Rehabilitation after an episode of SCN is initiated by ensuring that all neurologic symptoms and deficits have resolved. A physical therapy program that focuses on attaining a full and pain-free range of motion of the
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neck and extremities ensures that ligamentous and bony injury will not predispose the athlete to further injury. Muscular conditioning to regain a preinjury level of strength in the extremities and neck ensures that all neurologic deficits have been eliminated and also assists in prevention of injury.
Throughout the rehabilitation process the athlete should be counseled on the risk of recurrent injury. Only after receiving an explanation of the injury process and the possible predisposition to recurrence based on radiographs and MRI studies and after being fully informed of their risk and the serious consequences of neurologic injury can athletes and their families make an informed decision about return to play.
Surgery is reserved for destabilizing injuries. There has been no long-term study investigating the efficacy of spinal cord decompression such as a canal expansive laminoplasty in preventing a recurrent episode of SCN.
No special surgical procedures have been widely accepted for the purpose of returning an athlete to play. In circumstances of severe cervical spine canal stenosis and the development of myelopathy, surgery is necessary. In a younger patient population normal cervical lordosis should be maintained and in the absence of severe neck pain a canal expansive laminoplasty may be an option. Cervical laminoplasty has proven useful in expanding the space available for the spinal cord, obviating the need for a much more aggressive anterior procedure that may require a multilevel corpectomy or a posterior laminectomy with fusion. Unfortunately, it decreases range of motion of the neck due to the arthrodesis required at each level performed.
Prognosis
An estimate of the incidence of SCN in a group of collegiate football players in 1984 was 0.06%. Interestingly, five of the seven players who returned to play sustained a second episode of SCN. In another study, 35 of 62 athletes who returned to play after sustaining an SCN experienced second episodes of SCN.
Return to Play
Just as important as the initial management of the injured athlete, a thorough physical examination must be completed and pertinent radiographic studies must be reviewed before allowing the athlete who has sustained an SCN to return to play. Only after all studies remain normal, the athlete is completely asymptomatic, and the physical examination is unremarkable for injury may the athlete return to play. Controversy exists when the physical examination is normal but the radiographs or MRI scan show evidence of cervical stenosis. This situation requires careful counseling of players and their families about the possible consequences of a second injury before returning to play.
Cantu RC: The cervical spine stenosis controversy. Clinics Sports Med 1998;17:121.
Muhle C et al: Dynamic changes of the spinal canal in patients with cervical spondylosis at flexion and extension using magnetic resonance imaging. Invest Radiol 1998;33(8):444.
Torg JS et al: Cervical cord neuropraxia: classification, pathomechanics, morbidity, and measurement guidelines. J Neurosurg 1997;87(6):843.
Wilberger JE: Athletic spinal cord and spine injuries. Clinics Sports Med 1998;17:111.
Lumbar Spine Injuries in Athletes
Lumbar Sprain
Essentials of Diagnosis
Pathogenesis
Low back pain has been reported to affect approximately 85–90% of the population at least once during their lifetime. The incidence in the athletic population has been reported to be 1–30% and is one of the most common reasons for missed playing time in professional sports. Unfortunately, the specific etiology of the athlete's back pain often remains elusive. Muscle strain is the most common etiology of low back pain in adolescent, collegiate, and adult athletes. It is also the most common diagnosis in both acute and chronic low back pain.
Prevention
Strategies for prevention of lumbar strains and sprains have focused on increasing flexibility of the lumbar spine. It is thought that improved lumbar flexibility improves
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responses to high-energy demands and prevents episodes of low back pain in athletes. Although a definitive relationship between lumbar flexibility and low back pain has not been proven, most agree that athletes with poor flexibility are at higher risk for lumbar strain injuries. In regards to prevention of lumbar strain injuries during competition, it is likely that the timing of the pregame warm-up is important. Warm-up exercises are designed to increase core body temperature, improve extremity blood flow, and improve flexibility in an effort to prevent injury. Muscular strain injuries in the extremities have been linked to inadequate warm-up, weakness, decreased flexibility and muscle fatigue. Recently, it has been shown that the improved lumbar flexibility gained from pregame warm-up exercises is lost after 30 minutes of rest prior to game time. Although the link between the observed degree of increased stiffness and the subsequent risk of lumbar injury remains unclear, keeping athletes active immediately prior to the game and during rest periods on the sidelines should help decrease the risk of muscle strain injuries.
Ultimately, the best predictor of future occurrences of back pain in athletes is a history of low back pain. The risk of future episodes of low back pain is three times higher in athletes with a history of back pain than in athletes who do not have such a history. Core-strengthening paradigms have been proposed, however, there is no conclusive evidence that these programs decrease the incidence of back pain in athletes. It is likely that emphasis on form and technique combined with appropriate conditioning is the best preventive medicine.
Clinical Findings
Lumbar strains are defined as disruption of muscle fibers at various locations within the muscle belly or musculotendinous junction from excessive eccentric loading of the muscle–tendon unit. Lumbar sprains occur by subcatastrophic stretch of one or more of the spinal ligaments. Athletes with lumbar strains can present with either acute or chronic symptoms. In acute lumbar strain, athletes typically report an inciting injury with back pain beginning soon after, becoming most painful about 24–48 hours postinjury. The mechanism is often a twisting injury but can occur from a direct blow as well. Frequently, the intensity of the pain has diminished considerably by the time of presentation to the clinician's office. Athletes with chronic lumbar strains generally report fatigue-related back pain, worsening toward the end of a hard training week or cycle. The clinician should inquire about any recent or sudden increases in training frequency or intensity. It is important to ask the athlete about any previous episodes of back pain and previous treatments. The athlete should also be questioned about neurologic symptoms and variations in the intensity of the pain with coughing, sneezing, or changes in position. In lumbar strain injuries, radicular symptoms (radiating pain in the lower extremities) are absent and pain is limited to the back and paraspinal muscles. Increased pain intensity with a valsalva maneuver may indicate a herniated nucleus pulposus. Although cauda equina syndrome is extremely rare in the athletic population, the athlete should be asked about the presence of any difficulty with bowel or bladder function.
Typically, most athletes will have limitations in range of motion, predominantly from muscle spasm. Muscle spasms occur as the body's response to injury. Although the mechanism is not completely understood, it is thought that local inflammatory mediators trigger muscular contraction in an attempt to stabilize the injured segment. When muscle spasms are severe, a painful trigger point may develop after several days. Trigger points typically are palpated in the paraspinal musculature away from the midline. Lumbar sprains are thought to be due to injury to the interspinous process ligaments so midline tenderness may be present as well.
A full neurologic examination of the lower extremities should be performed and is normal in lumbar strain injuries. Nerve root tension signs such as the supine and seated straight leg raise and Laseques maneuver should also be negative. Pain worsening with lumbar extension in a young athlete raises concern for spondylolysis. The sacroiliac joints should also be palpated and stressed. Abnormalities in strength, reflex, or sensory testing are not consistent with lumbar strains and sprains and should prompt further work-up. It is important to assess all lower extremity joints for range of motion and pain as primary joint pathology may cause back pain. An examination of the athlete's gait and overall spinal balance concludes the physical examination.
Imaging is not necessary in the vast majority of lumbar strain injuries as 80–90% of these injuries resolve spontaneously. Imaging tests should be considered for the athlete whose pain is severe, was caused by an acute traumatic event, or whose symptoms have not responded to several weeks of conservative treatment. Any neurologic findings warrant radiographic evaluation. Teenage or younger athletes may benefit from earlier imaging as earlier identification of acute spondylolysis may influence outcomes. Plain radiographs including an anteroposterior, lateral, left and right oblique, and coned down lateral view of the lumbosacral junction should be obtained. These radiographs may reveal mild degenerative changes in older athletes but should otherwise be negative.
When considering the role of advanced imaging for spinal disorders, the high rate of false positive radiographic
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abnormalities (normal aging degenerative changes) should prompt the clinician to carefully consider what clinical question needs to be answered from the imaging study. Many athletes undergo unnecessary imaging studies for low back pain. These studies may reveal radiographic abnormalities not consistent with their current symptoms that unduly influence treatment. Degenerative changes are more frequent in the athletes, however, the incidence of low back pain is similar to the general population. Degenerative changes seen on MRI have not been shown to be predictive of the development or duration of low back pain. The main indication for obtaining an MRI scan is the presence of neurologic symptoms and signs. Occasionally, a bursal cavity may be seen between the spinous processes in athletes with chronic lumbar strain injuries, although the clinical significance of this finding is unknown.
Treatment
Rehabilitation
Lumbar strains and sprains are generally self-limited processes that respond very well to conservative treatments. A common sense approach to rehabilitation, including a short period of bed rest (no longer than 1–2 days to prevent deconditioning), ice for muscle spasms, nonsteroidal antiinflammatory medication, and physical therapy to strengthen the spinal musculature, is important. A three-cycle rehabilitation program for the treatment of nonradicular low back pain in athletes emphasizes differing degrees of rest, physical the-rapy, and time to return to play. Essentially, when symptoms are moderate to severe, the athlete is restricted from contact and emphasis is primarily on pain control and cardiovascular conditioning. As symptoms subside, the athlete is allowed to progress to limited practice sessions of increasing duration over time. Recently, motion-specific rehabilitation protocols have gained popularity. In a motion-specific protocol, athletes are placed into categories depending on which range of motion is least tolerated or exacerbates the athlete's symptoms. Treatment is directed first toward improving range of motion in the pain-free arc, then progressively improving motion in the opposite direction. For example, if an athlete's symptoms become worse with extension, flexion-based exercises are initiated and extension exercises are restricted.
Prognosis
Overall, the prognosis from lumbar strain and sprain injuries is quite favorable with resolution in 80–90% of patients. A history of low back pain is the best predictor of future occurrences. Although many athletes experience lumbar strain during their careers, rarely are symptoms debilitating enough to lead the athlete to early retirement. Multiple studies of collegiate wrestlers, rowers, and football players have shown that retirement from sport due to lumbar strain is rare.
Return to Play
Most athletes who experience an episode of lumbar strain or sprain will require a period of reduced activity and perhaps removal from competition for a short period. Return to competition is allowed once the athlete's pain is tolerable, flexibility is restored, and muscle spasms have diminished.
Aure OF et al: Manual therapy and exercise therapy in patients with chronic low back pain: a randomized, controlled trial with 1-year follow-up. Spine 2003;28:525.
Bono CM: Low-back pain in athletes. J Bone Joint Surg Am 2004;86A(2):382.
Fujiwara A et al: The interspinous ligament of the lumbar spine: magnetic resonance images and their clinical significance [Diagnostics]. Spine 2000;25(3):358.
George SZ, Delitto A: Management of the athlete with low back pain. Clinics Sports Med 2002;21:105.
Green JP et al: Low-back stiffness is altered with warm-up and bench rest: implications for athletes. Med Sci Sports Exerc 2002;34:1076.
Greene HS et al: A history of low back injury is a risk factor for recurrent back injuries in varsity athletes. Am J Sports Med 2001;29:795.
Nadler SF et al: The relationship between lower extremity injury, low back pain, and hip muscle strength in male and female collegiate athletes. Clin J Sports Med 2000;10:89.
Trainor TJ, Wiesel SW: Epidemiology of back pain in the athlete. Clinics Sports Med 2002;21:93.
Lumbar Fractures
An extensive discussion of all lumbar spine fractures is beyond the scope of this chapter, however, the sports medicine clinician may be called upon to treat minor fractures of the lumbar spine. These injuries include anterior compression fractures, spinous process and transverse process fractures, adolescent vertebral end plate injuries, and pedicle or sacral stress fractures. Anterior compression fractures generally result from a mechanism involving forced flexion. Spinous process and transverse process fractures generally result from a direct blow or torsional injury. Adolescent athletes may suffer avulsion injuries of the end plates as the spinal ligaments tend to be stronger than the vertebral end plates. Stress fractures of the lower lumbar pedicles have been reported, most commonly in fast bowling cricketers. Sacral stress fractures, although uncommon, are generally overuse injuries that may develop in running athletes.
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Essentials of Diagnosis
Prevention
Fortunately, fractures of the lumbar spine are rare injuries in sports competition. Prevention of such injuries includes emphasis on sound tackling techniques, adequate protective equipment, and maintaining abdominal and lumbar muscle conditioning.
Clinical Findings
The history of a violent or high-energy injury combined with symptoms of acute back pain alert the clinician to the possibility of a lumbar spine fracture. Pain that is worse when sitting up and is relieved by lying supine may indicate a compression fracture. The athlete should be carefully questioned for neurologic symptoms and for difficulties with bowel or bladder function. A history of the mechanism of injury and the energy associated with that injury should be obtained. Falls from significant height, violent collisions, and diving injuries raise the suspicion of fracture. Chronic low back pain refractory to conservative measures may represent a stress fracture of either the pedicles or sacral spine. In female athletes, a nutritional and menstrual history should be obtained to identify risk factors for osteoporosis. Additionally, positional variations that make such pain worse with extension could indicate a stress fracture of the posterior bony elements. In the chronic setting, it is important to ascertain any recent changes in frequency or intensity of training or competition. The clinician should also ask the athlete to attempt to pinpoint the area of most discomfort as sacral stress fractures may present as low back or buttock pain.
In the acute setting, spine precautions with log-rolling should be utilized during the evaluation. Palpation of the posterior spine should be performed looking for step-off, hematoma, and midline versus paraspinal tenderness. A complete neurologic examination including motor, sensory, and reflex testing should follow. A rectal examination should be performed to assess for perianal sensation and rectal tone.
In the chronic setting, active and passive lumbar range of motion should be assessed. Increased pain with extension should alert the clinician to the possibility of a posterior bony element injury. The sacral spine should also be examined because sacral stress fractures are usually tender to palpation. Asking the patient to perform single leg support and single leg hopping maneuvers may provide clues to a sacral stress fracture as well.
Plain films including anteroposterior, lateral, and oblique radiographs should be obtained. These radiographs should be examined for overall spinal alignment, presence of soft tissue swelling, interspinous process distance, vertebral body height, scoliosis, or evidence of instability. Anterior compression fractures are seen as a fracture of the anterior superior portion of the vertebral body. Anterior and posterior vertebral body height should be measured at the level of injury and compared to adjacent levels. The posterior interspinous process distance should be scrutinized. An increase in this distance indicates that the fracture may potentially be unstable. In simple anterior compression fractures, there is minimal loss of height, no increased interspinous process distance, and no rotational deformity on the anteroposterior radiograph.
Spinous process fractures are best visualized on the lateral radiograph. The interspinous process distance should be carefully evaluated and compared to adjacent levels. Although the fractured portion of the spinous process can be significantly displaced, the remaining portion should maintain its normal relationship with adjacent vertebrae.
Transverse process fractures are best visualized on the anteroposterior radiograph. Single transverse process fractures are considered minor injuries, however, the presence of multiple transverse process fractures raises the suspicion of a more serious injury.
Plain radiographs are usually unrevealing in stress fractures of the pedicles or sacrum. Occasionally, fracture callus or sclerotic lines may be seen as clues to the diagnosis.
Advanced imaging studies should be obtained in athletes with compression fractures, multiple spinous process or transverse process fractures, or for persistent symptoms despite previous conservative management. CT allows differentiation between compression and more complex (eg, burst or chance-type) fractures. CT will also rule out associated severe spinal fractures in athletes with multiple spinous process or transverse process fractures. Fracture lines with sclerotic margins
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may be seen in athletes with pedicle or sacral stress fractures. Athletes with multiple spinous process or transverse process fractures or any neurologic symptoms should undergo MRI. MRI allows excellent visualization of the neural elements as well as the integrity of the posterior ligamentous supporting structures.
If plain films and CT fail to provide a diagnosis, single-photon emission computed tomography (SPECT) or MRI may reveal stress reactions of the lumbar pedicles or sacral spine. In female athletes with compression or stress fractures of the lumbar spine, bone densitometry should be performed to assess for the presence of osteoporosis.
Treatment
Nonsurgical management is the mainstay of treatment for minor fractures of the lumbar spine. Nondisplaced or minimally displaced compression fractures should be supported with either a lumbosacral corset or thoracolumbosacral orthosis (TLSO) for 6–12 weeks. Frequent radiographs should be obtained because progressive collapse or instability can occur. Upright flexion and extension radiographs should be obtained at the conclusion of bracing and approximately 4–6 weeks postbracing to assess final alignment. Once clinical and radiographic healing has been obtained, the athlete may begin a physical therapy program emphasizing range of motion and cardiovascular conditioning. Strengthening exercises should begin after range of motion has been restored.
Spinous process and transverse process fractures should be managed with activity restriction and a lumbosacral corset for comfort. The majority of these fractures heal in approximately 6 weeks. As pain decreases and the athlete is comfortable, physical therapy is started with emphasis on range of motion and cardiovascular conditioning. As the athlete tolerates, therapy may shift toward a strengthening paradigm.
Sacral stress fractures are treated nonoperatively with rest and protected or non-weight bearing. As symptoms abate, progressive mobilization and weight bearing are begun and activities are resumed.
Pedicle stress fractures if detected early, prior to establishment of a nonunion, are treated with a TLSO for 6–12 weeks. Follow-up radiographs should be obtained frequently to assess for alignment and stability. CT scans may be necessary to document fracture union prior to discontinuation of brace treatment. Pedicle fractures that are detected late and have evidence of nonunion are managed surgically with bone grafting and instrumented fusion.
The literature regarding apophyseal ring injuries in the adolescent spine predominantly consists of case reports. There is no general consensus for treatment. Suffice to say, case series of asymptomatic patients treated conservatively have yielded good results. In symptomatic patients, with radicular or claudicatory (pain radiating into the extremities with exertion such as walking) symptoms, surgical decompression of the anterior thecal sac from the posteriorly protruding vertebral end plate has yielded good results.
Prognosis
Although there are no outcome data on minor fractures of the lumbar spine in athletes, extrapolating data from the adult nonathlete population would suggest that the prognosis should be good. Provided overall spinal alignment has been maintained a full recovery with minimal residual symptoms is expected.
Return to Play
Currently, there are no published guidelines regarding return to sports after lumbar fractures. Upon demonstration of clinical and radiographic healing it is appropriate for the athlete to begin functional restoration with physical therapy on a phased continuum. Full, painless range of motion should be achieved prior to engaging in sport-specific training.
Folman Y, Gepstein R: Late outcome of nonoperative management of thoracolumbar vertebral wedge fractures. J Orthop Trauma 2003;17(3):190.
Johnson AW et al: Stress fractures of the sacrum. An atypical cause of low back pain in the female athlete. Am J Sports Med 2001; 29:498.
Parvataneni HK et al: Bilateral pedicle stress fractures in a female athlete: case report and review of the literature. Spine 2004;29(2):19.
Spondylolysis
Essentials of Diagnosis
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Spondylolysis, a defect in the posterior neural arch, is seen in both athletic and nonathletic populations. It is most common at the L5 spinal level and is next most common at the L4 level. Although the precise etiology of spondylolysis is not known, it is widely thought that repetitive hyperextension of the lumbar spine leads to a stress fracture within the pars interarticularis. Epidemiologic studies have demonstrated a prevalence of 4–7% in the general population. Although athletes in certain sports (diving, gymnastics, weightlifting, wrestling, football, rowing) demonstrate a higher incidence of spondylolysis, occurrence in the athletic and nonathletic populations is similar. Spondylolysis is twice as common in boys as in girls and longitudinal studies suggest a familial predisposition.
Prevention
Strategies for prevention of spondylolysis are aimed at early detection of the pars at risk. If stress reactions with the pars interarticularis are detected, treatment can prevent progression to a lytic defect. In the future earlier detection of pending pars fractures may decrease the incidence of spondylolysis in athletes.
Clinical Findings
Symptoms of spondylolysis may range from a dull, persistent ache present within the low back to severe pain causing an awkward gait or limiting ambulation. The pain is often worse with lumbar extension and improves when leaning forward. Athletes may report difficulty sleeping or laying flat. Pain is usually limited to the low back but may radiate to the buttock or posterior thigh. Patients may also complain of hamstring tightness and loss of lumbar range of motion. Radicular symptoms may occur but are rare in spondylolysis.
Athletes with spondylolysis generally have few abnormalities on physical examination. Typically, lumbar range of motion is limited, predominantly with extension. Gentle passive extension of the lumbar spine often exacerbates symptoms. The single-leg hyperextension test is a provocative maneuver that can aid in the diagnosis of spondylolysis. When performing the test, the patient stands on one leg and extends the lumbar spine. In patients with spondylolysis, symptoms worsen with this maneuver on the side of the defect. Tenderness to palpation can often be elicited on the symptomatic side. If spondylolisthesis is not present, there should not be a palpable step-off. Provocative maneuvers for radiculopathy such as straight leg raising and the Laseques maneuver are negative and the neurologic examination is usually normal.
If spondylolysis is suspected, imaging should begin with plain radiographs. An initial radiographic series including anteroposterior, lateral, both left and right obliques, and a coned down lateral view of the lumbosacral junction will demonstrate a lytic defect of the pars interarticularis in 85% of cases of spondylolysis (Figure 7-5). The coned down lateral view centers the x-ray beam on the lumbosacral joint, not the lumbar spine. A break in the “neck” of the “Scottie Dog” may be seen. Radiographs should also be assessed for the presence of spondylolisthesis, which is present in 50–75% of initial radiographs when a lytic defect is seen. The older the athlete at the time of presentation, the higher the likelihood that spondylolisthesis is present.
If the initial radiographic examination is negative and the athlete has a compelling history and physical examination concerning spondylolysis, advanced imaging is indicated. This may consist of a bone scan, CT, SPECT,
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or MRI. Stress reactions in the pars may be detected by radionuclide imaging prior to progression to a lytic defect (Figure 7-6). Athletes with back pain and a pars defect on radiographs should undergo a bone scan to determine if active bone turnover is present. If uptake is not demonstrated on bone scanning, it is unlikely that spondylolysis is the cause of the athlete's symptoms. SPECT scanning is more sensitive and specific than the standard bone scan; it has shown uptake in the pars when bone scans were negative. SPECT has also been shown to be negative in asymptomatic athletes with spondylolysis. Given the high sensitivity and specificity of SPECT scanning for symptomatic spondylolysis, it is the imaging study of choice when initial radiographs are negative and the clinical suspicion is high.
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Figure 7-5. Oblique radiograph of the lumbar spine demonstrating a defect in the pars interarticularis of the L5 vertebrae. The defect is seen in the neck of the “Scottie Dog.” |
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Figure 7-6. SPECT scan of spondylolysis. Notice the area of increased uptake near the left L5 pars interarticularis. |
CT is more sensitive than plain radiographs for spondylolysis and the defect in the pars interarticularis is demonstrated well on the axial cuts. The defect may be unilateral or bilateral. The major disadvantages of CT include difficulty in determining the age of the defect as well as the clinical significance if a defect is present. Sclerotic margins and hypertrophic bone ends may indicate a chronic nonhealing defect. Given the prevalence of spondylolysis in the general population, an adjunctive bone scan may be necessary to determine the defect's clinical significance. If a bone scan does not show increased uptake, it is unlikely that the pars defect is the source of the athlete's symptoms.
MRI, which is not as sensitive as a bone scan in symptomatic spondylolysis, is not commonly used in the diagnosis. Additionally, the temporal relationship between clinical healing and reversal of MRI abnormalities has also not been elucidated.
Treatment
The treatment of spondylolysis depends on several factors including the athlete's age, the severity and duration of symptoms, and radiographic findings. Asymptomatic athletes with a radiographic finding of a pars defect do not require treatment and should be allowed to participate in sports. If the athlete's symptoms are mild and are limited to low back pain, core strengthening and cardiovascular conditioning should be emphasized. If neurologic symptoms are present or if the athlete's symptoms are severe, play should be restricted and further evaluation should be performed to establish a diagnosis. In athletes with back pain and radiographic findings consistent with spondylolysis, limitations in activity and bracing result in a greater than 90% rate of success.
The need for bracing and the best method of bracing are debatable. In a series of seven athletes with spondylolysis, rest and restriction of activity without bracing allowed clinical healing in all athletes. The results of that study have been challenged and have not been reproduced. A short period of brace treatment is the usual recommendation. Soft and rigid, lordotic and antilordotic braces have all been utilized with good success. An antilordotic brace (0° flexion) is thought to unload the posterior elements and aid the healing process and is our preference. Time spent within the brace has varied among series and does not appear to be linearly correlated with clinical success. We currently recommend continuous bracing during waking hours with sleeping permitted out of the brace. The duration of bracing is generally 6–8 weeks, accompanied by restriction from sports. In adolescent athletes the recommendation is to repeat the radiographs every 6 months until skeletal maturity. In skeletally mature athletes, repeat radiographs are indicated only if symptoms return.
The goal of treatment in athletes with stress reactions (increased uptake on SPECT imaging with negative plain radiographs) or fractures of the pars is bony healing of the defect. In athletes with stress reactions a quantitative reduction in uptake on SPECT imaging can be seen following brace treatment. In athletes with a pars defect and uptake on a bone scan, bony union is possible. The likelihood of osseous union is greatest in unilateral defects and least when a defect is present on one side and a stress reaction is present on the contralateral side. Importantly, the rate of return to sports has not been correlated with the achievement of osseous union. It is postulated that a stable fibrous union occurs at the site of the defect allowing resolution of symptoms. Most clinicians recommend a discontinuation of bracing and a return to sports when the athlete is asymptomatic.
After immobilization, the athlete is advanced to a rehabilitation program emphasizing flexion-type exercises and flexibility. The athlete may resume activities over the next 6–8 weeks.
Due to the clinical success of nonoperative management of spondylolysis, surgery is rarely indicated. Athletes
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with symptoms that persist for more than 6 months despite restriction of activity and bracing are candidates for surgical intervention.
Historically, the gold standard for the treatment of symptomatic spondylolysis in the adolescent athlete at the L5 level has been surgery consisting of in situ uninstrumented posterolateral L5–S1 fusion. Although successful, segmental motion is sacrificed. Over the past two decades there has been considerable interest in direct repair of the pars defect as an alternative to fusion. The major advantage of a direct pars repair versus fusion is preservation of motion. As many athletes with spondylolysis are in their adolescent to early adult years, fusion should not be considered lightly. Several techniques have been described for the direct repair of the pars including the Scott wiring technique, hook-wire constructs, the translaminar interfragmentary screw (ie, Buck) technique, and pedicle screw–rod-hook constructs with bone grafting (Figure 7-7). The pedicle screw–rod-hook technique is theoretically the most rigid construct. Direct repair of pars defects from L3 to L5 have been reported. In several series of competitive athletes, both the interfragmentary technique and wiring techniques have produced good to excellent results and return to sports at the same level of competition in over 90%. Given the good success with multiple techniques, it is likely that the most important aspect of the operation is autogenous bone grafting of the defect.
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Figure 7-7. Lateral radiograph of the direct repair of the pars interarticularis defect with wiring technique and bone grafting. |
Athletes treated operatively for symptomatic spondylolysis should show evidence of bony healing prior to beginning a rehabilitation program. Once healing has been achieved, a rehabilitation program stressing flexion-type exercises, flexibility, and trunk strengthening is begun.
Return to Play
Athletes treated nonoperatively for spondylolysis are allowed to return to sports after clinical resolution of symptoms. Athletes may return to play when they are pain free, regardless of radiographic evidence of pars healing. Athletes returning to high-risk sports such at football, soccer, or gymnastics are five times more likely to have a poor clinical outcome compared to athletes returning to low-risk sports such as baseball, track, or swimming.
Timing for return to sports in athletes treated by direct pars repair is controversial. We believe that once healing of the pars has been demonstrated, the athlete may return to sports participation when pain free, range of motion has been established and trunk strength has been regained. This may take between 5 and 12 months.
Eck JC, Riley LH: Return to play after lumbar spine conditions and surgeries. Clinics Sports Med 2004;23:367.
Herman MJ et al: Spondylolysis and spondylolisthesis in the child and adolescent athlete. Orthop Clin North Am 2003;34:461.
Lim MR et al: Symptomatic spondylolysis: diagnosis and treatment. Curr Opin Pediatr 2004;16:37.
Lonstein JE: Spondylolisthesis in children: cause, natural history, and management. Spine 1999;24(24):2640.
Reitman CA, Esses SI: Direct repair of spondylolytic defects in young competitive athletes. Spine J 2002;2(2):142.
Rubery PT: Athletic activity after spine surgery in children and adolescents: results of a survey. Spine 2002;27(4):423.
Standaert CJ, Herring SA: Spondylolysis: a critical review. Br J Sports Med 2000;34:415.
SPONDYLOLISTHESIS
Essentials of Diagnosis
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Spondylolisthesis is commonly divided into five types based on the Wiltse classification: Type I is dysplastic or congenital. In this type, a congenital deficiency of the L5–S1 facets allows slippage of L5 on S1. Type II is isthmic or spondylotic spondylolisthesis. The defect in the pars interarticularis allows forward slippage of the vertebral body while the posterior elements remain in place. The defect in the pars may be a lytic fracture, an acute pars fracture, or an elongated but intact pars. Type III is degenerative, occurring in older individuals with associated facet arthropathy and spinal stenosis. Type IV, traumatic, is an acute fracture in a vertebrae other than the pars. Type V, pathologic, involves a pedicular or pars lesion because of generalized bone disease or tumor. Isthmic spondylolisthesis is the most common type in athletes and will be the focus of this discussion.
Spondylolysis and spondylotic spondylisthesis appear to have a genetic predisposition and often coexist. Spondylolysis is present in 4–6% of the general population. Spondylolisthesis is present in 50–80% of athletes with a pars defect on initial radiographs. Athletes in high-risk sports (football, gymnastics, soccer) may develop symptoms at a higher rate than the general population, in which the incidence of symptoms is low. Recently, in a large study of high school and college football players, athletes with spondylolysis or spondylolisthesis were twice as likely to report an episode of back pain than athletes without these diagnoses. Natural history studies in young athletes have shown that about 40% of athletes with spondylolisthesis will show evidence of progression over a 5-year period, however, the progression is small (10%) and does not correlate with worsening symptoms.
Clinical Findings
The most common presenting symptom in spondylolisthesis is back pain, however, there are a significant number of athletes who will not report symptoms. The association of spondylolisthesis with disability and symptoms is difficult to establish. In studies of young athletes with spondylotic spondylolisthesis, frequent problems related to pain or disability have not been observed. Athletes with L4–5 isthmic spondylolisthesis, greater than a 25% slip, or degenerative disk disease at the level of the slip are more likely to complain of back pain. Athletes may complain of back or leg pain but few patients have associated neurologic complaints. If neurologic symptoms are present, they are usually radicular in nature.
The physical examination of athletes with isthmic spondylolisthesis is generally unrevealing. The two most common findings based on physical examination in adolescents are increased pain with lumbar extension and hamstring tightness. Decreased lumbar range of motion and tenderness may be present but are nonspecific findings. In athletes with high-grade slips, III or IV, a palpable step-off between spinous processes may be present. Low-grade slips are very difficult to detect on palpation. Nerve root tension signs are usually negative and the neurologic examination is usually normal. When neurologic deficits are noted, they are frequently seen as weakness of the muscles innervated by the lumbar root exiting at the level of the slip, such as extensor hallucis longus weakness in an L5 pars defect. An awkward gait may be demonstrated if hamstring contracture is present. Severe hamstring contracture or listhetic posturing of hip and knee flexion, anterior pelvic tilt, and lumbar lordosis may indicate spinal instability.
Spondylolisthesis is demonstrated on plain radiographs as anterolisthesis of the cephalad vertebrae on the caudad vertebrae (Figure 7-8). Isthmic spondylolisthesis may occur at any level in the lumbar spine but is most common at the L5–S1 level. The Meyerding classification system is used to grade the degree of slip: Grade I <25%, Grade II 25–50%, Grade III 50–75%, and Grade IV >75%. Grade V or spondyloptosis rarely occurs. In isthmic spondylolisthesis, the pars defect is more easily seen on plain radiographs. Approximately 75% of patients will be classified as Grade I or II at the time of presentation. Grades III, IV, and V account for only 5% of cases of spondylolisthesis. The slip angle defines the degree of lumbosacral kyphosis and the actual percentage of slip can be calculated by dividing the millimeters of anterolisthesis by the total width of the caudad
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vertebrae. Radiographic parameters associated with an increased risk of progression of spondylolisthesis include higher degree of slip at initial presentation and increased lumbosacral kyphosis. Although a dome-shaped sacrum and trapezoidal L5 vertebrae may be seen in high-grade slips, these findings are not prognostic for slip progression. Given the differences in interrater reliability with measurements of the degree of slip, documentation of progression requires a 10–15% change in slippage or an increase in subluxation of 4–5 mm. Flexion and extension views of the lumbar spine have not been proven to be useful in isthmic spondylolisthesis.
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Figure 7-8. Lateral radiograph of the lumbosacral spine demonstrating spondylolysis with Grade I spondylolisthesis. |
CT scans with fine cuts (1–2 mm slice thickness) can demonstrate the lytic defect in the pars interarticularis quite well. Additionally, CT is useful as a preoperative planning tool. Pedicle anatomy, size, and orientation can be easily determined. Associated dysplasia is also demonstrated well.
MRI is useful in evaluating the intervertebral disc at the level of the slip and at adjacent levels. Degenerative discs display less signal on T2-weighted images due to loss of water content. It is thought that spondylolisthesis may progress in adulthood as a result of continued disc degeneration. Additionally, MRI also details nerve root compression associated with spondylolisthesis. Nerve root compression is best visualized on T1-weighted images as loss of fat signal surrounding the nerve root. Importantly, it should be noted whether the root is being pinched from cephalocaudal collapse of the foramen or between the posterolateral aspect of the disc and the remaining pars of the cephalad vertebrae.
In athletes for whom operative intervention is planned, predominant cephalocaudal collapse of the foramen may be an indication for use of an interbody fusion technique to restore foramenal height. In addition, provocative discography may be useful in the selection of fusion levels. Although controversial, exact reproduction of low back pain during discography of an adjacent segment may indicate that the fusion level should be extended to include that segment.
Treatment
The goal in the treatment of isthmic spondylolisthesis is symptom reduction, not healing of the pars defect. In asymptomatic athletes with Grade I or II isthmic spondylolisthesis, there is no need for treatment or for restriction from activities or sports. In young athletes, serial radiographs are recommended every 4–6 months until the age of 10, semiannually from age 10 to age 15, and annually after age 15 until skeletal maturity. Asymptomatic athletes with Grade III or IV spondylolisthesis should not participate in contact sports. Surgical intervention is recommended even in the asymptomatic adolescent athlete with Grade III or IV spondylolisthesis.
In symptomatic athletes with Grade I or II spondylolisthesis, a short period of bracing (6–8 weeks), activity modification, and flexion-based trunk strengthening exercises should be instituted. Bracing is not intended to prevent slip progression but to decrease symptoms. Two-thirds of adolescent athletes with Grade I or II spondylolisthesis will respond to conservative treatment. Serial radiographs are recommended until skeletal maturity.
Less than 10% of symptomatic athletes with Grade III or IV spondylolisthesis respond favorably to bracing, activity modification, and rehabilitation. Most athletes with symptomatic Grade III or IV spondylolisthesis require surgical intervention.
We believe that nonoperative care of isthmic spondylolisthesis in adults should be similar to care for acute low back pain. Avoidance of long periods of bed rest and return to activities are recommended. Symptomatic treatment with ice or cold packs may be beneficial. The use of transcutaneous electroneural stimulation (TENS) units lacks demonstrable efficacy. Additionally, manipulative therapies have not been shown to provide long-term relief in this patient population.
Flexion exercises of pelvic tilts and seated chest-to-thigh maneuvers have shown favorable results in both short- and long-term symptom reduction. Short-term improvements can be seen with aggressive physical therapy and stretching combined with high-intensity resistance training. Recently, programs of cocontraction-specific stabilization exercises involving the deep abdominal and multifidus muscles proximal to the pars defect have shown promise in reducing pain and disability in this population.
Overall, significant progression, defined as a greater than 10% change, is seen in only a minority of patients. Minor progression, less than a 10% change, may be seen in up to 75% of adolescent athletes. The risk of progression is not influenced by the athlete's sport and progression has not been shown to lead to an increase in symptoms. Progression of spondylolisthesis is more common in adolescents during the growth spurt and is unlikely after skeletal maturity. Progression after skeletal maturity is associated with disk degeneration. In general, females and those with dysplastic spondylolisthesis show higher rates of progression.
The indications for surgical intervention in the adolescent athlete include persistent pain despite 6–12 months of conservative treatment, a progressive slip greater than 50%, an ongoing
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neurologic deficit, or gait changes due to the slippage and associated muscle spasm. High-grade spondylolisthesis is a relative indication for surgical intervention.
The gold standard for Grade I and II isthmic spondylolisthesis is uninstrumented in situ posterolateral fusion with iliac crest bone grafting. Decompressive laminectomy is indicated only if severe neurologic symptoms are present. For high-grade slips when the L5 transverse process is anterior and inferior to the sacral alae, extension of the fusion to L4 is recommended and postoperative spica casting is added. Bone graft that is placed in the lateral gutter between the transverse process of L5 and the sacral alae is under shear forces. Bone graft that is laid in the lateral gutter up to the L4 transverse process is more vertical and under less shear force. Recently, instrumentation in adolescent cases has been utilized to decrease the necessity of extending the fusion (Figure 7-9).
Over 90% of patients will obtain relief from pain and improvement in neurologic symptoms, independent of the grade of spondylolisthesis. Outcomes are improved in uninstrumented fusions for low-grade slips if patients are immobilized for 6 weeks postoperatively. We expect excellent results in more than 90% of cases with no low back pain and unrestricted activity at a minimum of 2-year follow-up.
Surgical intervention for adult athletes with isthmic spondylolisthesis is indicated if after 6–12 months of conservative management symptoms have not been reduced enough to maintain quality of life. Persistent radicular or claudicatory symptoms or ongoing neurologic deficit are also indications.
Low-grade slips are treated with an instrumented L5–S1 posterolateral fusion with iliac crest bone grafting. If preoperative studies indicate significant degenerative disc disease at the adjacent segment, consideration for extension of the fusion to include that segment should be given. A decompressive procedure should be added if radicular or claudicatory symptoms are present.
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Figure 7-9. Lateral radiograph of the lumbosacral spine demonstrating Grade III isthmic spondylolisthesis before (A) and after (B) posterior instrumented fusion with pedicle screw instrumentation. |
High-grade slips are treated with an instrumented L4–S1 posterolateral fusion with iliac crest bone grafting. Improved outcomes of surgery for adult isthmic spondylolisthesis have been associated with the achievement of a solid fusion. Interbody fusion techniques (anterior, posterior, and transforaminal lumbar interbody fusion) have been shown to improve fusion rates in isthmic spondylolisthesis. However, differences in clinical outcome between posterolateral fusion only and posterolateral plus interbody fusion procedures have not been demonstrated.
Return to Play
Few guidelines exist regarding return to play after lumbar fusion surgery in adolescents. A recent survey of surgeons in the Scoliosis Research Society revealed that about 50% do not permit return to noncontact activities for 6 months postoperatively. One-third of surgeons allow return to collision sports at 1 year. Sixteen percent do not allow athletes with low-grade slips to return to collision sports. Twenty-five percent of surgeons do not allow athletes with high-grade slips to return to collision sports. Unrestricted return to sports is possible in athletes with a stable fusion and who are fully rehabilitated without symptoms at 1 year.
There are currently no reports of return to competitive sports after lumbar fusion procedures in adults. Of concern is the risk of adjacent segment degeneration in
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this population. Adult athletes should be encouraged to participate in exercises for cardiovascular fitness, however, return to contact sports is not recommended.
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