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THE SPINE AND SPORTS

PREFACE

WILLIAM C. LAUERMAN, MD Guest Editor

It was indeed my pleasure to accept Dr. Millers invitation to put together an issue of Clinics in Sports Medicine dealing with spinal disorders and injury in athletes. I hope the reader will be pleased with the variety of topics presented, all dealing with either common or potentially very serious injuries or conditions involving athletes. The issue leads off with Dr. Robert McAlindon reviewing appropriate initial evaluation and treatment of athletes who have sustained a head and/or neck injury during competition. This is an up-to-date review dealing with one of the few times that orthopaedic surgeons come into contact with potentially lifethreatening injuries. Drs. Allen and Kang have contributed a manuscript on transient quadriparesis in the athlete. This overview brings us up to date on current thinking in terms of etiology, treatment, and return-to-play considerations. Drs. Brian Shannon and Klimkiewicz have contributed a very thorough review dealing with the subjunctive cervical burners in athletes. This is a common condition, relatively poorly understood and claried greatly, I believe, by this article. Drs. Greg Sassmannshausen and Smith have helped out with a discussion of what I believe to be one of the most difcult patient populations to treat, the young athlete with back pain. Their common sense approach to evaluation and management, I am quite sure, will be extremely helpful. Dr. R. Lane Wimberly and I have reviewed the all too common cause of back pain, spondylolisthesis in the athlete. We are then fortunate enough to have Dr. Kirkham Wood from the University of Minnesota and the Twin City Spine Center, who has reviewed the topic of spinal deformity, both scoliosis and kyphosis in the adolescent athlete. Dr. Robert Watkins has provided an overview of lumbar disc injuries in athletes and Dr. Anthony Delitto discusses for us the subject of low back rehabilitation in the athlete. Finally, Drs. Trainor and Wiesel review the epidemiology of low back pain in the athlete. Hopefully, this collection of articles will prove both entertaining and educational. There is much new information regarding etiology, evaluation, and treatment for many of these conditions and I hope that this issue of Clinic in Sports ix

Medicine will provide a valuable reference for physicians treating both adolescent and adult athletes. WILLIAM C. LAUERMAN, MD Guest Editor

Georgetown University Hospital 3800 Reservoir Rd., NW Washington, DC 20007

PREFACE

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ON FIELD EVALUATION AND MANAGEMENT OF HEAD AND NECK INJURED ATHLETES


Robert J. McAlindon, MD

All physicians who care for athletes must be able to recognize, evaluate, treat, and help to prevent recurrent head and neck trauma. The return of the injured athlete to collision sports is a complex issue. Careful evaluation of all injuries should be done on an individual basis. HEAD INJURIES The scalp, skull, meninges, and cerebral spinal uid form a multilayered barrier that protects the brain from injury. The brain in competitive athletics is injured in one of two ways. In one type of injury, an object strikes the resting, but movable, head, causing injury at the site of the impact. This is called a coup lesion. In another type, the moving head strikes a nonmoving object and produces an injury to the brain in an area opposite to the site of the impact. This is the so-called contrecoup lesion. Each mechanism is capable of generating rotational (angular) or translational (linear) forces through the brain tissue. Rotational forces produce a shearing mechanism across the nerve bers, commonly leading to a loss of consciousness. Translational forces lead to compression that can cause a skull fracture, hematoma, or cerebral contusion, but less frequently to a loss of consciousness. The brain tolerates compressive stresses better than shearing stresses. Cerebral spinal uid and the elastic properties of the brain tissue make the brain somewhat able to be compressed and therefore resistant to translational forces. Shear force

From the The Hughston Clinic, PC, Auburn, Alabama

CLINICS IN SPORTS MEDICINE


VOLUME 21 NUMBER 1 JANUARY 2002

McALINDON

travels parallel to the surface of the brain and imparts a linear zone of injury. The degree of head injury is related to the position and motion of the head at the time of impact. Classication of Head Injuries Head injuries can be broadly classied as focal or diffuse. Focal brain injuries are cerebral contusions or hematomas that result from translational energy. A diffuse brain injury, especially a concussion, occurs as the result of rotational energy and is associated with global disruption of neurologic function. A diffuse brain injury often is not associated with visible or objective brain lesions. Focal Brain Injuries Focal brain injuries include cerebral contusions, in which a small, illdened area of hemorrhage or edema is noted, and often are the result of a contrecoup-type lesion (Fig. 1). Intracerebral hematomas occur within the brain. The site and location of the hematoma determine symptoms.

Figure 1. Types of focal brain injury: subdural hematoma, hemorrhage in the subdural space between the dura and arachnoid membrane; epidural hematoma, accumulation of blood in the epidural space owing to damage in the middle meningeal artery; and intracerebral hematoma, hemorrhage in to the cerebrum. (Adapted from Jacko JG: Head injuries. In Baker CL [ed]: The Hughston Sports Medicine Book. Philadelphia, Williams & Wilkins, 1995, pp 112117; with permission.)

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES

Epidural hematomas result from a tear commonly of the middle meningeal artery. A rapidly expanding hematoma may prove to be life threatening by causing brain herniation. Subdural hematomas occur when the bridging veins between the brain and dura are torn. Nausea, vomiting, and seizures may ensue as an enlarging hematoma causes a slowly enlarging mass and pressure on the brain. Diffuse Brain Injuries Of all head injuries, a concussion is the most common. Sometimes, it is the most difcult to recognize. It is estimated that 250,000 concussions occur in the United States in football alone each year.5 Twenty percent of high school football players suffer concussions each year, and the chance of sustaining a second concussion is ve times higher than that of sustaining the rst. Contact with articial turf appears to be associated with more serious concussions. Only approximately 9% of concussions involve loss of consciousness. Eighty-six percent involve headaches. Thirty percent of football players who sustain concussions return to play the same day.12 The complexity of the brain and the lack of objective signs and symptoms in some patients make injury assessment difcult. Signs and symptoms present at the time of injury may quickly resolve, but the injury may be life threatening. Despite the use of protective equipment, the head and brain are susceptible to injury during athletic competition. Attempts to characterize and classify concussions have been difcult. Early detection by recognizing the signs and symptoms of concussion is critical to managing the head-injured athlete. Neural Biology Concussion is dened as a clinical syndrome characterized by immediate and transient post-traumatic impairment of neural function, such as alteration of consciousness, and disturbance of vision or equilibrium, because of brain stem involvement. However, we continue to lack a complete understanding of the pathology of a concussion. No objective neural, anatomic, or physiologic measurements can be used to assess the severity of a concussion. The athlete can remain in a state of viability after a concussion and therefore is susceptible to second-impact syndrome during this variable time period.7, 19, 23 In addition, the cumulative effects of injury remain a concern.11 It is now known that a metabolic disturbance arises in the damaged brain tissue.3 There is a notable increase in demand for glucose and a reduction in blood ow. This results in inability of the brain tissue to respond to increasing demands for energy. Neural tissue demands more fuel but is limited in its capacity to obtain it. The duration of this disturbance may be related to the duration of symptoms and, more importantly, the period of vulnerability to second impact. Calcium, he-

McALINDON

mostasis, or regulation may play a role in the posttraumatic cerebral blood ow, as well, with vasoconstriction present with high-calcium values.29 On-Field Evaluation Being prepared for head injuries is the key to on-eld management. In the event of an injury, the equipment needed to evaluate and, if necessary, to transport the injured athlete must be available. The most important objective of on-eld management is to prevent further injury. First, an accurate and complete diagnosis of the level of consciousness and evaluation of associated injuries, such as cervical spine injuries, must be obtained. When approaching an injured player, the examiner should observe the posture of the athlete and note any spontaneous motion or verbalization. Total lack of movement may alert the medical team to a potential spine injury. Incoherent or confused speech suggests a signicant concussion. Athletes with closed head injuries frequently have a blank expression and may appear confused or demonstrate inappropriate verbiage. The Glascow coma scale can provide insight into the level of consciousness (Table 1).29 A grade of 11 or higher on the coma scale is generally associated with an excellent prognosis for recovery. A

Table 1. GLASGOW COMA SCALE* Response Eye opening Spontaneously To verbal command To pain None Verbal Oriented, converses Disoriented, converses Inappropriate words Incomprehensible No response Motor Obeys verbal commands Localizes to painful stimuli Flexion withdrawal Abnormal exion Extension No response Point/s 4 3 2 1 5 4 3 2 1 6 6 4 3 2 1 Action Reticular activity system is intact; patient may not be aware Opens eyes when told to do so Opens eyes in response to pain Does not open eyes to any stimuli Relatively intact central nervous system; aware of self and environment Well articulated and organized, but disoriented Random, exclamatory words Moaning; no recognizable words No response or intubated Readily moves limbs when told to Moves limb in an effort to avoid pain Pulls away from pain in exion Decorticate rigidity Decerebrate rigidity Hypotonic, accid; suggests loss of medullary function or concomitant cord injury

*Normal, 15. From Wojtys EM, Hovda D, Landry G, et al: Concussion in sports. Am J Sports Med 27:676686, 1999; with permission.

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES

score of 7 or less is, of course, considered serious. The eye motions, verbal cues, and motor competency can be used to rapidly determine the initial severity of an injury. Retrograde amnesia is an important factor to test for. The presence of a headache, dizziness, and blurred vision should also be determined. After an associated spine injury has been ruled out and the level of consciousness is appropriate, the athlete may then be assisted into a sitting position. It is believed that a seated or standing position will help diminish intracranial pressure and help alleviate some symptoms. Once stable and seated, the athlete may be assisted to a standing position and helped off the eld. Bench Evaluation After the player is removed from the eld of play, a more thorough examination is begun.29 Dizziness, vertigo, double or blurred vision, photophobia, ringing in the ears, headache, and nausea can then be assessed. Vomiting is rare but may be present and should be a cause for concern. Careful inspection and palpation of the head should be undertaken at this time. A visual acuity examination should be done, and the presence of nystagmus should be noted. Nystagmus can indicate a rotational brain injury. A baseline neurologic examination with sensation and strength testing of the extremities must also be done. If initial ndings are abnormal, frequent re-examinations must be done to document progression of symptoms. Initially the player must be observed for 15 minutes on the sidelines. If any symptoms persist, return to play on the same day is not recommended. Maneuvers, such as a 40-yard dash, sit-ups, or deep squats, that increase intracranial pressure may help elicit some symptoms. If symptoms are present during these maneuvers, the player should not return to competition. If a player who is asymptomatic and has no difculty with maneuvers that increase intracranial pressure subsequently returns to play, he or she must be re-evaluated during the contest to detect any clinical changes. An athlete who develops seizures, focal neurologic signs, or deterioration in mental status should be transported to an appropriate medical facility. Concussion Grading The traditional concussion grading scale was introduced by Cantu.5 The grade of concussion represents severity of the brain injury and is based on the level of consciousness and duration of memory loss. Patients with grade 1 concussions have no loss of consciousness and memory loss of less than 30 minutes. Patients with grade 2 concussions have loss of consciousness of less than 5 minutes and memory loss lasting up to 24 hours. Patients with grade 3 concussions have loss of

McALINDON

consciousness of more than 5 minutes and memory loss exceeding 24 hours. In 1991, The Colorado Medical Society developed a grading system.8 According to its system, patients with mild concussions exhibit confusion but no amnesia and no loss of consciousness. Moderate concussions are characterized by amnesia as well as confusion. Loss of consciousness characterizes a severe concussion.10 In a recent study by Guskiewicz, 59% of collegiate and high school athletes with head injuries demonstrated mental confusion.13 Ninety-six percent had headaches. Thirty-two percent of these athletes had confusion lasting more than 10 minutes. Nine percent of their series demonstrated loss of consciousness. Disorientation and visual changes occurred much more frequently than amnesia. For athletes who had had multiple concussions, the injury severity increased with the number of recurrent injuries. In 1983, Gerberich found that an athletes risk for suffering a second concussion injury was four times greater than an athletes with no history of concussion.10 Return to Play Determining when an athlete can return safely to competition after an injury is one of the most controversial issues in sports medicine. It should be recognized that some symptoms, such as amnesia and headache, are sometimes delayed. In general, if the athlete has any symptoms on the eld that are related to the concussion, he or she should not be allowed to return to play. The sport itself should not be a determining factor with respect to return-to-play issues. All concussions warrant monitoring for at least 15 minutes. If, after 15 minutes, if there has been no loss of consciousness and all signs and symptoms are normal, participation may resume. If residual symptoms remain, the athlete should be disqualied for that days competition. Only after the athlete has become asymptomatic, has passed memory testing, and has no symptoms with provocative testing, can he or she be returned to play. The injured athlete must be continually monitored throughout the remainder of the event. The stress of the competition can produce signs and symptoms not seen off the eld. Any episodes of loss of consciousness, no matter how brief, should preclude return to play at that time. Reportedly, 30% of high school and collegiate football players return to participation on the same day of injury.13 Of these players, 14 had grade 2, or moderate, concussions. The players who returned to play on the same day were held out for only an average of 13 minutes. The remaining 70% of football players with concussions were held out an average of four days for a mild grade 1 concussion, and those with grade 2 injuries returned to play 8 days after injury. Twenty percent of players with concussions do not leave the game because the symptoms were either not reported or not identied until after the competition ended.

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES

Many authors have warned against the dangers involved in returning to athletics too early,5, 8, 9, 16, 17, 27 but many times these warnings are ignored. If an athlete returns to play on the same day, he or she must be asymptomatic for at least 15 minutes both at rest and during exertion. He or she must have a normal neurologic examination, and certainly have had no loss of consciousness at any time. Delayed return to play is reserved for athletes who are not asymptomatic within 15 minutes or who develop symptoms or worsening signs on exertion. Any loss of consciousness precludes play on the same day. Ninety-six percent of athletes have a headache at some point after the concussion. Any new headache after 48 hours or a change in the character of the headache warrants further medical evaluation. Dizziness, slowing of response, difculty concentrating, or memory loss precludes participation at any time. An athlete who feels ne is not necessarily normal. It is not known how quickly brain healing occurs after neural function returns to normal. The absence of neural cognitive decit is used to judge return-to-play criteria but does not necessarily relate to the brain-healing process. Symptoms that last more than 15 minutes preclude same-day play, but exact guidelines regarding play after a longer period of symptoms are not yet dened. Five to 7 days of rest may benet some athletes, whereas others may be able to play much sooner. Our current medical knowledge does not address this situation. CERVICAL SPINE INJURIES Each year, more than 1,000,000 students participate in high school football and 200,000 in collegiate and professional football. Cervical spine injuries occur in 10% to 15% of football players.1, 2 Most of these injuries are self-limiting, and a full recovery can be expected. In 1976, Albright found that 50% of incoming freshman football players with a previous neck injury had radiographic changes in their cervical spine that indicated instability, compression fracture, or neural arch derangement.1 Although relatively uncommon, a neck injury can be devastating. Proper and prompt management is absolutely essential. The spacial and geometric orientation of the cervical facet joints allows a high degree of mobility, and this mobility allows for a high degree of injury. Soft-tissue injuries including muscle, ligament, and tendon injuries occur frequently as well. The cervical spine comprises the rst seven vertebrae of the spinal column. C1, or the atlas, is essentially a ring without a vertebral body. It articulates with the base of the skull by means of two synovial joints formed with the occipital condyles. C2, or the axis, includes a true vertebral body and an upward projection, the dens, that articulates with C1. A strong ligamentous component maintains structural integrity and alignment between C1 and C2. This anatomy allows a high degree of mobility and rotation. Fifty percent of cervical spine rotation occurs at the C1-C2 articulation. The remaining 50% of rotation occurs over the

McALINDON

inferior ve segments, C3 through C7. The spinal cord is protected within the spinal canal. Paired laminae provide the roof of the canal. There are two facet articulations at each level oriented obliquely to provide stability in the anterior-posterior direction. Each vertebral body is separated from the adjacent body by an intervertebral disc made up of a semisolid nucleus pulposus contained within a brous annulus. Anterior and posterior ligaments connect the vertebral bodies and provide structural support to the cervical spine (Fig. 2). The muscles may be broadly grouped into those of the posterior cervical spine that extend the head and neck, those of the lateral cervical spine that function in rotation and lateral exion, and those of the anterior cervical spine that ex the head and neck. The spinal cord is a continuation of the central nervous system and is widest in the midcervical region. The cervical spine injury that occurs most frequently in football players is neurapraxia of the nerve roots or brachial plexus. As many as 50% of linemen, linebackers, and defensive ends have one or more episodes per season.26 Stingers or burners are caused by compressive or traction injuries to the multiple roots or the brachial plexus itself. The upper roots or trunk are stretched by a shoulder depression and lateral head exion away from the involved side. Neurapraxia can also be caused by direct compression of the brachial plexus. Athletes may complain of a multitude of ndings. Careful examination is required to prevent attribution of a burning or stinging sensation to a benign condition when, in fact, it may be the result of a much more serious problem.

Figure 2. The ligaments of the upper cervical spine (Adapted from Kelley LA: Functional anatomy of the spine. In Baker CL [ed]: The Hughston Sports Medicine Book. Philadelphia, Williams & Wilkins, 1995, pp 17383; with permission.)

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES

Most often, stingers or burners are unilateral in nature. The presence of symptoms in both upper extremities suggests a spinal cord rather than a nerve root or plexus injury. The athlete may complain of a dead arm with shoulder or arm pain and unilateral muscle paresis. Symptoms are generally self-limiting, and strength usually returns within 24 to 48 hours. A variable degree of weakness in the muscles innervated by the specic portion of plexus or trunk that is irritated can last up to 6 weeks, and certainly permanent changes may be seen as well in severe cases. Examination of the cervical spine should be free of any painful palpation. There should be no midline tenderness over the bony architecture. Range of motion should be basically normal with the exception of some muscle spasm that may cause some tightness to rotation as well as exion and extension, but overall the arc of motion should be quite normal. If symptoms resolve quickly and the neurologic examination is otherwise normal, once full motor strength returns the patient may be allowed to return to play. Persistence of symptoms or lack of pain-free range of motion with palpable pain over the bony architecture requires further evaluation and cervical spine radiographs. The player should be restricted from further play until he or she has recovered full muscle strength. Stingers and burners may be preventable by working on tackling technique. Certainly, the head up position must be maintained. Cervical collars or shoulder pad orthotics can also help with prevention of burners and stingers. Intervertebral Disc Lesions Acute traumatic herniation of a disc with resultant cord compression can result in transient quadriplegia or permanent quadriparesis or quadriplegia. Affected athletes experience bilateral pain, numbness, and tingling in the extremities. In severe cases, paralysis may be noted. Immediate transport to an appropriate medical facility, radiographs, and further imaging, such as computed tomography or magnetic resonance imaging, may be warranted. Decompression by discectomy and interbody fusion may be warranted in patients with symptoms of persistent radiculopathy or myelopathy. Transient Quadriplegia Transient quadriplegia is caused by neurapraxia of the cervical cord.25 The symptoms include bilateral burning pain, tingling, and loss of sensation in the arms or legs. Motor symptoms vary from mild weakness to complete paralysis. Episodes are transient, and complete recovery usually occurs within 10 to 15 minutes, but it can take as long as 48 hours. Radiographs are negative for fractures or dislocations but frequently reveal congenital stenosis. Cord compression without residual radiographic abnormality may

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occur by means of a pincer-like mechanism. When the cervical spine is hyperextended, the cord is compressed between the inferior margin of the superior vertebra and the anterior and superior laminae of the subjacent vertebra. The posterior longitudinal ligament and ligamentum avum may become infolded and contribute to the central canal narrowing. Athletes with congenital or acquired cervical stenosis are predisposed to cord neurapraxia with hyperextension or hyperexion loading. Stenosis is dened on the basis of a diameter in which the cervical canal is believed to be narrow.21 To assess for narrowing, the canal diameter is measured on a lateral radiograph from the midpoint of the posterior aspect of the vertebral body to the nearest point along the spinolaminar line. The normal midsagittal diameter should be between 14 mm and 23 mm. Stenosis is dened on the basis of a diameter of less than 13 mm. Variations and technique as well as lm distances and anatomy often contribute to inaccurate measurements. To minimize these areas, Torg and Pavlov proposed using a ratio of the segmental sagittal diameter of the canal to the width of the vertebral body (Fig. 3).24 A ratio of less than 0.8 has been used to dene canal stenosis. It has been found that 93% of players with transient quadriplegia, 12% of asymptomatic nonathletes, and 48% of asymptomatic football players have spinal stenosis. A threefold increase in the incidence of stingers has also been noted in athletes with spinal stenosis.4 Unstable Cervical Fractures Most patients with football-related spinal cord injuries have had concomitant unstable fractures and dislocations. Through the late 1960s

Figure 3. The Torg ratio is calculated by dividing the shortest distance between the posterior vertebral body and the spinolaminar line (a) by the vertebral body width (b). (Adapted from Torg JS, Pavlov H: Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med 6:115133, 1987; with permission.)

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES

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and early 1970s, the incidence of severe head injuries decreased, whereas the incidence of severe cervical spine injuries increased.27 The act of tackling by defensive players was associated with the greatest risk of injuries that resulted in quadriplegia.27 Most catastrophic events resulted from either a combined fracture dislocation or anterior compression fracture. Improvements in helmet design and construction have decreased head injuries, but as athletes have become stronger, faster, and more agile, the cervical spine has been placed at substantial risk of injury. Tackling techniques such as using the head as a spear also increase the risk of catastrophic cervical spine injury.6 Axial loading of the cervical spine is the primary mechanism for severe neck injuries.26 The cervical spine can absorb much of the energy of collision by dissipation through the paravertebral musculature, the intervertebral discs, and the normal lordotic curve of the cervical spine. When the neck is exed beyond 30 degrees, the normal lordotic curve is attened and forces applied along the top of the head are now directed into a straight column (Fig. 4).28 In this position, the cervical spine is much less able to disperse the forces that are being exerted. With continuing load, compression forces occur within the vertebral disc causing irregular deformation and buckling. Intervertebral disc pathology may occur. Eventually, should the force continue, the spine fails in exion with a resultant fracture or dislocation. Although axial loading accounts for most fracture dislocations, it does not account for all patterns. A

Figure 4. A, When the neck is in a normal, upright, anatomical position, the cervical spine is slightly extended because of the natural cervical lordosis. B, When the neck is slightly exed to approximately 30, the cervical spine is straightened and converted into a segmented column. (Adapted from Torg JS, Vegso JJ, ONeill MJ, et al: The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 18:5057, 1990; with permission.)

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combination of rotation and compression can produce a variety of recognized spinal injuries. A couple of motions can lead to extensive injury. Flexion, extension, rotational, and shear forces within adjacent regions of the cervical spine can place the cervical spinal cord at risk. Field Evaluation And Early Treatment Initial involvement of the sports medicine physician in the care of an athlete with a cervical spine injury begins on the eld. Essential sideline equipment should include a stretcher, tools necessary to remove a face mask, a spine board, and airway protective equipment. Preparedness is paramount to timely management. It is necessary to remove the face mask for airway control of the unconscious athlete while simultaneously protecting the cervical spine.20 In general, newer cage-type masks are removed by cutting the plastic attachment loops with a scalpel or utility knife. Most of these masks are also held on with a series of screws that can easily be removed by using Phillips head screwdrivers. The chin strap and helmet are best left in place. Spinal malalignment is noted when the shoulder pads are left in place and the football helmet is removed. Recent studies have also shown that hockey helmets that are removed while leaving the shoulder pads in place also cause spinal malalignment.18 In general, it is probably safest to leave the helmet in place while protecting the airway after facemask removal. The jaw-thrust technique is probably safe as well in providing and maintaining good airway alignment. Transportation to a medical facility is necessary for any athlete with mental status changes, neck pain or tenderness, limited cervical motion, and symptoms referable to a cord injury. The patient must be fully immobilized on a spine board with the helmet and shoulder pads remaining in place. The helmet should be removed only when permanent mobilization in a controlled setting can be instituted after lateral cervical spine radiographs have been taken. Only at that time should the chin strap be removed, the ear aps of the helmet spread, and the helmet gently pulled in line with the cervical spine while the head is supported under the occiput. Return To Play Sideline evaluations are often a difcult matter. The player must be examined to determine the specic location of pain, the presence of numbness, tingling, or weakness, and the duration of symptoms. Again, a complete motor and sensory neurologic evaluation of the upper and lower extremities should be performed. Mental status should also be evaluated at this time. An athlete with tenderness over bony prominences must have radiographic documentation of normality before returning to play. Any signs or symptoms of neurologic decit on both sides of the body should

ON FIELD EVALUATION AND MANAGEMENT OF INJURED ATHLETES

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preclude return to play for the same day as well. Transient unilateral mild numbness and tingling that resolves quickly, as in the situation of a stinger or burner, may not preclude a players return to play. In general, when normal pain-free motor strength and normal sensation return, these athletes can be allowed to return to competition. The return of the injured athlete to collision sports is a complex issue. Each athlete must be evaluated carefully on an individual basis. Frequent serial examinations are necessary to help guide the physician in his or her treatment regimen. Although the decision to allow an athlete to return to play after some injuries can be complicated and equivocal, the medical sequelae of certain cervical spine injuries are absolute contraindications to a return to contact sports. Neck injuries that result in permanent central nervous system dysfunction, permanent and signicant peripheral nerve dysfunction, and spinal fusion at the C4 level or above are examples of such contraindications. Anatomic abnormalities such as spinal stenosis are relative contraindications to an athletes to return to play even after a full clinical recovery.

References
1. Albright JP, McAuley E, Martin RK, et al: Head and neck injuries in college football: An eight-year analysis. Am J Sports Med 13:147152, 1985 2. Albright JP, Moses JM, Feldick HG, et al: Nonfatal cervical spine injuries in interscholastic football. JAMA 236:12431245, 1976 3. Bergsneider M, Hovda DA, Shalmon E, et al: Cerebral hyperglycolysis following severe traumatic brain injury in humans: A position emission tomography study. J Neurosurg 86:241251, 1997 4. Bruce D, Schut L, Sutton L: Brain and cervical spine injuries occurring during organized sports activities in children and adolescent. Clin Sports Med 1:495514, 1982 5. Cantu RC: Guidelines for return to contact sports after cerebral concussion. Physician Sportsmed 14:7583, 1986 6. Cantu RC, Mueller FO: Catastrophic spine injuries in football (19771989). J Spinal Disord 3:227231, 1990 7. Cantu RC, Voy R: Second impact syndrome: A risk in any contact sport. Physician Sportsmed 23:172177, 1995 8. Colorado Medical Society. Report of the Sports Medicine Committee: Guidelines for the Management of Concussion in Sports (revised). Denver, Colorado Medical Society, 1991 9. Evans RW: The postconcussion syndrome: 130 years of controversy. Semin Neurol 14: 3239, 1994 10. Gerberich SG, Priest JD, Boen JR, et al: Concussion incidences and severity in secondary school varsity football players. Am J Public Health 73:13701375, 1983 11. Gronwall D, Wrightson P: Cumulative effects of concussion. Lancet 2:995997, 1975 12. Guskiewicz KM, Perrin DH, Gansneder BM: Effect of mild head injury on postural stability in athletes. J Athl Train 31:300306, 1996 13. Guskiewicz K, Weaver NL, Padua DA: Epidemiology of concussion in collegiate and high school football players. Am J Sports Med 28:643650, 2000 14. Jacko JG: Head injuries. In Baker CL (ed): The Hughston Sports Medicine Book. Philadelphia, Williams & Wilkins, 1995, pp 112117 15. Kelley LA: Functional anatomy of the spine. In Baker CL (ed): The Hughston Sports Medicine Book. Baltimore, Williams & Wilkins, 1995, pp 17383 16. Kelly JP, Nichols JS, Filley CM, et al: Concussion in sports: Guidelines for the prevention of catastrophic outcome. JAMA 266:28672869, 1991

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17. Kelly JP, Rosenberg J: Diagnosis and management of concussion in sports. Neurology 48:575580, 1997 18. LaPrade RF, Schnetzler KA, Broxterman RJ, et al: Cervical spine alignment in the immobilized ice hockey player. A computed tomographic analysis of the effects of helmet removal. Am J Sports Med 28:800803, 2000 19. McCrory PR, Berkovic SF: Second impact syndrome. Neurology 50:677683, 1998 20. Palumbo MA, Hulstyn MJ, Fadale PD, et al: The effect of protective football equipment on alignment of the injured cervical spine: Radiographic analysis in a cadaveric model. Am J Sports Med 24:446453, 1996 21. Pavlov H, Torg JS, Robie B, Jahre C: Cervical spinal stenosis: Determination with vertebral body ratio method. Radiology 164:771775, 1987 22A. Robertson WC Jr, Eichman PL, Clancy WG: Upper trunk brachial plexopathy in football players. JAMA 241:14801482, 1979 23. Saunders RL, Harbaugh RE: The second impact in catastrophic contact sports head trauma. JAMA 252:538539, 1984 24. Torg JS, Pavlov H: Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med 6:115133, 1987 25. Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:13541370, 1986 26. Torg JS, Sennett B, Vegso JJ, et al: Axial loading injuries to the middle cervical spine segment: An analysis and classication of twenty-ve cases. Am J Sports Med 19: 620, 1991 27. Torg JS, Truex R Jr., Quedenfeld TC: The national football head and neck injury registry: Report and conclusions 1978. JAMA 241:14771479, 1979 28. Torg JS, Vegso JJ, ONeill MJ, et al: The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 18:5057, 1990 29. Wojtys EM, Hovda D, Landry G, et al: Concussion in sports: Am J Sports Med 27: 676686, 1999 Address reprint requests to Dr. McAlindon at The Hughston Clinic, PC 161 E. University Drive Auburn, AL 36832 e-mail: auburn@hughston.com

THE SPINE AND SPORTS

02785919/02 $15.00 .00

TRANSIENT QUADRIPARESIS IN THE ATHLETE


Christina R. Allen, MD, and James D. Kang, MD

SYNOPSIS Transient quadriparesis is a rare cervical spine injury caused by axial loading of the neck in extension or exion. Transient quadriparesis is associated with sensory or motor functional changes or a combined sensorimotor decit. The athlete may complain of total body numbness and moderate to severe weakness in all four extremities. The episodes, by denition, are not permanent, and complete sensory and motor recovery occurs in 10 minutes to 48 hours. In all cases of the above phenomenon, radiographs are negative for fractures and dislocations but frequently demonstrate evidence of congenital spinal stenosis, acquired stenosis, cervical instability, or congenital abnormalities such as KlippelFeil syndrome. A considerable amount of controversy exists regarding return-to-play criteria and the risk for more severe injury after an athlete experiences an episode of transient quadriparesis. Introduction One of the most disturbing and dramatic clinical syndromes associated with cervical spine injury in athletics is transient quadriparesis. Also referred to as transient neurapraxia and cervical cord neurapraxia, transient quadriparesis may be considered a concussion of the cervical spinal cord. It was perhaps rst described in 1879 by Obersteiner when

From the Division of Sports Medicine (CRA), Division of Spine Surgery (JDK), Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania

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he used the term spinal cord concussion to describe spinal cord injuries that resulted in complete neurologic recovery in 24 to 48 hours.17 The phenomenon, although rare in incidence, has been noted to occur most frequently in football athletes, but also has been documented in athletes participating in boxing, hockey, basketball, and wrestling,21 generally as the result of axial loading of the neck in extension or exion. Transient quadriparesis is associated with sensory or motor functional changes, or a combined sensorimotor decit. Sensory changes include burning pain, numbness, tingling, and sensory losses. Motor changes range from weakness to complete paralysis of both the upper and lower extremities. The athlete may complain of total body numbness and moderate to severe weakness in all four extremities. The episodes, by denition, are not permanent, and complete sensory and motor recovery occurs in 10 minutes to 48 hours.5, 20, 21 Except for burning paresthesias, neck pain is not present at the time of injury, and there is complete return of full, pain-free cervical motion. A variant of this phenomenon, described by Maroon, is burning hands syndrome. Thought to be a mild form of central cord syndrome, burning hands syndrome causes burning dysesthesias and weakness of the hands and arms. An anteroposterior compressive force causes an injury to the corticospinal and spinothalamic tracts. Most symptoms resolve within 24 hours, but the athlete may demonstrate reversible abnormalities on magnetic resonance imaging and electrophysiologic studies.10, 11 In all cases of the above phenomenon, radiographs are negative for fractures and dislocations, but frequently demonstrate evidence of congenital spinal stenosis, acquired stenosis, cervical instability, or congenital abnormalities such as Klippel-Feil syndrome. As a result of an NCAA football study performed by Torg in 1984, the incidence of transient quadriparesis has been estimated at 1.3 episodes of transient weakness with paresthesias per 10,000 athletes, with an additional estimated incidence of 6 episodes of transient paresthesias alone per 10,000 athletes.21 MECHANISM AND PATHOPHYSIOLOGY The pathophysiology of transient quadriparesis is not entirely understood. It is believed to be a neurapraxia, implying that the injury is caused by a physiologic conduction block that causes peripheral nerve axon dysfunction without anatomic disruption. This conduction block is usually caused by compression or contusion, resulting in segmental demyelination and prolongation of the absolute refractory periods of long-tract axons. This increases the time during which axons are unresponsive to subsequent stimulation, resulting in a postconcussive effect.8, 31 Torg has postulated that disruption of cord function is a result of the effects of local cord anoxia and the increased concentration of intracellular calcium. He performed experiments involving the mechanical deformation of squid axons and determined that recovery of neuro-

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logic function is directly proportional to the intracellular calcium concentration, which is directly proportional to the amount and rate of tension applied to the axon.25 The spinal cord is narrower in the anterior-posterior direction than in the transverse plane and is most susceptible to congenital narrowing between the third and fth cervical vertebrae. As previously mentioned, the mechanism of injury in transient quadriparesis has been documented to be an axial load applied to the cervical spine while held in extension or exion. The greatest dynamic compression of the spinal cord occurs with hyperextension because it is known to produce maximal narrowing (up to an additional 2 mm) of the anterior-posterior diameter of the spinal canal,4 thereby placing athletes with acquired or congenital cervical stenosis at increased risk for cord injury. Penning has described the pincer mechanism effect of hyperextension on the cervical spinal cord.13, 25 During hyperextension, the distance decreases between the posterior-inferior aspect of the superior vertebral body and the anteriorsuperior aspect of the spinal laminar line of the subjacent vertebra (Fig. 1). The cord is therefore pinched between the processes of the two opposing bodies, with the degree of compression dependent of the sagittal diameter of the canal, the degree of extension, the presence of spondylitic degenerative spurs, and the infolding of soft tissues such as the ligamentum avum and posterior-longitudinal ligaments. In fact, Taylor reported that infolding of the laminar ligaments during hyperextension might decrease canal size an additional 30%.3, 4, 18 Conversely, in hyperexion, the distance decreases between the spinal laminar line of the superior vertebra and the posterior superior aspect of the body of

Figure 1. Hyperextension pincer mechanism, as described by Penning. During hyperextension, the distance decreases between the posterior inferior aspect of the superior vertebral body and the anterior superior aspect of the spinal laminar line of the subjacent vertebra (double-headed arrow). The cord is, therefore, pinched between the processes of the two opposing bodies.

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the subjacent vertebra. In each hyperextension or hyperexion scenario, a rapid decrease in sagittal diameter occurs, with resultant compression of the spinal cord.13 CERVICAL STENOSIS The sagittal diameter of the cervical spinal canal is cited as a signicant predictor of acute and chronic neurologic dysfunction.2, 4, 7, 29 However, a considerable amount of controversy and opinion exists regarding whether the presence of cervical stenosis makes an athlete more prone to sustaining permanent neurologic injury or transient quadriparesis.2, 15, 16, 20, 22, 23 Traditionally, the anteroposterior diameter of the spinal canal (measured from the posterior aspect of the vertebral body to the most anterior point on the spinal laminar line) was determined from lateral cervical spine radiographs and used to determine the presence of spinal stenosis (measurement A in Fig. 2A, 13 mm in Fig. 2B ). The accepted opinion is that between C3 and C7, anteroposterior canal dimensions of more than

Figure 2. A, Lateral cervical spine radiograph. The space between the midpoint of the posterior cortex of the vertebral body anteriorly and the spinolaminar line posteriorly (A) is the sagittal width of the spinal canal. The Pavlov ratio represents the ratio of the width of the spinal canal (A) to the width of the vertebral body (B, or A:B). B, Lateral cervical spine radiograph demonstrating a 13 mm width of the spinal canal at C6, and a corresponding Pavlovs ratio of 13:22 or 0.59. Additionally, the lms demonstrate evidence of absolute stenosis at the C5 level, with a canal diameter of 12 millimeters.

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15 mm are normal, whereas cervical stenosis is present if the canal diameter is less than 13 mm.7, 21, 30 The variability of technique used and the structural anatomy of the subject can signicantly affect the quality of measurement of cervical spine canal dimensions determined from lateral cervical spine radiographs. Variations in landmarks used for measurement, changes in target distances for making the radiographs, positioning of the neck while the radiograph was taken, differences in the triangular cross-sectional shape of the canal, and magnication of the canal because of a patients large body habitus all may affect canal measurements. Herzog demonstrated that athletes with large shoulders might have a magnication factor of up to 21% (versus the standard 10%15% in the general population) on lateral radiographs of the cervical spine.6 In an effort to eliminate the variability in absolute measurements caused by confounders such as body habitus, Torg and Pavlov designed a ratio method for determining the presence of cervical stenosis. They compared the sagittal diameter of the spinal canal to the sagittal midbody diameter of the vertebral body at the same level, designating a normal Pavlov ratio as 1:1 (Fig. 2). Torg and Pavlov further asserted that a Pavlov ratio of less than 0.8 indicates signicant cervical stenosis.12, 21 In contrast, Herzog actually demonstrated a high correlation coefcient when comparing plain lm sagittal measurements adjusted for magnication to those measured from a midline sagittal computed tomography image. The plain lm canal size measurements were more accurate than those obtained from magnetic resonance images. He also made note of the high sensitivity but low positive predictive value of the Pavlov ratio in predicting the true presence of spinal stenosis.6 In his study, 41% of the professional football players tested had a Pavlov ratio 0.80 but a normal developmental sagittal diameter of the cervical spinal canal. Herzog proposed that screening players with the Pavlov ratio might result in labeling many athletes as stenotic when they have adequately sized canals but large vertebral bodies. He stated that the Pavlov ratio should be utilized as a screening tool for spinal stenosis when one does not have knowledge of the magnication factors needed to determine the true developmental sagittal diameter. Many authors have pointed out the utility of computed tomography myelograms, plain lm myelography, and magnetic resonance imaging in determining the hidden impact of ligamentous hypertrophy and disk protrusion on spinal canal size, what some authors refer to as functional spinal stenosis (Fig. 3).3, 14 Although more accurate and indicative of all potentially compressive structures and effects within the spinal canal, these studies are more costly and difcult to institute as potential screening tools. RISK OF INJURY In 1996, Torg published his results on the evaluation of 45 athletes who experienced transient quadriparesis during athletic participation.

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Figure 3. MR image demonstrating the presence of critical cervical stenosis in a 25-yearold patient. The coexistence of bulging/herniating disks at C3-4, C4-5, and C5-6 would be considered a relative contraindication to participating in contact sports by Torgs standards.

By his criteria, 42 of 45 athletes (93%) had cervical stenosis at one spinal level or more or a Pavlov ratio of 0.80 or less.20 Of note, these same athletes had a mean anteroposterior canal diameter of 15.3 mm, considered to be a low-normal dimension by current standards, but not stenotic. In contrast, 41% and 42% of asymptomatic college and professional football athletes tested met Pavlovs criteria for cervical stenosis, and their average canal sagittal diameters were greater than 18 millimeters at each level. The incidence of stenosis by absolute criteria and the Pavlov ratio in Torgs control non-athlete group was not delineated, but the average canal sagittal diameter was greater than 18 mm at each level, and the average Pavlov ratio was well over 0.95 at each cervical level. In Torgs previous study published in 1986, only two of 49 control subjects had a Pavlov ratio of 0.80, in contrast to 17 of 24 athletes showing radiographic evidence of stenosis who experienced an episode of transient quadriparesis.21 Applying his 1996 data to the results of his 1984 study that demonstrated an incidence of transient neurapraxia (sensory and/or motor changes) of 7.3 per 10,000 athletes who played football, Torg estimated that the positive predictive value of having a Torg ratio less than 0.80 and subsequently experiencing an episode of

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transient neurapraxia is 0.2%.20, 21 Torg concluded that a Pavlov ratio of 0.80 in an asymptomatic athlete should not preclude participation in contact sports, and he recommended against screening with plain radiographs to assess for stenosis and suitability for play in contact sports. Torgs 1996 study also involved interviews and radiographic examination of 77 individuals who were permanently quadriplegic as a result of an injury while playing high school or college football. Interestingly, this cohort demonstrated a mean Pavlov ratio of more than 0.90, and an average canal size of 18.9 mm. Torg argued that a smaller mean anteroposterior diameter would be an expected nding in this group of permanently quadriplegic patients if developmental narrowing of the spinal canal played an important role in the etiology of their permanent neurologic decits.20 In fact, data collected revealed that the anteroposterior dimensions of the vertebral bodies in this group were signicantly smaller than those of the asymptomatic athletes and those athletes who experienced an episode of transient neurapraxia, indicating that catastrophic neurologic injury may result from collapse or fracture of a proportionally smaller vertebral body that fails during axial loading. He also noted that none of the 77 individuals interviewed recalled having an episode of transient neurapraxia before their catastrophic injury, and none of the 45 athletes who experienced transient neurapraxia episodes ever became quadriplegic. Given all of these factors combined, Torg felt that developmental narrowing of the cervical canal in a spine that has no evidence of instability is neither a predictor of nor a contributor to permanent neurologic injury. In further support of his research, Torg has more recently published statistics on 110 cases of cervical cord neurapraxia caused by a sportsrelated injury. In this study, 36% of athletes experienced transient paralysis, 26% transient weakness, and 38% experienced sensory changes only. Symptoms tended to last less than 15 minutes (73% of athletes), but some lasted more than 24 hours (10%). The average Pavlov ratio was 0.69, with an average canal diameter measured by magnetic resonance imaging of 9.6 millimeters.19 Of the 65% of athletes who returned to their sport, 56% experienced a recurrent episode of transient quadriparesis. The risk of recurrence increased with a smaller Pavlov ratio, a smaller disk-level canal diameter, and less space available for the cord. Cervical cord neurapraxia was not associated with permanent neurologic injury, and no permanent morbidity occurred in patients who returned to contact sports. He therefore reiterated that individuals with cervical stenosis who experience an episode of uncomplicated cervical cord neurapraxia could be allowed to return to play without an increased risk of permanent injury, but they may have recurrent episodes of neurapraxia.19, 23 Although Torg believes that cervical stenosis in the absence of instability or degenerative changes is not a rm contraindication to continued participation in contact sports, there are others with an opposing viewpoint. Specic details are not available on his series of patients,

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but Schneider asserted that he had treated a large group of athletes who sustained neck injuries resulting in permanent neurologic decits and were later found to have cervical stenosis.15, 16 Cantu also strongly asserts that athletes with documented spinal stenosis should not participate in collision sports, citing the works and recommendations of Penning, Eismont, Wolfe, and Ladd and Scranton.2, 4, 9, 39 Cantu reports that, unlike Torg, he has seen permanent quadriplegia occur in a stenotic patient after an initial episode of transient quadriplegia without fracture or dislocation.2 Additionally, Cantu states that in the data from the National Center for Catastrophic Sports Injury, cases of quadriplegia without spine fracture have been seen only when functional spinal stenosis is present and that the complete neurologic recovery rate after cervical spine fracture/dislocation is 0% when cervical stenosis is present, compared to 21% in the absence of stenosis.2, 3

EVALUATION An evaluation of athletes who have experienced an episode of transient quadriparesis includes obtaining a complete history and physical. The history may be helpful in delineating the occurrence of previous neck injuries or episodes of transient quadriparesis, as well as clarifying the mechanism of injury. A complete and thoroughly documented neurologic exam is mandatory because it will be used to document the progress of neurologic recovery and serve a role in determining when an athlete may return to play. Radiographic evaluation includes anteroposterior, lateral, oblique, and open-mouth odontoid views. Because the superior endplate of T1 is often difcult to see radiographically in this patient population, axial computed tomography scanning with 3-mm cuts may be necessary to evaluate any areas not adequately visualized on plain radiographs. Dynamic exion-extension radiographs may be helpful in evaluating cases of suspected ligamentous instability but should be obtained only when the patient can actively perform the maneuvers while supervised by a physician. Instability is dened as radiographic evidence of more than 3.4 millimeters of translation in the anteroposterior direction or 11 degrees of angulation in the sagittal plane between two adjacent vertebrae.21, 28 The radiographs are closely inspected for evidence or fracture, instability, congenital or developmental stenosis, spondylosis, or congenital abnormalities (Klippel-Feil syndrome, odontoid agenesis or hypoplasia, developmental os odontoidium, spina bida occulta). Radiographic evaluation frequently leads to the discovery of one of these abnormalities in the patient who has experienced an episode of transient quadriparesis.21 Any athlete with a documented history of transient quadriparesis or an abnormal neurologic exam after a suspected episode is evaluated with magnetic resonance imaging to rule out ongoing extrinsic cord or

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nerve root compression (herniated disk), intrinsic cord abnormalities, or evidence of ligamentous injury. Electromyographic or nerve conduction studies may be helpful in some cases to differentiate a brachial plexus traction injury from radiculopathy. Somatosensory-evoked potentials may be useful in documenting physiologic cord dysfunction, which may preclude a return to sports.2 Herzog designed an algorithm for assessment of symptomatic athletes with cervical stenosis as determined by their developmental sagittal diameter. He believed that the symptomatic athlete with a developmental sagittal diameter 12.5 mm should be further evaluated with a functional magnetic resonance imaging study to determine the size of the spinal cord and to assess the functional reserve of the spinal canal. Additionally, exion-extension radiographs should be obtained on all symptomatic athletes (whether or not they meet the criteria for stenosis) to assess spinal stability. If horizontal translation exceeded 3 mm, a functional magnetic resonance imaging study should also be performed. The main aim of testing is to determine the impact of a small developmental sagittal diameter or instability on the functional reserve of the spinal canal.6, 13

RETURN-TO-PLAY CRITERIA There is a general consensus that an athlete should be completely asymptomatic with a normal sensory and motor neurologic examination and a full, painless range of motion of the cervical spine before returning to his or her sport. The main controversy involves the disposition of the athlete with imaging abnormalities such as evidence of instability, disk herniation, congenital or developmental stenosis, congenital abnormalities (Klippel-Feil syndrome, odontoid agenesis or hypoplasia, os odontoidium, spina bida occulta), or spear tacklers spine. Torg recently recommended guidelines for the management of athletes with documented spinal stenosis who participate in contact sports.23 He stated that an asymptomatic athlete with a Pavlov ratio of 0.8 or less has no contraindications to play. However, in slight contrast to his comments in earlier publications, Torg considered a Pavlov ratio of 0.8 or less with one episode of cervical cord neurapraxia a relative contraindication to return to play. Documented episodes of cervical cord neurapraxia associated with intervertebral disk disease and/or degenerative changes was also considered a relative contraindication to returning to play. A single documented episode of cervical cord neurapraxia associated with magnetic resonance imaging evidence of a cervical cord defect or cord edema was considered a relative or absolute contraindication to return to play, evaluated on a case-by-case basis. Finally, cervical cord neurapraxia associated with ligamentous instability, neurologic ndings or symptoms lasting more than 36 hours, or multiple

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episodes of neurapraxia are considered to be absolute contraindications to return to sport. As delineated in a previous section, Cantu believes that the athletes with documented cervical stenosis should not engage in collision sports such as football because he feels they are predisposed to both transient quadriparesis and permanent neurologic injury. If a patient without documented evidence of cervical stenosis experiences an episode of transient quadriparesis, Cantu states that return to play is probably safe in the absence of spinal stenosis, bony or ligamentous injury, and if no evidence of spinal cord injury exists. A second incident of transient quadriparesis should initiate a repeat full evaluation including radiographs and magnetic resonance imaging. If tests are all normal, the player may return to sport, with full consideration given to limiting participation in contact sports, given the recurrence of symptoms.2 Watkins created a scoring system to determine whether athletes experiencing an episode of transient quadriparesis should be allowed to return to play.27 Points are assigned based on the athletes symptoms or measurements in three categories: extent of neurologic decit, duration of symptoms, and severity of cervical stenosis. The sum of points is utilized to determine the players risk for cervical spine injury. Bailes has categorized sports-related cervical spine injuries into three groups, which provides useful information when making returnto-play decisions.1, 11, 26 Type I injuries involve a permanent spinal cord injury (major decits), or a minor neurologic injury associated with spinal cord hemorrhage, cord contusion or swelling as demonstrated on magnetic resonance imaging. Athletes with Type I injuries should not be allowed to return to contact sports. Type II injuries, specically transient quadriparesis or burning hands syndrome, are transient neurologic decits. As dened previously, radiographic studies show no evidence of fracture or instability. Magnetic resonance imaging studies show no evidence of cord lesion. Return to play is permissable if neurologic symptoms fully resolve and there is truly no evidence of radiographic abnormality, including instability, stenosis, fracture, or congenital abnormalities. Patients with recurrent episodes of transient quadriparesis should be restricted from participation in contact sports. Individuals with type III injuries comprise a heterogeneous group of athletes with solely radiographic or imaging abnormalities, including fractures, fracture-dislocations, pure ligamentous and soft-tissue injuries, and herniated disks. The neurologic exam of the athlete is normal. Because of the variety of injury types or abnormalities in this group, the decision about whether an athlete can return to play must be determined on a case-by-case basis, primarily by considering how stable the injury will be when the athlete is subjected to large forces during contact play. Those with signicant bony or ligamentous injury or spinal cord contusion should be advised not to return to contact sports. Disruption of the anterior and posterior elements or evidence of ligamentous instability prohibits further participation.28 Players with stable healed fractures (lamina fractures, spinous process fractures, minor vertebral body fractures) should be evaluated for stability using exion-extension radio-

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graphs before return to play. Any individual requiring atlantoaxial fusion caused by fracture or ligamentous instability should be restricted from contact sports. Relative contraindications to return to sport include healed non-displaced Jefferson fractures, type I and II odontoid fractures, and asymptomatic lateral mass fractures.23 There are several congenital anomalies of the cervical spine that are absolute contraindications to continued participation in contact sports. The presence of odontoid agenesis, odontoid hypoplasia, or os odontoidium is an absolute contraindication to participation in collision sports because small injury to weakened or compromised structures may result in marked C1-2 instability and neurologic injury. Additionally, the presence of a congenital atlantooccipital fusion is an absolute contraindication to participation in contact sports.22, 24 Torg has subdivided congenital Klippel-Feil deformities into two types. A type I Klippel-Feil deformity is a mass fusion of the cervical or upper thoracic vertebrae. It constitutes an absolute contraindication to participation in contact sports because spinal mechanics are altered, predisposing the patient to injury. A type II Klippel-Feil deformity is a fusion of only one or two interspaces. In this group, if a player has signs of limited cervical spine motion, instability, disk disease, or spondylosis, contact sports participation should be precluded. In contrast, there is no contraindication to participation of an asymptomatic athlete with a type II Klippel-Feil deformity involving interspaces at C3 and below with an absence of other cervical spine abnormalities.22 SPEAR TACKLERS SPINE There is one special subset of football players who merit special discussion. Torg in 199324 identied a group of athletes who are at high risk for cervical quadriplegic injury because of their habits when playing football. He identied 15 athletes from the National Football Head and Neck Injury Registry who sustained a cervical spine injury and demonstrated ndings of congenital cervical stenosis (Pavlov ratio of 0.8 or less), persistent straightening or reversal of the normal cervical lordotic curve on radiographs, radiographic evidence of pre-existing posttraumatic cervical spine abnormalities, and a history of using speartackling techniques. These athletes chronically employed the technique of spearing while performing tackles (using the top of the helmet to ram the opponent in the chest or back). This method of applying repetitive axial loads to a straightened cervical spine can result in developmental stenosis, loss or even reversal of the normal lordotic curve of the cervical spine, compression fractures, disk bulging or herniation, or ligamentous instability. Dubbed by Torg spear tacklers spine, it is an absolute contraindication to continued participation in contact sports. Four of the 15 athletes examined sustained permanent neurological injury.24 Torg determined that axial loading applied to the straightened cervical spine resulted in permanent spinal cord injury in these athletes. With the neck slightly exed and its lordotic curve straightened, the

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cervical spine becomes a segmented column. Axial loads (spearing) impair bending, and the energy of impact is directly transmitted to the spinal structures, to the point that the spine may buckle in exion with large enough axial loads. Fractures, dislocations, and neurologic injury may result if the axial load is not absorbed by controlled motion in the spinal segments.24 As mentioned previously, because of the potential for sustaining catastrophic neurologic injury, Torg recommended that athletes with the syndrome of spear tacklers spine be withheld from participation in contact sports. However, Torg recognized that return to play could be considered if the loss of cervical lordosis was reversible and if the athlete could be trained to employ proper and safe tackling techniques.24

SUMMARY A considerable amount of controversy persists regarding return-toplay criteria and the risk for more severe injury after an athlete experiences an episode of transient quadriparesis. Similarly, the implication of the presence of congenital stenosis in an athlete participating in contact sports elicits great debate in the literature in terms of the athletes risk for neurologic injury. The relatively infrequent occurrence rate of both transient quadriparesis and permanent cervical cord injury make it difcult to predict with certainty whether or not an episode of transient quadriparesis is a risk factor for permanent neurologic injury. The decision-making process in determining player eligibility in the face of congenital stenosis or after a documented spinal injury is difcult and at times confusing. Every injury and athlete should be evaluated on an individual basis in terms of cause, symptoms, radiographic ndings, and previous history. It is hoped that the guidelines for return-to-play delineated in this article will help the physician and the athlete make an informed and rational decision regarding the criteria for and relative risks of returning to participation in a contact sport.

References
1. Bailes JE, Hadley MN, Quigley MR, et al.: Management of athletic injuries of the cervical spine and spinal cord. Neurosurgery 29:491497, 1991 2. Cantu RC: Stingers, transient quadriplegia, and cervical spinal stenosis: Return to play criteria. Med Sci Sports Exerc 29(suppl):S233S235, 1997 3. Cantu RC, Bailes JE, Wilberger JE: Neurologic athletic head and neck injuries: Guidelines for return to contact or collision sport after a cervical spine injury. Clin Sport Med 17:137146, 1998 4. Eismont FJ, Clifford S, Goldberg M: Cervical sagittal spinal canal size in spinal injury. Spine 9:663666, 1984 5. Engle CA, Kang JD, Lauerman WC: Cervical stenosis in the athlete. Op Techniques Orthopaed 5:218222, 1995 6. Herzog RJ, Wiens JJ, Dillingham MF, et al: Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players: Plain lm

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7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31.

radiography, multiplanar computed tomography, and magnetic resonance imaging. Spine 16(suppl 6):S178S186, 1991 Kang JD, Figgie MP, Bohlman HB: Sagittal measurements of the cervical spine in subaxial fractures and dislocations. An analysis of 288 patients with and without neurological decits. J Bone Joint Surg Am 76:16171628, 1994 Kline DG, Hudson AR: Acute injuries of peripheral nerves. In Youmans (ed): Neurological Surgery. Philadelphia, WB Saunders, 1990, pp 24232510 Ladd AL, Scranton PE: Congenital cervical stenosis presenting as transient quadriplegia in athletes: Report of two cases. J Bone Joint Surg Am 68:13711374, 1986 Maroon JC: Burning hands in football spinal cord injuries. JAMA 238:20492051, 1977 Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21:22942299, 1996 Pavlov H, Torg JS, Robie B, et al: Cervical spinal stenosis: Determination with vertebral body ratio method. Radiology 164:771775, 1987 Penning L: Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology 12:513519, 1962 Resnick D: Degenerative disease of the spine. In Diagnosis of Bone and Joint Disorders. Philadelphia, WB Saunders, 1981, pp 14081415 Schneider RS: Serious and fatal neurological football injuries. Clin Neurosurg 12: 226236, 1966 Schneider RS, Reifel E, Grisler H: Serious and fatal football injuries involving the head and spinal cord. JAMA 177:362367, 1961 Sonntag VKH, Hadley MN: Nonoperative management of cervical spine injuries. Clin Neurosurg 34:630649, 1988 Taylor AR: The mechanism of injury to the spinal cord in the neck without damage to the vertebral column. J Bone Joint Surg Br 33B:543547, 1951 Torg JS, Corcoran TA, Thibault LE, et al: Cervical cord neurapraxia: Classication, pathomechanics, morbidity, and management guidelines. J Neurosurg 89:687690, 1997 Torg JS, Naranja RJ, Pavlov H, et al: The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players: An epidemiological study. J Bone Joint Surg Am 78:13081314, 1996 Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:13541370, 1986 Torg JS, Ramsey-Emrhein JA: Management guidelines for participation in collision activities with congenital, developmental, or post-injury lesions involving the cervical spine. Clin Sport Med 16:501530, 1997 Torg JS, Ramsey-Emrhein JA: Suggested management guidelines for participation in collision activities with congenital, developmental, or postinjury lesions involving the cervical spine. Med Sci Sports Exerc 29(suppl):S256S272, 1997 Torg JS, Sennett B, Pavlov H, et al: Spear tacklers spine: An entity precluding participation in tackle football and collision activities that expose the cervical spine to axial energy inputs. Am J Sports Med 21:640649, 1993 Torg JS, Thibault L, Sennett B, et al: The pathomechanics and pathophysiology of cervical spinal cord injury. Clin Orthop 321:259269, 1995 Warren WL, Bailes JE: Neurologic athletic head and neck injuries: On the eld evaluation of athletic neck injury. Clin Sport Med 17:99110, 1998 Watkins RG, Dillin WH, Maxwell J: Cervical spine injuries in football players. Spine State Art Rev 4:391408, 1990 White AA, Johnson RM, Panjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 109:8596, 1975 Williams JP: Biomechanical factors in spinal injury. Br J Sports Med 14:14, 1990 Wolfe BS, Khilnani M, Malis L: The sagittal diameter of the bony cervical spinal canal and its signicance in cervical spondylosis. J Mount Sinai Hosp 23:283292, 1956 Zwimpfer TJ, Bernstein M: Spinal cord concussion. J Neurosurg 72:894900, 1990 Address reprint requests to James D. Kang, MD Associate Professor, Department of Orthopaedic Surgery University of Pittsburgh Medical Center 3471 Fifth Avenue Suite 1010 Pittsburgh, PA 15213

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CERVICAL BURNERS IN THE ATHLETE


Brian Shannon, MD, and John J. Klimkiewicz, MD

Approximately 1.2 million high school athletes and 200,000 college and professional athletes participate in American football each year.13 For the thousands of physicians responsible for the medical care of these athletes, no situation is fraught with more danger or elicits more anxiety than that of the injured player who demonstrates symptoms consistent with spinal cord dysfunction. Neck injuries have been perennial problems in American football. Nineteen instances of death or paraplegia in 1904 prompted Theodore Roosevelt to demand either an end to the brutality involved in football or elimination of the game. Roosevelts demands resulted in the formation of the National Collegiate Athletic Association.1 Since that time, safety of the athlete has continued to be of primary importance in the evolution of American football. In 1973, Schneider stated that The football elds of our nation have been a vast proving ground or laboratory for the study of the tragic neurologic sequelae of head and neck trauma in man. These concerns were taken to heart, and at the conclusion of the 1975 football season, governing bodies at both the interscholastic and the intercollegiate levels outlawed the use of the helmet or facemask in blocking and tackling (NCAA rule 99-1-2-N and 0-1-2-1 and National Federation of High School Athletic Association rule 9-3-2-k and 9-3-1). Furthermore, in 1977 and 1980 additional rule changes were implemented, allowing offensive players to use their hands and arms to block. These changes appear to have been followed by a reduced incidence of catastrophic injuries because there have been less than 10 catastrophic spinal injuries reported since the implementation of these changes in the years 19771990.1, 6
From the Department of Orthopaedic Surgery, Division of Sports Medicine, Georgetown University Medical Center-MedStar Health, Washington, DC

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Statistics of catastrophic injury, however, are not reective of the more common stingers and neck sprains. The stinger syndrome represents one of the most common injuries seen in tackle football. The stinger syndrome or burner is thought to be caused by trauma to the brachial plexus and/or nerve roots. The injury most typically is characterized by unilateral shoulder and/or arm pain with burning dysesthesias and often muscle weakness involving the biceps, deltoid, and spinatus muscles. Because the pain, paresthesias, and weakness typically last only a few seconds or minutes, these injuries often go unreported to medical staff. The transient nature of these symptoms have classied these neurologic injuries into the category of a neuropraxia.18 The actual incidence of these injuries may in fact approach 50% to 65% of college football players throughout a 4-year collegiate career.17 Persistent sensory changes are rare with these injuries. The subjective manifestations are usually short lived, but in some instances weakness may persist for days to weeks. Prolonged weakness, when present, is generally found in the deltoid, biceps, and spinatus muscles. Overall, 5% to 10% of these injuries are more serious, presenting with a neurologic decit lasting several hours or longer.2, 19 Those injuries with neurologic disturbances lasting more than 2 weeks represent examples of greater stretch to the brachial plexus resulting in axonotmesis as described by Seddon.18 The differential diagnosis for these athletes include cervical radiculopathy, cord contusion, and brachial plexus injury. When considering these other possibilities, a variant injury described by Torg and colleagues known as transient quadriplegia represents a neurapraxia at the level of the cervical spinal cord.20 This syndrome differs from cervical burners in that it represents injury to the actual spinal cord. It often involves bilateral upper extremity and lower extremity neurologic involvement with no associated fracture or dislocation, and usually resolves within 36 hours. The incidence of transient quadriplegia, or cervical cord neuropraxia, has been estimated to be 7.3 per 10,000 football participants. MECHANISM OF INJURY Based on the typical clinical presentation of cervical burners, general consensus is that the C5-C6 nerve distributions are the most commonly affected, which would implicate either the root level or a brachial plexus upper trunk lesion as a cause for the symptoms. Initially, Clancy et al characterized the pathology in cervical burners as occurring at the brachial plexus level, secondary to traction mechanisms.7, 17 Although others have supported this mechanism as the etiology for some cervical burners, controversy has arisen about the potential for a cervical root injury secondary to compression at this level as an additional explanation for these injuries.4, 11, 14, 16, 17 In Meyers study of 40 collegiate and professional players with stingers, 34 (85%) had extension-compression mechanisms thought to involve the nerve root, whereas only six (15%) athletes had

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brachial plexus stretch mechanisms.14 Similiary, Levitz et al characterized neck extension combined with ipsilateral-lateral deviation as the mechanism in 83% of patients presenting with chronic or recurrent burners. In this series, the pathology was thought to occur at the nerve root level based on clinical examination and roentgegnographic work-up.11 Finally, a third potential causative mechanism thought to result from direct trauma of the shoulder pads to the brachial plexus has been proposed.12 Neither of the previous two reports mentioned this mechanism as an explanation for the stingers. These somewhat conicting studies concerning both the mechanism and point of injury in cervical stingers leaves three main hypothetic mechanisms to explain stingers or transient neuropraxia in this population: (1) nerve root compression in the neural foramen (extension-compression), (2) Brachial plexus stretch (traction injuries), and (3) A direct blow to the plexus (Fig. 1). Cervical hyperextension with or without concomitant lateral exion is thought to compress or pinch the nerve root at the interverteral foramen. Extension-compression burners occur in more mature athletic populations (collegiate and professional). They are generally associated with pre-existing radiologic evidence of cervical disk disease or arthritic change. These patients usually exhibit a positive Spurlings test on physical examination indicating compression at the nerve root level. A study conducted by Watkins and Odor focused on 12 professional and

Figure 1. Proposed areas of brachial plexus involvement with different mechanisms of cervical burners. A, Extension-ipsilateral compression. B, Flexioncontralateral exion (traction) or direct trauma. (Modied from Grants Atlas of Anatomy Williams & Wilkins, 1983, 8th Edition.)

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several intercollegiate football players who had a mechanism of extension and ipsilateral compression.23 These players had the severest symptoms of those studied. They attributed the symptoms to injury of the nerve root at the intervertebral foramen. Brachial plexus stretch or traction injuries occur if the head is forced away from the symptomatic side with concomitant ipsilateral shoulder depression. These injuries occur more commonly in younger athletes without cervical stenosis or degenerative changes of the cervical spine. Spurlings test is usually negative. Sallis stated that lateral neck exion with contralateral shoulder depression was the mechanical stimulus for a traction injury to the plexus most commonly at the C5-C6 level. This is the most frequent mechanism cited in the literature as cause of these injuries.7, 17, 19 The third mechanism of compression of the xed brachial plexus between the shoulder pads and the superior medial scapula that can occur when the pad is pushed into the area of Erbs point, where the brachial plexus is most supercial has been described by Markey et al.12 ROLE OF CERVICAL STENOSIS The signicance of cervical spinal stenosis in this active population has long been a topic of debate. Several investigators have noted an association of cervical spinal stenosis and burner syndrome. Meyer et al noted an incidence of 47% of spinal stenosis on the University of Iowa football team in players who sustained a cervical burner compared to only 25% in assymtomatic players.14 Players with this condition were thought to have a threefold increased risk of sustaining a stinger than those without cervical stenosis. Similarly, Kelley et al reported an association between cervical stenosis and this syndrome.10 These investigators have proposed that a narrowed canal with accompanying shortened pedicles leads to narrow neural foramina increasing the risk of burners caused by nerve root compression. The actual denition of what constitutes cervical spinal stenosis in this population and how it is measured continues to evolve as different theories about its association with cervical burners continues to develop. The most commonly employed method for determining the sagittal diameter of the spinal canal is measuring the distance from the middle of the posterior surface of the vertebral body to the nearest point of the corresponding spinal laminar line on the lateral radiograph. The use of the actual measurement in millimeters on the lateral view of the cervical spine to document spinal stenosis can be misleading, and the dimensions considered to be signicant vary as reported in the literature.5, 9 The second method, designated as the Pavlov ratio or ratio method, compares the sagittal spinal canal diameter measured from the posterior surface of the vertebral body to the nearest point of the corresponding spinal laminar line, with the sagittal diameter of the corresponding vertebral body measured at its midpoint.15 When Torg compared actual measure-

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ments, as previously described, with the ratio method, the ratio method was more then 2.5 times as sensitive as the conventional method with use of a cutoff value of 0.82 representing signicant stenosis. There was a 92% accuracy rate compared with a 62% accuracy rate with the conventional method.21 The Pavlov ratio has proven to be a reliable tool for determining cervical spinal stenosis and is independent of technical factor variables. However, the main criticism of using this method in this athletic population lies in the fact that these individuals usually are larger in size than the general population with inordinately larger vertebral bodies. This may generate falsely low values overstating the signicance of spinal stenosis in this population.8, 10 Although the previously mentioned studies have demonstrated a potential for cervical stenosis to contribute to cervical stingers in a classic sense, one should be aware of relationship of this phenomenon with cervical cord neuropraxia. Torg et al compared football players at different skill levels to a control group of 105 nonathletes to determine the relationship, if any, between a developmentally narrowed cervical canal and reversible and irreversible injury of the cervical cord. A Pavlov ratio of 0.80 or less had a high sensitivity (93%) for transient neurapraxia. The low positive predictive value of this ratio (.02%), however, precludes its use as a screening mechanism for determining the suitability of an athlete for participation in contact sports.21 These authors concluded from this analysis that symptoms may result from a transient reversible deformation of the spinal cord in a developmentally narrowed osseous canal, yet developmental narrowing of the cervical canal in a stable spine did not appear to predispose an individual to permanent catastrophic neurologic injury, and therefore should not preclude an athlete form participation in contact sports. TREATMENT Treatment issues are often difcult decisions as a result of the transient nature of the majority of these episodes, yet the substantial potential risk associated with cervical spine injuries. Criteria involving a return to play after a cervical burner emphasize a complete and thorough physical examination. In addition to an intact neurologic exam focusing on normal strength and sensation within the upper extremities, the cervical spine exam must be normal. Cervical range of motion, head compression test, Spurling and Adsons maneuvers, and resistive head pressures should all be within normal limits. Watkins states criteria for removing a player form a game usually involve two predominant ndings.23 First is any radiating arm pain and neurologic decit that can be an indicator of a more serious problem, and second is a nding of loss of cervical range of motion, because many times unstable cervical spine lesions without a neurologic decit may present only with loss of cervical range of motion. Any positive ndings as listed above mandate removal from compe-

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tition and further evaluation.3, 22, 23 Watkins in his experience with professional, collegiate, and high school football players noted that when the symptoms persist, the numbness usually settles into the C6 area of the index nger and thumb, whereas the initial weakness presents in shoulder abduction and wrist and thumb extension.23 The player classically holds himself with a head-forward posture and stiff neck and attempts to avoid any extension and rotation. Once the symptoms persist emphasis should be placed on the chestout posturing and thoracic outlet obstruction exercises. The chest-out posturing produces three effects: (1) it opens the intervertebral foramina to its maximum size, (2) it reduces the effect of the weight of the head as the head is brought back over the body in this position, and (3) it opens the thoracic outlet by changing the alignment of the scalene muscles and the clavicle relative to the neck. A stoop-shoulder, headforward posture will cause the symptoms of brachial plexus irritation to persist. Neck strengthening and stretching is also important component of therapy. Neck isometrics should be done with the head in the midline position, and resisting forces should be applied perpendicularly to the head from every direction. Emphasis has also been placed on midline stretching through a full range of motion. Electrodiagnostic studies have been performed on cases in which the symptoms have persisted. Continued muscular weakness at 72 hours after the actual injury seems to correlate with positive electrodiagnostic testing performed at 4 weeks.19 These ndings at 4 weeks from the time of injury have been shown to persist at up to 4 years from the time of the initial event in up to 80% of the cases studied; however, clinically these ndings have not contributed to substantial strength decits or limitation of function.4, 19

PREVENTION OF BURNERS The primary equipment needed to prevent burners includes wearing properly tting shoulder pads.23 Shoulder pads should accomplish four basic functions: (1) absorb shock, (2) protect the shoulders, (3) t the chest, and (4) x the mid cervical spine to the trunk. A proper shoulder pad should encompass many of the qualities of a well-tted cervicothoracic orthosis. Important characteristics of a proper shoulder pad include a modied A-frame shape, rm circumferential xation to the chest, and xation of the neck to the chest by the t of the shoulder pad at the base of the neck. Thick, comfortable, stiff pads at the base of the neck are essential. It is this support laterally at the base of the neck that offers xation to the cervical spine. A common method of adapting pads is to add lifters and neck rolls. The lifters provide a pad at the base of the neck that can provide additional support, whereas the neck rolls attempt to limit compression but are often compromised in their function by poorly tted shoulder pads.

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References
1. Albright JP, McAuley E, Martin RK, et al: Head and neck injuries in college football: An eight-year analysis. Am J Sports Med 13:147152, 1985 2. Archambault JL: Brachial plexus stretch injury. J Am Coll Health 31:256260, 1983 3. Bailes JE, Hadley MN, Quigley MR, et al: Management of athletic injuries of the cervical spine and spinal cord. Neurosurgery 29:491496, 1991 4. Bergfeld, JA Hershman E, Wilbourne A: Brachial plexus injury in sports: A ve-year follow up. Orthop Trans 12:743744, 1988 5. Boijsen E: Cervical spinal canal in intraspinal expansive processes. Acta Radiol 42: 101115, 1954 6. Cantu RC, Mueller FO: Catastrophic spine injuries in football. J Spinal Disord. 3: 227231, 1990 7. Clancy WG, Brand RL, Bergfeld JA: Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 5:209216, 1977 8. Herzog RJ, Wiens JJ, Dillingham MF, Sontag MJ: Normal cervical spine morphometry and cervical spine stenosis in asymptomatic professional football players. Spine 16: 51785186, 1991 9. Hinck VC, Hopkins CE, Savara BS: Sagittal diameter of the cervical spinal canal in children. Radiology 79:97108, 1962 10. Kelly JD, Aliquo D, Sitler MR, et al: Association of burners with cervical canal and formaminal stenosis. Am J Sports Med. 28:214217, 2000 11. Levitz CL, Reilly PJ, Torg JS: The pathomechanics of chronic, recurrent cervical root neuropraxia: The chronic burner syndrome. Am J Sports Med 25:7376, 1997 12. Markey KL, DiBenedetto M, Curl WW: Upper trunk brachial plexopathy: The stinger syndrome. Am J Sports Med 21:650655, 1993 13. Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21:22942298, 1996 14. Meyer SA, Schulte KR, Callaghan JJ, et al: Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med 22:158166, 1994 15. Pavlov H, Torg JS, Robie B, Jahre C: Cervical spinal stenosis: determination with vertebral body method. Radiology 164:771775, 1987 16. Rockett FX: Observations on the burner. Traumatic cervical radiculopathy. Clin Orthop 164:1820, 1982 17. Sallis RE, Jones K, Knopp W: Burners: Offensive strategy for an under-reported injury. Physician Sportsmed 20:4755, 1992 18. Seddon H: Surgical Disorders of the Peripheral Nerves. Edinburgh, Churchill Livingstone, 1992 19. Speer KP, Bassett FH: The prolonged burner syndrome. Am J Sports Med 18:591594, 1990 20. Torg JS, Corcoran TA, Thibault LE, et al: Cervical cord neuropraxia: Classication, pathomechanics, morbidity, and management guidelines. J Neurosurg 87:843850, 1997 21. Torg JS, Naranja RJ, Pavlov H, et al: The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players. J Bone Joint Surg 78A:13081314, 1996 22. Warren WL, Bailes JE: On the eld evaluation of athletic neck injury. Clin Sports Med 17:99110 23. Watkins RG: Neck injuries in football players. Clin Sports Med 5:215246, 1986 Address reprint requests to John J. Klimkiewicz, MD Department of Orthopaedic Surgery Georgetown University Medical Center-MedStar Health 3800 Reservoir Road NW Washington, DC 20007

THE SPINE AND SPORTS

02785919/02 $15.00 .00

CERVICAL DISC DISEASE IN THE ATHLETE


Steven C. Scherping, Jr, MD

In the medical literature, considerable attention has been devoted to the evaluation and management of athletes with a traumatic cervical spine injury.10, 15 Similarly, great emphasis has been placed on determining appropriate guidelines for participation in contact sports in athletes with a cervical spinal stenosis.13, 14 Both of these topics are addressed elsewhere in this issue. In contrast, comparatively little focus has been directed at the topic of cervical disc disease in the athlete. The notable exception is cervical disc disease that results in a signicant spinal stenosis. Though cervical disc disease is a frequent cause of pain and disability in the general population, it tends to predominately afict those that are in their mid-30s and older, and is thus a less frequent problem in the younger athletic population.8 Nevertheless, as all age groups are at some risk, even the well-conditioned young athlete is not immune to the problem. As the age of the athlete increases, so too does the incidence of symptomatic cervical disc disease. Moreover, it should be recognized that some sporting activities, particularly football and wrestling, likely increase the incidence of cervical disc disease over the lifetime of the high-performance athlete.1 For these reasons, it is important that all clinicians providing medical care for athletes have an understanding of the clinical syndromes and sequelae of cervical disc disease. The purpose of this article is to review the basic principles of cervical disc disease, and to outline strategies for the evaluation and treatment of this disorder. It is also intented to outline some guidelines regarding the difcult return to play decision for athletes with cervical disc disease.

From the Georgetown University Hospital, Washington, DC

CLINICS IN SPORTS MEDICINE


VOLUME 21 NUMBER 1 JANUARY 2002

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PATHOPHYSIOLOGY Cervical disc disease is a common cause of neck, shoulder, and brachial pain in the adult population. The prevalence of neck pain in the adult population is estimated to be 9%.9 Cervical disc disease is largely responsible for the frequent complaint of neck pain. Most acute disc herniations occur posterolaterally and involve the C5-C6 and C6C7 levels, followed by the C4-C5 level. Disc herniations at C3-C4 and C7-T1 are appreciably less frequent, and disc herniations at C2-C3 are quite rare. The levels that are most prone to acute disc herniations are similarly subject to the onset of the more chronic, degenerative process of cervical spondylosis. Cervical disc disease can be thought of as consisting of two basic forms, commonly referred to as soft-disc and hard-disc disease. Although the underlying pathophysiology may be similar, the clinical expression of these two forms of cervical disc disease may be quite different. The terminology soft-disc disease is used when there is an acute herniation of the gelatinous nucleus pulposus into or through the annulus of the cervical disc. Such an event is typically accompanied by acute neck pain and paraspinal muscular spasm, with or without radiating periscapular or arm pain. Associated neurologic signs and symptoms may accompany the acute event. The clinical hallmark of soft-disc disease is the absence of previous or more chronic symptoms of neck or arm pain. Patients with an acute soft-disc herniation tend to be younger and are more likely, although by no means consistently, to have an identiable event leading to symptom onset. This event may be a highenergy injury to the head or cervical spine or be as minimal as an awkward or unusual twisting to the head and neck that can accompany more ordinary activities. Acute soft-disc herniations that arise in the absence of a precipitating traumatic event and as a result of normal physiologic stresses are probably more accurately identied as the early stages of degenerative cervical disc disease. The second and more common form of cervical disc disease, harddisc disease, represents progressive degeneration of the cervical disc in conjunction with the more global process of cervical spondylosis. Harddisc disease is characterized rst by changes in the intervertebral disc to include a disturbance in the normal production of the components that comprise the extracellular matrix, dessication of the nucleus pulposus, and a loss of annular elasticity (Fig. 1). These changes are typically associated with loss of the disc space height along with bulging or frank herniation of the degenerative nuclear contents. In turn, secondary changes frequently include the development of osteophytes or traction spurs at the disc-vertebral body interface as well as the unconvertebral and facet joints (Fig. 2). The anatomical changes at the disc and facet joint level are associated with an alteration in the kinematics at the spinal motion segment. The symptoms of hard-disc disease tend to be more insidious in their onset, often rst presenting as episodic neck stiffness and pain that tends to wax and wane. During longer periods

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Figure 1. Some of the earliest radiographic changes consistent with cervical disc disease. At the C6-C7 level there is loss of the disc space height with osteophyte formation. Subtler changes are visible at the C5-C6 level.

Figure 2. Cervical spondylosis in the advanced stages with multilevel involvement. Note the disc space narrowing, anterior and posterior body osteophytes, and loss of the typical lordotic cervical alignment.

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of time, the symptoms may become more severe and persistent. The development of neurologic signs and symptoms is dependent on several factors and is not a consistent nding. It is believed that cervical disc degeneration is a cascading process of biochemical and subsequent biomechanical alterations that is rst initiated in the nucleus pulposus. This process of cervical disc degeneration is inextricably linked to that of cervical spondylosis. There is a gradation of cervical disc degeneration that begins with a prevalence of 10% by the mid-20s and progresses in a near-linear fashion to age 70 when it approaches a 95% to 100% prevalence.9 It is therefore widely held that disc degeneration is a consequence of the normal aging process.4 It should be recognized, however, that there is a relatively poor correlation between the radiographic presence of cervical disc disease and the expression of clinical signs and symptoms consistent with this process.2, 6 As morphologic changes occur at the level of the cervical disc, either from an acute nuclear herniation or more gradual changes after the evolution of a degenerative cervical disc, there is risk of sufcient anatomical distortion that the spinal cord or nerve root may come under a xed or dynamic compression. Compression of the nerve root may be on the basis of a disc protrusion or herniation, or foraminal narrowing from any one or more of osteophyte formation, ligamentous hypertrophy, or foraminal height narrowing. The nerve root and spinal cord may also come under compression as a consequence of dynamic changes with altered motion at the disc-vertebral body interface. The end result of such compression of the neural elements may produce pain or neurologic signs and symptoms. CLINICAL PRESENTATION AND EVALUATION The syndrome of cervical disc disease is just one potential cause of neck and brachial pain in the athlete. Because there are a myriad of other potential pathologic culprits, and extensive differential diagnosis must be sorted through in every patient. Most patients with an acute cervical disc herniation complain of a sudden onset of severe posterior neck pain. Depending on the location and level of the disc herniation, the neck pain may be the only symptom, or it may be in association with a referred pain to the shoulder, arm, or hand (Fig. 3). At or below the C4-C5 disc level, if there is compression of the nerve root, the patient will generally have pain extending to or below the level of the deltoid. The referred extremity pain may be associated with other neurologic symptoms such as paresthesias/dysesthesias or a sense of muscular weakness. Dening a dermatomal pattern for the referred extremity symptoms may allow a presumptive clinical diagnosis of the involved root level. Central disc herniations may produce signs and symptoms of a cervical myelopathy or myeloradiculopathy. Questions pertaining to the presence of a LHermittes sign, disturbances in balance or gait, lower extremity weakness, or alterations in normal bowel/bladder func-

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Figure 3. Sagittal T2-weighted MR scan of the cervical spine. Midline soft-disc herniations are identied at the C5-C6 and C6-C7 levels. These herniations are not associated with a signicant cervical stenosis, and thus with management of the acute symptoms and appropriate counseling, a return to play may be possible.

tion will generally provide clues to the presence of any compromise in spinal cord function. Although patients with an acute cervical disc herniation may have a more dramatic presentation than the patient with a recurrent bout of symptoms from an underlying degenerative cervical spine, the neurologic manifestations and pain associated with the radiculopathy may be quite similar. The distribution of any head, neck, shoulder, or arm pain is used with the physical exam ndings to localize the level of pathology. A disc herniation usually affects the nerve root exiting at that segment, and therefore a C2C3 disc herniation causes a C3 radiculopathy, a C3C4 disc herniation a C4 radiculopathy, a C4C5 disc herniation a C5 radiculopathy, a C5C6 disc herniation a C6 radiculopathy, a C6C7 disc herniation a C7 radiculopathy, and a C7T1 disc herniation a C8 radiculopathy. When the third cervical nerve root is compressed, no reex change or motor weakness can be identied. The pain radiates to the posterior neck and toward the mastoid process, possibly to include the pinna of the ear. Involvement of the fourth cervical nerve root again leads to no readily detectable reex change or motor weakness. The pain radiates into the back of the neck and into the superior aspect of the scapula. Occasionally, the pain will radiate into the anterior chest wall just below the level of the clavicle. Unlike the more cephalad roots, the fth through the eight cervical roots have discernable motor functions. Compression of the fth cervical root is characterized by weakness of

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shoulder abduction and extension. The biceps reex is often depressed, and the pain radiates from the side of the neck to the top of the shoulder and into the deltoid. A loss of sensation may be noted on the lateral aspect of the shoulder. Involvement of the sixth cervical nerve root produces biceps and wrist extensor weakness. A diminished brachioradialis reex may be appreciable. The pain radiates from the neck down the lateral arm and forearm into the radial half of the hand. Loss of sensation may be detected in the dorsal forearm and wrist, as well as in the radial three digits of the hand. Compression of the seventh root produces reex loss at the triceps level along with weakness in the triceps, wrist exors, and nger extensors (Fig. 4). The pain typically radiates from the lateral neck down the posterior arm above the elbow and into the dorsal forearm, nally terminating in the middle nger of the hand. Sensory changes are characteristically found in the middle three digits. Lastly, involvement of the eighth cervical root is typied by weakness in the nger exors and hand intrinsics. The radicular pain radiates into the ulnar border of the forearm and hand, often involving the ulnar two digits. Sensory loss is found in a similar distribution. The physical exam focuses on an assessment of posterior cervical tenderness and the range of motion of the neck. The other essential component of the initial exam includes an assessment of the shoulder and scapulothoracic articulation because these are frequent sources of pathology in the athlete giving rise to pain in and around the shoulder girdle. A neurologic exam to include a detailed evaluation of the motor and sensory function of the upper extremities is always necessary. It is also essential to examine both upper and lower extremity reexes to look for evidence of an isolated reex loss, or in some cases with cord compression, hyperreexia in the lower extremities. Examining the patient for evidence of upper motor neuron signs (Hoffmans reex; ankle clonus, Babinski sign, etc.) will prove useful if there is suspicion of cord compression by history or the preliminary exam ndings. Provocative maneuvers such as the head compression test and the Spurlings sign are helpful in conrming the clinical diagnosis of a radiculopathy stemming from a compressive cervical spine lesion. Another helpful though less commonly used test is the shoulder abduction test. The shoulder abduction test is performed in the sitting position and is positive if radicular symptoms decrease when the patient lifts a hand above the head with the shoulder held in an abducted position. The head compression test, Spurlings sign, and shoulder abduction test are quite specic for a radiculopathy, but lack sensitivity. The radiologic evaluation begins with a complete set of plain lms to include the following views: anteroposterior, lateral, oblique, and open-mouth odontoid. If these lms demonstrate no evidence of any signicant osseous pathology or suspicion of a spinal instability, then lateral exion/extension lms are obtained. The static plain lms will screen for evidence of disc-space narrowing or other ndings consistent with cervical spondylosis, congenital abnormalities, or destructive lesions from an infection or a tumor. Importantly, the sagittal spinal canal

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Figure 4. A, Sagittal T1-weighted MR scan of the cervical spine. Acute left arm pain prompted investigation of the cervical spine with this study. A disc herniation at the C6-C7 level is clearly visible on these images. B, The T2-weighted axial images at the C6-C7 level conrm the presence of a left-sided soft disc herniation. Compression of the exiting C7 nerve root was the cause of the left arm pain. A conservative treatment regimen including a series of selective nerve root injections brought lasting relief of the radicular symptoms.

dimensions can also be measured from these lms and a determination made as to the presence of a cervical stenosis on a congenital basis. When so indicated by either the persistence of pain despite appropriate nonoperative measures or the presence of neurologic signs and symptoms, further imaging with magnetic resonance scanning is useful. Magnetic resonance scanning provides superior delineation of the softtissue anatomy and therefore is the preferred method for visualizing the intervertebral disc and surrounding structures. Any site of disc dessication or other early degenerative changes as well as any site of a nuclear herniation, are consistently identied with magnetic resonance imaging.

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Also identiable are any sites of compression of the neural elements and, if present, any changes within the neural elements reective of parenchymal edema or myelomalacia.12 It must be recognized, however, that not all cervical disc herniations or other ndings consistent with degenerative disc disease detected on magnetic resonance images are symptomatic. It is well established that there is a signicant incidence of asymptomatic cervical disc disease and that this incidence increases with age.2, 11 When imaging with magnetic resonance is contraindicated, myelography with postcontrast computed tomography scanning is the preferred test to evaluate a patient presumed to have cervical disc disease. MANAGEMENT The treatment of cervical disc disease in the athlete and non-athlete alike is initially supportive and includes rest or other activity modication, immobilization, anti-inammatory medication, and local modalities such as heat and massage. The focus of this initial treatment is to gain some measure of pain relief and restoration of functional capacity. Rarely is surgical treatment considered initially unless there is a rapidly progressive neurologic decit or evidence of a frank myelopathy. Most patients with cervical disc disease will respond to a multifaceted nonoperative treatment approach. In the athlete with acute symptoms, the initial treatment should include activity restrictions with a temporary suspension of play. A soft collar worn with the neck in slight exion provides a limited means of immobilization and a continual reminder of the imposed activity restrictions. Moist heat and massage may prove useful for the neck pain and muscular spasm. Intermittent traction is most helpful as a means of relieving the pain associated with a radiculopathy. These measures are supplemented by the use of anti-inammatories and other analgesics as needed. As the acute symptoms subside, the institution of a physical therapy program to emphasize cervical isometrics and a gradual restoration of the cervical range of motion is often helpful. Passive modalities may be used during the more acute phase of the patients care. Active modalities to include an exercise program with dynamic and isometric neck strengthening exercises, neck and shoulder stretching, and aerobic activities are then implemented in a progressive manner to patient tolerance. This regimen is often successful in relieving the acute symptoms associated with a cervical disc herniation, particularly the neck and referred shoulder pain. For patients that continue to have persistent radicular pain or other neurologic symptoms but for whom operative treatment is still not considered necessary or appropriate, a trial of selective nerve root injections may be warranted. Selective nerve root injections involve the delivery of a local anesthetic and long-acting steroid around the inammed nerve root sheath. It is done under uoroscopic imaging to

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deliver the steroid to a precise anatomic location and does require technical competence to achieve optimal results. In one prospective study of patients with a cervical radiculopathy, satisfactory clinical results with avoidance of surgery were reported with the use of selective nerve root injections.5 The indications for surgical treatment in patients with cervical disc disease include persistent or recurrent radicular pain unresponsive to appropriate conservative measures, progressive or persistent neurologic decit, cervical myelopathy. This is assuming that other potential pathologic entities to explain the patients symptoms have been excluded, and imaging studies (magnetic resonance imaging, myelography) conrm compression of the neural elements in the expected distribution. In the absence of a progressive or dense neurologic decit, surgical treatment is generally not a consideration within the rst 6 to 8 weeks of symptom onset. Surgical treatment of a radiculopathy from cervical disc disease may be accomplished from either an anterior or posterior approach. In my opinion, a posterior approach with a laminoforaminotomy and limited disc excision is a consideration in a relatively small group of patients. These include those with a single-level soft-disc herniation that is outside the sagittal boundaries of the spinal cord. The plain radiographs should demonstrate no evidence of disc-space narrowing, osteophyte formation, or motion on exion-extension lms. In all other patients, my preference is an anterior approach with a discectomy and fusion. This approach appears to have a more favorable clinical outcome compared to the posterior approach with a laminoforaminotomy.7 However, because the return to play may be more expeditious with a laminoforaminotomy, a reasonable argument can be made for slightly expanding the indications for a posterior approach in the athlete with a limited recuperation period. The advantages and disadvantages of such an approach must be discussed among all involved parties to arrive at a mutually acceptable decision. An anterior approach with a discectomy and fusion can be expected to result in relief of the radicular symptoms in more than 90% of patients; there is no role for an anterior cervical discectomy without a fusion.3 RETURN TO PLAY Established standards or guidelines for an athletes ability to return to play after either conservative or surgical treatment of a cervical disc disorder are lacking. Because of the medical, social, and medicolegal implications of such decisions, the return to play decision is often difcult and frequently surrounded by questions and controversy. Certainly in all of these decisions, the unquantiable factor of the risk versus benet to the patient of a expeditious return to play must be considered. The criteria used to determine an athletes ability to return to contact activities are insufciently rigid so that they are best arbitrarily divided

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into three broad categories: no contraindication to play, relative contraindication to play, and an absolute contraindication to play. An athlete with a conservatively treated cervical disc herniation has no contraindication for return to contact sports once the neck pain and neurologic symptoms have resolved and a full, painless range of motion has been restored. This is assuming that the disc herniation has not resulted in a central spinal stenosis. In that instance, the severity of the spinal stenosis becomes the critical issue, and any return to play, even in the asymptomatic individual, must take that into consideration. An athlete who has required operative treatment of a cervical disc herniation with a single-level anterior cervical discectomy and fusion may return to unrestricted play with no contraindication once radiographs demonstrate a solid fusion and there has been resolution of any preoperative neurologic symptoms. The athlete must also have a return of a painless range of motion of the cervical spine. The only exception to this rule is a fusion in the upper cervical spine at the C2-C3, and perhaps C3-C4 level, where there exists at least a relative contraindication to return to play. After a posterior approach to a cervical disc herniation with a laminoforaminotomy, an athlete may return to contact activities with no contraindication once all neck pain and preoperative neurologic symptoms have resolved, cervical spine range of motion has been fully restored, and exion-extension radiographs demonstrate no instability at the operative level. A relative contraindication to return to play exists in the athlete after a two-level or three-level anterior or posterior fusion. A fusion of more than, and some would argue equal to, a three-level fusion represents an absolute contraindication to further participation in contact activities. Some element of subluxation without frank instability at the level of a degenerative disc or previous posterior decompression also represents a relative contraindication to continued play. An absolute contraindication for a return to play exists when there is an acute or chronic central disc herniation associated with any neurologic symptoms from cord or root compression. A central disc herniation that results in a painful or stiff neck with a loss of the normal neutral to lordotic cervical alignment is also an absolute contraindication for a return to play until the pain resolves and there is a full restoration of the range of motion with a normal sagittal alignment.

References
1. Albright JP, Moses JM, Feldich HG, et al: Non-fatal cervical spine injuries in interscholastic football. JAMA 236:12431245, 1976 2. Boden SD, McCowin PR, Davis DO, et al: Abnormal magnetic resonance scans of the cervical spine in asymptomatic subjects. J Bone Joint Surg 72A:11781184, 1990 3. Bohlman HH, Emery SE, Goodfellow DB, et al: Robinson anterior cervical discectomy and arthrodesis for cervical radiculopathy: Long-term follow-up of one hundred and twenty-two patients. J Bone Joint Surg 75A:12981307, 1993

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4. Buckwalter JA: Aging and degeneration of the human intervertebral disc. Spine 20: 13071314, 1995 5. Bush K, Hillier S: Outcome of cervical radiculopathy treated with periradicular/ epidural corticosteroid injections: A prospective study with independent clinical review. Eur Spine J 5:319325, 1996 6. Gore DR, Sepic SB, Gardner GM, et al: Neck pain: A long term follow-up of 205 patients. Spine 12:15, 1987 7. Herkowitz HN, Kurz LT, Overholt D: Surgical management of cervical soft disc herniation: A comparison between the anterior and posterior approach. Spine 15: 10261030, 1990 8. Kelsey J, Githens PB, Walter SD: An epidemiology study of acute prolapsed cervical intervertebral disc. J Bone Joint Surg 66A:907, 1984 9. Lawrence JS: Disc degeneration: Its frequency in relationship to symptoms. Annals Rheum Dis 28:121137, 1969 10. Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21:22942299, 1996 11. Matsumoto M, Fujimura Y, Suzuki N, et al: Magnetic resonance imaging of cervical intervertebral discs in asymptomatic subjects. J Bone Joint Surg (Br) 80B:1924, 1998 12. Modic MT, Ross JS, Masaryk TJ: Imaging of degenerative disease of the cervical spine. Clin Orthop 239:109120, 1989 13. Torg JS, Pavlov H, Genuario Se, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg 68A:13541370, 1986 14. Torg JS, Vegso JJ, Sennett B: The National Football Head and Neck Injury Registry: 14year report on cervical quadriplegia., 1971 through 1985. JAMA 254:34393443, 1985 15. Warren WL, Bailes JE: On the eld evaluation of athletic neck injury. Clin Sports Med 17:99110, 1998 Address reprint requests to Steven C. Scherping, Jr, MD Dept. of Orthopaedic Surgery 3800 Resevoir Rd, NW 1-Gorman Washington, D.C. 20007

SPECIAL ARTICLE

02785919/02 $15.00 .00

MR IMAGING IN CERVICAL SPINE TRAUMA


Deepak Takhtani, MD, and Elias R. Melhem, MD

Cervical spine trauma is a serious and often disabling injury that can have a potentially devastating effect on the patient. Motor vehicle accidents, recreational sports, and diving-related accidents account for most civilian cervical spine injuries.3 These injuries usually affect young men, frequently during a time of peak activity and productivity in their lives. A plethora of resources are devoted to the medical and surgical management and the rehabilitation of cervical spine trauma victims. Cervical spine and spinal cord injuries are classied according to several factors: neurologic decits (Table 1), type (blunt or penetrating trauma) and mechanism of injury (Table 2), and anatomic location of injury (cervicocranial junction or lower cervical spine). These classication schemes should serve as guidelines when considering fundamental issues in spinal injury management. To plan an effective therapeutic regimen and to formulate a prognosis, two fundamental issues specically associated with spinal trauma need to be addressed. The rst relates to the characterization of the direct injury to the spinal cord, and the second relates to identication of spinal instability and the spinal cord at risk.19 To address these issues thoroughly, the spinal injury must be evaluated radiographically. Plain-lm radiographs and radiographic CT scanning continue to be instrumental in the evaluation of the acutely injured cervical spine, particularly for the identication of spinal instability. These imaging modalities, however, are less than optimal for the characterization of direct spinal cord injury and the identication of nonosseous causes of cord compression.2
From the Department of Radiology and Radiological Sciences, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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Table 1. FRANKELS FUNCTIONAL CLASSIFICATION OF SPINAL CORD INJURY Grade A B C D E Neurologic Decit Complete motor and sensory loss Preserved sensory function Preserved motor activity (nonfunctional) Preserved motor activity (functional) Complete neurologic recovery

Within the last decade, MR imaging of acute cervical trauma has demonstrated enormous potential in the characterization of direct injury to the spinal cord and in the timely and denitive identication of spinal instability. The newly established and critical role that MR imaging has assumed in the multidisciplinary evaluation of the acutely injured spine is the result of several recent parallel advancements: The development of support (ventilators), xation (halo), and monitoring (ECG) devices compatible with MR imaging Innovations in MR software and hardware technologies, including fast spin echo-based pulse sequences and surface coils The increasing availability of MR scanners for emergency spine imaging The increasing comfort and familiarity of the radiologist and spine surgeon with using MR images to evaluate the injured spine

Table 2. FUNCTIONAL CLASSIFICATION OF CERVICAL SPINE FRACTURES AND DISLOCATIONS Mechanism of Injury Hyperexion Type Anterior subluxation (sprain) Bilateral interfacetal dislocation Simple wedge fracture Clay-shovelers fracture Teardrop fracture Dislocation (sprain or strain) Avulsion fracture of the anterior arch of C1 Fracture of the posterior arch of C1 Tear drop fracture of C2 Laminar fracture Hangmans fracture Fracture or dislocation Jeffersons fracture Burst fracture Unilateral interfacetal dislocation Pillar fracture Uncinate process fracture Atlanto-occipital disassociation Odontoid fractures

Hyperextension

Vertical compression Hyperexion and rotation Hyperextension and rotation Lateral exion Indeterminate

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This article emphasizes the technical aspects of MR imaging in acute cervical trauma and details the specic protocols used at the Johns Hopkins Medical Institutions. It discusses the systematic approach to the evaluation of MR images in the setting of trauma and denes the use of MR imaging in the characterization of spinal cord injury and identication of spinal instability. The correlations between MR imaging ndings and patient functionality and outcome are outlined. The article concludes with a review of the various classications of cervical spine injuries. TECHNICAL CONSIDERATIONS Recently, signicant progress has been made in device compatibility, use of fast pulse sequences for MR imaging, and surface coil technology. These advances have facilitated the routine use of MR imaging in the evaluation of cervical spine trauma. Compatibility Acutely traumatized patients often require continuous hemodynamic monitoring and respiratory support. External xation devices are also commonly used to provide stability before MR imaging. Monitoring devices and external xation devices are associated with risks or artifacts resulting from interference with the magnetic eld of the MR imaging scanner, but monitors and external xation designed to preclude such problems have greatly improved MR imaging of the acutely traumatized patient. The introduction of monitoring devices that have effective radiofrequency (RF) shielding or that operate at frequencies outside the RF spectrum of the MR imaging scanner have facilitated the safe imaging of the hemodynamically unstable patient.30 The use of MR-compatible materials (i.e., aluminum, graphite, and plastic) for cervical spine orthoses has signicantly reduced the risks and artifacts, such as induction of electric currents, heating, dislodgment, and image-degrading artifacts, that can be encountered in MR imaging of the spine.23 Image Quality Issues Fast spin-echo imaging has revolutionized cervical spine imaging.21, 22 Because of the acquisition of multiple data lines in k-space per TR interval (a signicant improvement in scanning efciency) and the maintenance of spin-echo contrast, fast spin-echo imaging has replaced conventional spin-echo imaging and, to a large extent, has replaced gradient-echo sequences in routine T2- and T2*-weighted imaging of the cervical spine. The signicant improvement in time resolution offered

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by fast spin-echo techniques has allowed timely imaging of the critically injured patient, improved image spatial resolution, signal-to-noise ratio, and routine implementation of formerly time-consuming short tau inversion-recovery (STIR) and uid attenuated inversion-recovery (FLAIR) MR sequences.20 Fast spin-echo techniques have also reduced gross motion-related artifacts. The multiple 180 RF pulses and the relatively short echo spacing implemented in fast spin-echo techniques is also important in reducing susceptibility-related artifacts originating from paramagnetic or ferromagnetic hardware.11, 29 Multiple 180 RF pulses and short echo-spacing, however, render fast spin-echo techniques suboptimal for detecting subtle acute hemorrhage in the spinal cord and necessitate routine implementation of a T2*-weighted gradient-echo sequence in spine trauma imaging. Another disadvantage of fast spin-echo techniques in imaging the traumatized spine is related to the bright signal originating from fat within the bone marrow and paraspinal soft tissue. This bright signal complicates the detection of edema in the bony spine and paraspinal ligaments on T2weighted imaging. Thus, fat-suppression (frequency- or T1-relaxation selective) techniques coupled with fast spin-echo readouts have become routine in imaging the traumatized cervical spine.9 Recently, circularly polarized (quadrature) phased-array coils functioning in receive mode have become the mainstay in imaging the traumatically injured cervical spine. The phased-array coil is a series of small coils linked in a ladder-like conguration, which allows the examination of a large anatomic area while taking advantage of the high signal-to-noise ratio offered by smaller coils. Although the Helmholtzlike volume coil conguration may provide a slightly superior signal-tonoise ratio than the phased-array coil in imaging the cervical spine, the use of xation and monitoring devices often precludes the use of the Helmholtz-like volume coil in MR imaging of the traumatized patient.

MR Imaging Protocols At the Johns Hopkins Medical Institution, all patients with neurologic decit referable to the spinal cord or evidence of cervical spine fracture or dislocation are imaged using a set MR imaging protocol under the supervision of an emergency department physician and a radiologist (Table 3). The need for cardiac and respiratory monitoring during MR imaging is determined by the trauma team. All MR imaging of the cervical spine is done using surface coils functioning in receive mode (quadrature phased-array). If the patients clinical condition permits, the following MR imaging protocol is routinely implemented: Sagittal T1-weighted spin-echo imaging is used for assessing alignment of the cervical spine, integrity of the individual vertebral bodies, and the caliber of the spinal cord (focal swelling).

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Table 3. MR IMAGING SEQUENCES USED IN IMAGING CERVICAL SPINE INJURY Type of MR Imaging Sequence Sagittal T1 Sagittal T2 fast spinecho Sagittal fast STIR Sagittal T2* gradientrecalled echo Axial T1 Axial T2 fast spinecho Parameters TR/TE: 500/15 Slice thickness/gap (mm): 3.0/0.3 TR/TE/ETL: 2000/80/8 Slice thickness/gap (mm): 3.0/0.3 TR/TI/TE/ETL: 2000/160/20/5 Slice thickness/gap (mm): 3.0/0.3 TR/TE/Flip angle: 480/25/25 Slice thickness/gap (mm): 3.0/0.3 TR/TE: 574/17 Slice thickness/gap (mm): 4.0/0.4 TR/TE/ETL: 3000/100/8 Slice thickness/gap (mm): 4.0/0.4 Utility Epidural hematoma, cord swelling Cord edema, spondylosis, cord compression Bone marrow edema, ligamentous and soft tissue injury Cord hematoma, disk herniation, bone fragments Epidural hematoma, posterior element fractures Cord edema, cord compression

STIR short tau inversion-recovery; ETL echo train length

Sagittal T2-weighted fast spin-echo imaging used for detecting cord edema (Fig. 1), cord compression, and spondylotic changes. Sagittal fast STIR imaging is used for detecting subtle paraspinal ligamentous injury (Fig. 2) and bone marrow edema. Sagittal T2*-weighted gradient-recalled echo imaging is used for exquisite demonstration of acute cord hemorrhage (Fig. 3) and acute posttraumatic disk herniation. This sequence maintains a high signal within the disks even in the presence of severe degeneration, facilitating the differentiation between a herniated disk and a bone fragment. Axial T1-weighted spin-echo and T2-weighted fast spin-echo imaging are used for detecting posterior element fractures. These sequences also conrm and reveal the precise location of abnormalities detected on sagittal imaging. All MR images are systematically analyzed (Table 4) and correlated with other available imaging modalities (plain radiographs and CT scans) and the patients neurological examination. Based on this information, the on-call radiologist provides an immediate impression of the stability of the cervical spine and the status of the spinal cord. USE OF MR IMAGING IN THE CHARACTERIZATION OF SPINAL CORD INJURY There is considerable variation in the response of the spinal cord to penetrating and blunt injury. Factors that affect spinal cord abnormality

Figure 1. Twenty-ve-year-old man with hyperexion injury resulting in quadriplegia. Sagittal (A) and axial (B) fast spin-echo (FSE) T2-weighted (3056/104: TR/TE) images display cord edema (large black arrow), and disruption (small black arrow) and edema (large white arrow) of the posterior longitudinal ligament. There is a fracture of left posterior body of C3 (small white arrow) better seen on axial images.

Figure 2. Forty-six-year-old man with hyperexion injury resulting in neck pain without neurological impairment. Sagittal FSE T2-weighted (3692/104: TR/TE) (A) and fast short inversion time inversion-recovery (STIR) (2000/160/20: TR/TI/TE) (B) images show edema (asterisks), disruption of the interspinous ligaments (arrow), and aring of the spinous processes at C5C6. Note the better demonstration of ligamentous and soft tissue injuries on STIR image because of fat suppression.

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Figure 3. Twenty-ve-year-old man with hyperexion injury and paraplegia. Sagittal T2*weighted gradient-recalled echo (GRE) (480/25/25: TR/TE/ip angle) image best demonstrates acute intramedullary hemorrhage at the C6 level as a focal area of hypointensity resulting from magnetic susceptibility effects (arrow).

Table 4. SYSTEMATIC INSPECTION OF THE MR IMAGES IN CERVICAL SPINE TRAUMA Alignment Spinal cord Subluxation/Dislocation Edema Swelling Hemorrhage Compression Disk herniation Bone fragment Hematoma Vertebral body fracture Posterior element fracture Bony edema Spondylosis Anterior longitudinal ligament Posterior longitudinal ligament Interlaminar ligaments (ava) Supra or interspinous ligaments Vertebral artery (see Fig. 5)

Epidural space Spinal column

Ligaments

Vascular

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after an injury include the site, intensity, and distribution of impact associated with the injury and the biochemical, electrophysiologic, and hemodynamic derangements.6 Spinal cord injuries can be categorized as concussive, contusive, or compressive.2 Concussion of the cord is a purely functional and fully reversible derangement that has been attributed to transient deciencies in the cords microcirculation.8 Demonstration of cord edema on T2weighted MR images is uncommon and transient. The severity of spinal cord contusion ranges from simple edema or petechial hemorrhages to severe hemorrhagic and liquefaction necrosis and even complete transection.12 Subsequent demyelination, micro- and macrocystic myelomalacia, and arachnoiditis are common. Frequently, contusion can result from transient compression or stretching of the spinal cord. Cord compression may produce the same range of spinal cord injury as contusion, with the notable addition of the compressive lesion (bone fragment, subluxation or dislocation, disk herniation, epidural hematoma, or spondylotic bar). It has been suggested that for spinal cord compression to be denitely determined, a 50% or greater reduction in the anterior-posterior dimension of the spinal canal must be present. In many trauma centers, acute compressive lesion mandates immediate surgical intervention; therefore, the identication of a compressive lesion is of utmost clinical importance.24 MR imaging is undoubtedly superior to other imaging modalities in dening spinal cord injuries and particularly in distinguishing cord contusion from cord compression. Kulkarni et al17 described three MR imaging patterns of spinal cord injury (Table 5). The rst pattern is characterized by an area of hypointensity relative to the normal cord on T2-weighted images in the acute phase, with the development of a thin rim of hyperintensity on short-term follow-up in 3 to 7 days. On the axial T2-weighted images, the foci of hyperintensity are often seen at the gray matterwhite matter junction. T1-weighted images demonstrate focal cord swelling. The second pattern is characterized by a spindleshaped area of hyperintensity relative to the normal cord on T2-weighted images (see Fig. 1). Follow-up imaging demonstrates rapid resolution of the hyperintensity. The third pattern is characterized by a small area of hypointensity surrounded by a thick rim of hyperintensity on T2weighted images (Fig. 4). Follow-up imaging demonstrates partial reso-

Table 5. MR IMAGING SIGNAL PATTERN IN ACUTE SPINAL CORD INJURY MR Imaging Pattern I II III T1-weighted Images Heterogeneous Normal Normal Central T2-weighted Images Peripheral Thin rim of hyperintensity Hyperintensity Thick rim of hyperintensity

Large area of hypointensity Hyperintensity Small area of hypointensity

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Figure 4. Twenty-ve-year-old man with hyperexion injury and paraplegia. Sagittal T2weighted FSE (2000/80: TR/TE) image demonstrates Kulkarnis third pattern, which is characterized by a small area of hypointensity representing acute intramedullary hemorrhage at the level of C6, surrounded by a thick rim of hyperintensity representing cord edema. A small epidural hematoma (arrow) behind the C6 vertebral body compressing the cord, and disruption of the posterior longitudinal ligament also are demonstrated.

lution of the lesion, which appears as a lling in of the central lesion by hyperintense signal. One of the most signicant characteristics of these three patterns is their strong correlation with the neurologic functionality at admission and discharge of patients suffering from spinal cord injury. The rst pattern is associated with the highest degree of acute neurologic decit and the least degree of improvement. The second and third patterns are associated with less acute neurologic decit and more improvement. Also, MR imaging of spinal cord injury has very high positive and negative predictive values for neurologic decits.12 The poor correlation between plain-lm radiographic and CT scan ndings and neurologic functionality in patients with cervical spine injury has been well documented; as a result, these modalities have been supplanted by MR imaging as the sole modality used for patient stratication and prognostication.14 The importance of distinguishing cord contusion from direct cord compression is based on experimental and clinical evidence that indicates improvement or resolution of acute and chronic neurologic decits after surgical spinal decompression.4 Although the benet of emergency spine decompression is somewhat controversial, most authorities agree that immediate intervention is necessary in patients with acute cord

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Figure 5. Twenty-nine-year-old man with a burst fracture secondary to axial loading injury. A, Axial T2-weighted FSE (2000/80: TR/TE) image demonstrates hyperintensity in the left transverse foramen (arrow) where ow void in the vertebral artery would have been expected. B, Occlusion of the left vertebral artery (arrow) secondary to post-traumatic dissection was conrmed on digital subtraction angiography.

compression, regardless of the severity of neurologic decit.24 This controversy surrounding emergency spine decompression may arise from inaccurate characterization of cord injury, signicant cord compression, or satisfactory decompression different types and approaches of surgical intervention inaccurate assessment of initial neurologic decits Currently, MR imaging is the method of choice for identifying and characterizing the causes of cord compression. Nonosseous causes, such as disk herniation (Fig. 6) and epidural hematoma (Fig. 7), are especially well demonstrated on MR imaging when compared with plain-lm radiographs, radiographic CT scans, or myelography. When MR imaging is used as a standard frame of reference, CT has approximately 33% and 44% sensitivity for the detection of posttraumatic spinal cord compression and disk herniation, respectively.12 Even when other modalities provide denite evidence of osseous cord compression, emergency MR imaging is still needed. After cervical reduction, an unsuspected extruded disk fragment can worsen cord compression and neurologic function28; emergency MR imaging is necessary to identify or rule out

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Figure 6. Forty-one-year-old woman with hyperexion injury and anterior cord syndrome. Sagittal T2-weighted FSE (2000/80: TR/TE) image demonstrates a hyperintense, moderately sized acute disk herniation at the C4C5 level causing cord compression. In addition, there was type 3 Kulkarni cord changes, minimal anterior subluxation of C4 on C5, mild prevertebral edema (arrow), and disruption of the posterior longitudinal ligament.

this entity. Furthermore, patients with severe cervical spine spondylotic changes who experience hyperextension injury may present with neurologic decits (central cord syndrome) despite an unremarkable plainlm radiographic or CT examination.25 In these patients, MR imaging is invaluable for demonstrating spinal cord injury and compression (Fig. 8). On MR imaging, the neurologic level of injury corresponds precisely to the site of compression. ROLE OF MR IMAGING IN THE IDENTIFICATION OF SPINAL INSTABILITY Instability of the cervical spine is dened as the inability to maintain a normal association between vertebral segments while under a physiologic load.31 Instability, in the setting of trauma, results from the loss of structural integrity of the bony spine and ligaments. This loss of structural integrity can lead to damage of the spinal cord and nerve roots or to pain and incapacitating deformity of the spinal column. Several clinical criteria have been established to indicate spinal instability. Denis7

Figure 7. Forty-year-old man with minor hyperextension injury and no abnormality on plain radiography of the cervical spine. A, Sagittal T2-weighted FSE (2000/80: TR/TE) and sagittal T1-weighted SE (500/15: TR/TE) (B) images demonstrate a spindle-shaped acute posterior epidural hematoma compressing the cord (arrow). The epidural hematoma was hypointense on the T2-weighted FSE image and isointense to cord on the T1-weighted SE image.

Figure 8. Sixty-nine-year-old man with minor hyperextension injury and moderate spondylotic changes in the cervical spine. Sagittal T2-weighted FSE (2000/80: TR/TE) image demonstrates moderate spinal stenosis at the C3C4 and C5C6 levels secondary to spondylotic disease and cord edema (arrow) at the C4 level resulting from the hyperextension injury.

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Table 6. COMPONENTS OF THE THREE COLUMNS OF THE CERVICAL SPINE Column Anterior Middle Posterior Components Anterior longitudinal ligament Anterior annulus brosus Anterior vertebral body Posterior vertebral body Posterior annulus brosus Posterior longitudinal ligament Posterior elements Facet capsules Interlaminar ligaments (ava) Supra or interspinous ligaments

Instability requires disruption of at least two columns

divides the spine into three columns (Table 6) and denes instability as disruption of at least two of these columns (Fig. 9). Other, more objective criteria depend solely on imaging. These criteria include the observation of a displacement greater than 3.5 mm between two adjacent vertebrae and angulation greater than 11.31 The role of MR imaging is less well dened in the evaluation of

Figure 9. Sagittal T2-weighted FSE (2000/100: TR/TE) image demonstrating Denis three columns of the cervical spine: anterior (A), middle (B), posterior (C).

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spinal instability. Patients who may not need an MR imaging evaluation of the cervical spine include those with clear evidence of instability on plain-lm radiographs, who have no signs of spinal cord injury, or in whom reduction of misalignment is not contemplated. If the clinical evaluation and plain-lm radiographic or CT scanning ndings are inconclusive but suggest instability, MR imaging may be necessary for conrmation. The reliability of cervical spine exion-extension radiography is questionable in the acute setting; this lack of reliability and the superiority of MR imaging in the detection of ligamentous injuries or tears have made MR imaging the imaging method of choice for the conrmation of instability.18 Using high-resolution CT scanning as a standard control, the reported sensitivity of MR imaging ranges from 25% to 100% for demonstrating cervical spine fractures.12 This wide range of reported sensitivity reects signicant differences in the ability of MR imaging to demonstrate vertebral body or posterior element fractures and the variability of the MR imaging techniques employed. Bony fractures of the posterior elements, which may be the only evidence of a second column disruption, can be difcult to dene using current MR imaging techniques (Fig. 10). At present, this limitation secures a role for high-resolution CT scanning in the evaluation of cervical spine trauma. CLASSIFICATIONS OF CERVICAL SPINE INJURIES Penetrating Trauma Penetrating trauma to the cervical spine can be further divided into missile injuries and puncture wounds. In civilians, missile injuries are

Figure 10. Thirty-year-old man with hyperexion injury and multiple cervical spine fractures. A, Axial CT image demonstrates fracture of right pedicle and two fractures through the right lamina (white arrows). B, Axial FSE T2-weighted (5000/104: TR/TE) image through the same region reveals edema surrounding the laminar fractures (black arrow). Fracture lines are poorly dened on the MR image.

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most commonly caused by bullet fragments (Fig. 11). Spinal cord damage from missile injuries can be caused by direct passage of the missile through the cord or, more frequently, by displaced bone fragments and blast effects.32 Puncture wounds are the result of stabbing with a sharp instrument. The bony posterior elements, particularly the laminae and spinous processes, provide signicant protection to the spinal cord. Therefore, most puncture-wound entry sites are off-midline through the interlaminar ligaments. Most injuries involve the dorsolateral aspect of the cord. MR imaging is important in the evaluation of penetrating trauma. Many puncture wounds are limited to the soft tissues and the spinal cord, and abnormalities are not observed on plain-lm radiographic and CT examinations. MR imaging can provide critical information regarding

Figure 11. Twenty-four-year-old man with gunshot wound to the neck. A, Axial CT image demonstrates bullet tract and fracture of the right transverse process and foramen (curved arrow). B, Axial FSE T2-weighted image (5100/102: TR/TE) image reveals concentric hyperintensity in the region of the right vertebral artery (arrow). Right subclavian arteriogram (C) shows occlusion of the vertebral artery (arrow).

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the location, extent, and type of cord injury and a precise correlation with the level of neurologic decit (Fig. 12). MR imaging, however, may occasionally be limited by ferromagnetic susceptibility artifacts induced by the instrument that caused the missile injury. Blunt Trauma Blunt trauma to the cervical spine is classied according to the anatomic location of injury (cervicocranial junction or lower cervical spine). Injuries at the cervicocranial junction are further divided into those involving the atlanto-occipital articulation or the atlantoaxial articulation. Lower cervical spine injuries are more common because of increased mobility and are commonly classied by the underlying mechanism of injury (see Table 2).27 Atlanto-occipital Disassociation Atlanto-occipital disassociation is any separation of the atlantooccipital articulation.13 This injury is usually fatal. The separation may be complete (dislocation) or partial (subluxation) with posterior, anterior,

Figure 12. Twenty-six-year-old man who developed BrownSequard syndrome after a penetrating injury to the neck. A, Sagittal and axial (B) T2-weighted SE (2000/80: TR/TE) images demonstrate focal swelling and hyperintensity involving the left posterolateral aspect of the cord at the C2C3 level representing contusion.

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or superior (distraction) displacement of the skull (Figs. 13 and 14). The primary injury associated with atlanto-occipital disassociation is disruption of the ligaments that provide structural support to the cervicocranial junction. The ligaments affected are the atlanto-occipital capsular ligaments, anterior and posterior atlanto-occipital membrane ligaments, paired lateral atlanto-occipital ligaments, longitudinal component of the cruciate ligament, apical ligament, paired alar ligaments, and tectorial membrane. Multiplanar capability and sensitivity to ligamentous injury make MR imaging the best modality for demonstrating the relationship between the basion and the tip of the dens, between the occipital condyle and the superior facets of the atlas, or the disruption of the supporting ligaments. Pre-existing cord injuries, common in many patients, are also well demonstrated with MR imaging.13 Atlantoaxial Disassociation Atlantoaxial disassociation may be caused by distraction, with superior displacement of the atlas and skull (Fig. 15), or by odontoid fractures with resultant anterior or posterior displacement of the atlas. The former is commonly associated with atlanto-occipital disassociation and is primarily the result of ligamentous disruption. Odontoid fractures, how-

Figure 13. Four-year-old girl with atlanto-occipital dissociation after high-speed motor vehicle accident. Sagittal FSE T2-weighted (5000/100: TR/TE) image demonstrates anterosuperior distraction of the skull. The apical ligament is disrupted, with increase in the basion (b)odontoid tip (o) distance. The tectorial membrane is lifted up and possibly torn (black arrow), with accumulation of an epidural hematoma posterior to the clivus. There is ligamentous disruption posteriorly, between C1 and C2, with edema (asterisks) and prevertebral edema (arrowhead).

Figure 14. Eighteen-month-old girl with atlanto-occipital dissociation after high-speed motor vehicle accident. A, Sagittal SE T1-weighted (500/11.9: TR/TE) and sagittal FSE T2weighted (3500/88: TR/TE); B, images show superior distraction of skull, with increased distance between the fractured odontoid process (white arrow) and basion, an epidural hematoma posterior to clivus (asterisk), with distraction of the tectorial membrane, cord contusion with hemorrhage (black arrow), and prevertebral (A, white arrow) and paraspinal (H) edema.

Figure 15. Four-year-old boy with a disassociation injury at the cervicocranial junction. A, Sagittal T2-weighted FSE (2000/80: TR/TE) and sagittal fast STIR (2000/160/20: TR/TI/TE) (B) images demonstrate posterior ligamentous injury (arrows) and mild superior displacement of the atlas and skull with respect to C2. Mild prevertebral edema anterior to C2 is also noted.

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Table 7. CLASSIFICATION OF ODONTOID FRACTURES Type I II III Description Avulsion fracture of the tip of the dens Transverse fracture of the dens above the body of C2 Fracture of the superior body and the superior articulating facets of C2

Adapted from Anderson LD, Alonzo RT: Fractures of the odontoid process of the axis. J Bone Joint Surg (Am) 56:16631691, 1974; with permission.

ever, are the most frequent cause of bony injury. In general, the mechanism of injury in odontoid fractures is not well understood, although hyperexion is believed to play a major role. These fractures have been classied by Anderson and DAlonzo1 based on the location of the fracture in the axis (Table 7) (Figs. 16 and 17).1 Atlantoaxial dissociation is also well dened on MR imaging. The disruption of the supporting ligaments and the relationship of the atlas to the axis is clearly represented, and spinal cord injury and compression are optimally displayed. MR imaging of atlantoaxial disassociation injuries caused by odontoid fractures may often demonstrate the fracture lines and associated bone marrow edema, especially when fat-saturation techniques are used. High-resolution CT scans, plain-lm tomography, or technetium 99m-methyleneliphosphonote (99m Tc MDP) bone scans may, however, be superior to MR imaging for detecting subtle cortically based fractures (e.g., type I fractures). Hyperexion Injuries Flexion injury of the cervical spine results in the forward rotation or translation of the vertebra in the sagittal plane. This injury is caused by direct trauma to the head and neck in the exed position or by forces that cause hyperexion of the neutral cervical spine. Flexion injuries are classied according to the degree of cord injury and instability (see Table 2). The degree of injury depends on the severity of traumatic force and the position of the neck at the time of impact. The injury tends to be more severe if the cervical spine is exed at the

Figure 16. Different types of dens fractures.

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Figure 17. Forty-year-old man with a previous type 2 odontoid fracture. Sagittal FSE T2weighted (4951/103: TR/TE) image displays type 2 odontoid fracture. The fracture surfaces are well corticated (white arrow), and there is evidence of fatty replacement of the marrow subjacent to the fracture. Small area of myelomalacia also is seen in the cord (black arrow).

time of impact.15 Anterior subluxation of the vertebral body, reversal of cervical lordosis, anterior narrowing and posterior widening of the intervening disk space, anterior displacement of the superior facets, and fanning of the spinous processes are common features of exion injury. These features result from the disruption of the posterior ligament complex (inter- and supraspinous ligaments), the interlaminar ligaments, the facet capsules, the posterior longitudinal ligament, and the posterior portion of the annulus brosus. The degree of anterior displacement may be minimal (hyperexion sprain) or obvious (bilateral interfacetal dislocation and teardrop fracture). The clay-shovelers fracture (Fig. 18) and the simple wedge fracture tend to be stable, whereas the bilateral interfacetal dislocation and the teardrop fracture16 are unstable fractures (Figs. 19 and 20). These latter two fractures frequently result in cord injury and compression. Hyperexion sprain results in delayed instability. Most exion injuries are well demonstrated on MR imaging. In addition to demonstrating alignment abnormalities and fractures, MR imaging provides unique information regarding the ligamentous injury, cord abnormalities, and acute disk herniations commonly associated with hyperexion injury.26 One of the most useful characteristics of MR

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Figure 18. Twenty-ve-year-old man with hyperexion injury resulting in clay shovelers fractures. Sagittal (A) and axial (B) FSE T2-weighted (2000/80: TR/TE) images show mildly displaced fractures of spinous processes of C6 and C7 (A, arrows, and B, arrowheads).

Figure 19. Sixty-ve-year-old man with severe hyperexion injury resulting in bilateral interfacetal dislocation. A, Sagittal T1-weighted SE (500/15: TR/TE) and sagittal T2weighted FSE (2000/80: TR/TE) (B) images demonstrate complete disruption of all three columns, with marked anterior translation of C5 vertebral body on C6, resulting in cord compression. Moderate prevertebral edema from C6 to T1 also is noted.

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Figure 20. Thirty-one-year-old man with severe hyperexion injury resulting in exion teardrop fracture. A, Sagittal T1-weighted SE (500/15: TR/TE) and sagittal T2-weighted FSE (2000/80: TR/TE) (B) images demonstrate reverse curvature of the cervical spine, with compression fracture of the C5 vertebral body on C6, producing the characteristic triangular fragment that comprises the anteroinferior aspect of the vertebral body (arrow). The retropulsed fragment caused cord compression and contusion. Also, there was disruption of the posterior longitudinal ligament, moderate prevertebral edema extending from C2C4, and bruising of the C6 vertebral body.

imaging is its ability to determine whether anterior subluxation is the result of chronic spondylotic changes or of hyperexion sprain. Unlike exion-extension radiography, MR imaging is capable of demonstrating acute posterior ligamentous injury, providing a denite conrmation of hyperexion sprain.18 Because of the questionable reliability of exion-extension radiography, MR imaging has become a valuable alternative. Hyperextension Injuries Extension injury of the cervical spine results in the backward rotation or translation of the vertebra in the sagittal plane. It often results from an anterior impact on the mandible, face, or forehead or from sudden deceleration.15 The classication of extension injuries is similar to that of exion injuries. Extension injuries are also classied according to degree of cord injury and instability (see Table 2), with the severity of the extension injury depending on the direction and magnitude of the

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hyperextensive force. These subtypes can be further categorized as stable or unstable fractures. Avulsion fracture of the anterior arch of the atlas and extension teardrop fracture are limited to the anterior column of the cervical spine, whereas isolated fracture of the posterior arch of the atlas and laminar fractures are limited to the posterior column. Because of the limited involvement of these fractures, they are considered relatively stable. In more severe hyperextension injuries, however at least two columns are disrupted, with resultant instability. Such fractures include hangmans fracture, hyperextension dislocation, and hyperextension fracture and dislocation (Fig. 21). Hangmans fracture, or C2 traumatic spondylolisthesis (Fig. 22), is a fracture involving the pars interarticularis and adjacent structures. This fracture is categorized by Effendi et al10 into three types. Type 1 is dened as an isolated hairline fracture of the pars without displacement of the body or facets of C2. Type 2 is dened as a fracture of the pars with anterior displacement of the body of C2. Type 3 is dened as a fracture of the pars with anterior displacement of the body of C2 in a position of exion and associated bilateral facet dislocation. Some investigators believe that type 3 hangmans fracture is not a pure hyperextension injury but rather results from a combination of hyperexion

Figure 21. Twenty-eight-year-old woman involved in a high-speed motor vehicle accident that resulted in hyperextension fracturedislocation injury. Sagittal (A) and parasagittal (B) T2-weighted FSE (2000/80: TR/TE) and parasagittal T1-weighted SE (500/15: TR/TE) (C) images demonstrate complete disruption of all three columns, with mild to moderate paradoxical anterior translation of C6 vertebral body on C7. There was complete interfacetal dislocation of the right C6 on C7 (curved arrow) and fracture of the left C7 superior facet (B, arrowheads). Also, note the severe cord contusion and posterior buckling of the disrupted C6C7 disk behind C6.

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Figure 22. Twenty-six-year-old woman with hyperextension injury resulting in a type 2 hangmans fracture. A, Parasagittal reformation from high resolution axial radiographic CT data and parasagittal T2-weighted FSE (2000/80: TR/TE) image (B) demonstrate fracture of the pars interarticularis of C2 (arrow), with edema in the superior facet, seen only on MR imaging.

followed by rebound hyperextension. Hyperextension dislocation injury is a predominantly ligamentous injury resulting in distraction of the anterior column, buckling of the middle column (posterior longitudinal ligament), and transient posterior intervertebral dislocation. This dislocation is usually reduced immediately after impact. Despite the serious neurologic decits commonly associated with this injury, plain-lm radiographic ndings can be subtle and include prevertebral soft tissue swelling, avulsion fracture arising from the inferior endplate of the distracted vertebra, widening of the disk space, and a vacuum disk. MR imaging is critical in dening the type of spinal cord injury responsible for the neurologic decit and the extent of ligamentous injury and in identifying an associated acute compressive herniated disk.5 Vertical Compression Injuries Axial loading injury of the cervical spine results from forces transmitted through the skull and occipital condyles to a voluntarily straightened spine.15 Such injury gives rise to the well described Jeffersons fracture of the atlas and the bursting fracture in the lower cervical spine. The Jeffersons fracture consists of simultaneous disruption of the

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anterior and posterior arches of C1 with or without disruption of the transverse atlantal ligament. Identication of transverse ligament disruption, with resultant atlantoaxial instability, is crucial in the thorough evaluation of this injury. Because of its superior multiplanar capability and sensitivity to ligamentous injury, MR imaging is highly suitable for the display of the lateral displacement of the lateral masses of C1 on coronal images, the increase in the atlantodental interval on sagittal images, and the disruption of the transverse ligament on axial images. As the vertical force is transmitted to the lower cervical spine, it is dissipated by compression of the intervertebral disk. The build-up of pressure within the disk results in either an acute herniated disk or a comminuted fracture in the adjacent vertebral body with associated retropulsion of the posterior body fragments (bursting fracture) (Fig. 23). In either case, MR imaging is invaluable in dening the relationship of the herniated disk or retropulsed fragment to the spinal cord and demonstrating cord injury. In conclusion, continual improvements in MR imaging technology and MR imaging-compatible monitoring and xation devices have allowed the incorporation of this relatively new imaging modality into standard algorithms for cervical spine trauma assessment. The ability of MR imaging to dene the type of spinal cord injury, the cause and severity of spinal cord compression, and the stability of the spinal

Figure 23. Twenty-nine-year-old man with a burst fracture of C7 secondary to axial loading injury. Sagittal T2-weighted FSE (2000/80: TR/TE) image demonstrates burst fracture of the C7 vertebral body, with the retropulsed fragment compressing the cord. There is mild prevertebral edema extending from C4T2. Note the normal alignment of the cervical spine.

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column is unmatched. The heavy reliance of the spine surgeon on MR imaging for decisions regarding the type of therapy, the timing, the approach of surgical intervention, and for predicting patient outcome attests to the usefulness of this modality. Future implementation of fast, high-resolution three-dimensional MR imaging sensitized to bone marrow edema and the application of relatively artifact-free functional MR imaging may enhance the ability to detect cervical spine instability and early, possibly reversible, spinal cord injury. References
1. Anderson LD, DAlonzo RT: Fractures of the odontoid process of the axis. J Bone Joint Surg (Am) 56:16631691, 1974 2. Benedetti PF: MR imaging in emergency medicine. Radiographics 16:953962, 1996 3. Bracken MB, Freeman DH, Hellenbrand K: Incidence of acute traumatic hospitalized spinal cord injury in the United States, 19701977. Am J Epidemiol 113:615622, 1981 4. Brodkey JS, Miller CF, Harmody RM: The syndrome of acute cervical spinal cord injury revisited. Surgical Neurology 14:251257, 1980 5. Davis SJ, Teresi LM, Bradley WG, et al: Cervical spine hyperextension injuries: MR ndings. Radiology 180:245251, 1991 6. De La Torre JA: Spinal cord injury: Review of basic and applied research. Spine 6: 315335, 1981 7. Denis F: The three column spine and its signicance in the classication of acute thoracolumbar spinal injuries. Spine 8:817831, 1983 8. Dohrmann GJ, Wagner FC, Buey PC: The microvasculature in transitory traumatic paraplegia: An electron microscopic study in the monkey. J Neurosurg 35:263271, 1971 9. Dwyer AJ, Frank JA, Sank VJ, et al: Short T1 inversion-recovery sequence: analysis and initial experience in cancer imaging. Radiology 168:827836, 1988 10. Effendi B, Roy D, Cornish B, et al: Fractures of the ring of the axis: A classication based on the analysis of 131 cases. J Bone Joint Surg (Br) 63:319327, 1981 11. Eustace S, Goldberg R, Williamson D, et al: MR imaging of soft tissues adjacent to orthopaedic hardware: Techniques to minimize susceptibility artifact. Clin Radiol 52: 589594, 1997 12. Flanders AE, Schaefer DM, Doan HT, et al: Acute cervical spine trauma: Correlation of MR imaging ndings with degree of neurologic decit. Radiology 177:2533, 1990 13. Goldberg AL, Baron B, Daffner RH: Clinical images. Atlantooccipital dislocation: MR demonstration of cord damage. J Comput Assist Tomog 15:174178, 1991 14. Goldberg AL, Rothfus WE, Deeb ZL, et al: Hyperextension injuries of the cervical spine. Skeletal Radiol 18:283288, 1989 15. Harris JR, Edeiken-Monroe B: The Radiology of Acute Cervical Spine Trauma, ed 2. Baltimore, Williams & Wilkins, 1987 16. Kim KS, Chen HH, Russell EJ, et al: Flexion teardrop fracture of the cervical spine: Radiographic characteristics. AJR Am J Roentgenol 152:319326, 1989 17. Kulkarni MV, McArdle CB, Kopanicky D, et al: Acute spinal cord injury: MR imaging at 1.5 T. Radiology 164:837843, 1987 18. Lewis LM, Docherty M, Ruoff BE, et al: Flexion-extension views in the evaluation of cervical-spine injuries. Ann Emerg Med 20:117121, 1991 19. Masaryk TJ: Spinal trauma. In Modic MT, Masaryk TJ, Ross JS (eds): Magnetic Resonance Imaging of the Spine, ed 2. St. Louis, Mosby, 1994 20. Melhem ER, Jara H, Shakir H, et al: Fast inversion recovery MR imaging: The effect of hybrid-RARE read-out on the null points of CSF and fat. AJNR Am J Neuroradiol 18:16271633, 1997 21. Melki PS, Jolesz FA, Mulkern RV: Partial RF echo planar imaging with the FAISE method: I. Experimental and theoretical assessment of artifact. Magn Reson Med 26: 328341, 1992

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22. Melki PS, Jolesz FA, Mulkern RV: Partial RF echo planar imaging with the FIASE method: II. Contrast equivalence with spin-echo sequences. Magn Reson Med 26: 342354, 1992 23. New PF, Rosen BR, Brady TJ, et al: Potential hazards and artifacts of ferromagnetic and nonferromagnetic surgical and dental materials in nuclear magnetic resonance imaging. Radiology 147:139148, 1983 24. Quencer RM, Nunez D, Green BA: Controversies in imaging acute cervical spine trauma. AJNR Am J Neuroradiol 18:18661868, 1997 25. Regenbogen VS, Rogers LF, Atlas SW, et al: Cervical spinal injuries in patients with cervical spondylosis. AJR Am J Roentgenol 146:277284, 1986 26. Rizzolo SLJ, Piazza MR, Cotler JM, et al: Intervertebral disc injury complicating cervical spine trauma. Spine 16 (suppl 2):187189, 1991 27. Roaf R: A study of the mechanisms of spinal injuries. J Bone Joint Surg (Br) 42: 810823, 1960 28. Robertson PA, Ryan MD: Neurological deterioration after reduction of cervical subluxation. J Bone Joint Surg (Br) 74:224227, 1992 29. Rockwell D, Melhem ER, Bhatia R: GRASE (gradient-and spin-echo) MR imaging of the brain. AJNR Am J Neuroradiol 18:19231928, 1997 30. Roth JL, Nugent M, Gray JE, et al: Patient monitoring during magnetic resonance imaging. Anesthesiology 62:8083, 1985 31. White AA, Southwick WO, Panjabi MM: Clinical instability in the lower cervical spine: A review of past and current concepts. Spine 1:1527, 1976 32. Yashon D, Jane JA, White RJ: Prognosis and management of spinal cord and cauda equina bullet injury in 65 civilians. J Neurosurg 32:163170, 1970 Address reprint requests to Elias Melhem, MD Department of Radiology Johns Hopkins School of Medicine 600 North Wolfe Street Baltimore, MD 21287 e-mail: emelhem@rad.jhu.edu

THE SPINE AND SPORTS

02785919/02 $15.00 .00

SPINAL DEFORMITY IN THE ADOLESCENT ATHLETE


Kirkham B. Wood, MD

More and more young people are participating in sports, especially women, who are involving themselves in increasingly strenuous and vigorous competitive activities at an earlier age than ever before.41 Knowledge about the effect sports have on the developing spine and about the capacity of a youngster aficted with a spinal deformity to compete in sporting activities is especially pertinent today. NORMAL SPINAL GROWTH The growing spine increases in size and length by a combination of longitudinal and latitudinal growth. Individual vertebral bodies and their posterior elements enlarge circumferentially by a combination of appositional growth while they elongate by endochondral ossication. The primary ossication center of the vertebral body is initially associated with a spherical physis, similar to epiphyseal ossication.39 After birth, the ossication center enlarges towards the sides of the vertebrae and the intervertebral discs. Gradually, this spherical growth center expands to demarcate increasingly parallel growth plates at the cephalad and caudad ends of the vertebra. The physis remains the major mechanism for enlargement of the axial skeleton. The physis is principally involved with longitudinal growth; however, it also contributes to circumferential expansion of the centrum. There is a growth plate present anteriorly at each neurocentral synchondrosis and similarly posteriorly at the spinous processes, which

From the University of Minnesota, Minneapolis, Minnesota

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allow increased length of the laminae and pedicles. These growth plates generally close much earlier so that the posterior elements are mature by the end of the rst decade, and longitudinal growth anteriorly continues until age 16 to 18. If there are any asymmetric closures here, it may be a predisposing factor for spinal deformity. Latitudinal growth of the vertebrae occurs via two mechanisms: the perichondrium, which surrounds the body, and diametric growth within the physis and the adjacent epiphysis, both of which are responsive to physiologic and mechanical stresses. SPINAL DEFORMITY (SCOLIOSIS, KYPHOSIS) Despite extensive research, the etiology behind the development of idiopathic adolescent spinal deformities such as scoliosis and kyphosis (Scheuermanns kyphosis) remains obscure. The prevalence of adolescent idiopathic scoliosis in the general population has been estimated to be between 2% and 3%.3, 56, 57 It is one of the most common childhood deformities and typically more common in girls than boys especially in the adolescent period (Fig. 1). Scoliosis is normally a painless condition no matter what the degree of curvature. It is not until the adult years that pain normally becomes any sort of factor in the process. Yet it is important to remember that many adolescents, including those with scoliosis, will report varying degrees of back ache on presentation. Hence, it is necessary to determine whether any pain complaints are in fact benign and not caused by the scoliosis itself. Other conditions that may be the cause of a painful deformity in a growing child include fracture, benign tumors (osteoblastoma, osteoid osteoma), syringomyelia, and malignancy. Scheuermanns kyphosis is a developmental roundback deformity principally of the thoracic spine, believed to be principally caused by abnormal growth and development of the vertebral endplates over many segments resulting in an abnormal increase in the normal thoracic spine4 (Fig. 2). Scheuermann43 rst described the abnormal thoracic kyphosis as three consecutive anterior vertebral bodies wedged at least 5% each along with visible end-plate alterations, Schmorls nodes, and even apophyseal ring fractures. Its incidence has been estimated at between 2% and 8%.35, 44 As with scoliosis, milder degrees of kyphosis are normally well tolerated; however, as the degree of curvature increases, or if the deformity comes to involve parts of the lumbar spine, pain reports become more frequent and in advanced cases may be severe enough to limit the patients participation in sports. RISKS OF ATHLETICS ON SPINAL DEVELOPMENT The development of the musculoskeletal system in growing individuals is strongly inuenced by external forces acting upon them.10, 26

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Figure 1. AP (A) and lateral (B) radiographs of a 19-year-old athlete with adolescent idiopathic scoliosis. (From Asher MA, Strippgen WE, Heinis CF, et al: Isola Instrumentation. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

Sporting activities can provide just such large forces from muscular exertion and body motions. Studies have shown some sport-specic permanent anthropometic changes5, 21: Jantz and Brehme26 showed that directional asymmetry was more common in females and wondered whether this might explain the increased incidence of spinal deformity in young women in certain sports. Immature bone is much more sensitive to cyclic loading than mature bone.12, 24 In highly competitive sports, the spine of the growing athlete may be at risk because it is the conduit for transferring mechanical power between the upper and lower extremities during rapid and forceful movements.61 Hellstrom et al23 reviewed radiographs of 143 athletes and found abnormalities in the vertebral ring apophyses especially in male gymnasts and wrestlers. Most athletic training and competition exposes the spine to large loads as muscle forces rapidly accelerate and decelerate body segments. Intense competi-

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Figure 2. A, Scheuermanns kyphosis lateral radiograph showing hyperkyphosis and wedging of the thoracic spine. B, Clinical view. (From Ascani E, La Rosa, G: Scheuermanns kyphosis. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

tion increases that exposure because of multiple repeated loading cycles and could increase the chances of a spinal deformity. Ohlen, et al40 showed that young skeletally immature women participating in a vigorous gymnastics program had more developed lumbar lordosis than their nongymnastic peers. There is a small but noticeable increase in scoliosis amongst adolescent and preadolescent swimmers, especially girls. It has been suggested5 that this may be evidence of the direct-effect external forces brought on by intense exercise may have on the skeletal growth of the vertebrae. As the normal spinal growth in girls stops at an average of ages 14 to 15, and between ages 16 and 17 in boys, this would be considered prime time for the development of any growth-related deformity. INCIDENCE OF SPINAL DEFORMITY IN SPORTS Although the overall prevalence of idiopathic scoliosis has been reported to be between 2% and 3% in athletes, it may be higher, and

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estimates have ranged from 2% to 33%.31, 33, 54 There are well-known risk factors that have been identied for the development and progression of scoliosis. Certainly, a familial pattern plays a role.15, 16 Delayed puberty and menarche, situations commonly seen in the young female athlete, are two more risk factors for the development of scoliosis.18, 53 It is believed that the endocrine imbalances may actually affect vertebral development and predispose to curvature development. An extended growth period would also just increase the chances of spinal deformity developing. Sports that seem to lend themselves particularly to an increased incidence of scoliosis are those involving extreme torque and potential asymmetric muscle development, such as dancing, ballet, swimming, table tennis, and some overhead throwing sports such as tennis, hurling, or javelin throwing.5, 21, 23, 54, 53, 32, 51, 55 The increased incidence of scoliosis in swimmers has been studied by many researchers.5, 33, 27, 22 Jensen and Bullow27 wrote that the drag and inertial forces of swimming produce a sufcient load to produce functional changes in the paraspinal musculature and the risk of subsequent spinal deformity. Hauser,22 has suggested that any inability of the spinal musculature of young swimmers to keep up with the demand can lead to muscular imbalances and an increase in sagittal deformity as well, i.e., roundback kyphosis. Tanchev et al32 found in Bulgaria a 10-fold higher incidence of scoliosis in rhythmic gymnastic trainees, a sport marked by long hours of training typically begun at or before the sixth birthday, than their normal coevals. Most rhythmic gymnasts are thin, with height and weight signicantly lower than nontrainees and manifest obvious delays in growth and maturation. Could asymmetric mechanical loading alter vertebral end-plate development and alignment? Studies on growing rat tails wherein asymmetric loads were applied to the growth plates affected normal spinal development and led to spinal deformities such as kyphosis.36, 48 Scheuermanns kyphosis has also been linked with competitive swimming during the adolescent years,61, 2, 60 although a true causal relationship has yet to be established. Solomon et al47 described increased kyphosis in young dancers as a development to rebalance the torso over the pelvis. Actual wedging at the apex of the compensating kyphosis such as in Scheuermanns kyphosis can be seen. Proper treatment has been exibility exercises for the tight lumbodorsal fascia and hamstrings, and even antilordotic bracing in resistant cases. Sports such as water skiing have a reported high incidence of Scheuermanns kyphosis, especially when competitive skiing has begun at the age of 6.50 Arvidson and Micheli2 have described an atypical kyphosis seen in the thoracolumbar junction involving one or two vertebrae, often occurring in gymnasts who begin their career before the age of ve. A gibbus deformity may be present, and on radiographs actual collapse of the vertebral bodies can be seen. Recommended treatment has been stretching, strengthening exercises,

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and even hyperextension bracing. Surgery may be suggested in painfully resistant or progressive cases. ATHLETIC PARTICIPATION WITH SPINAL DEFORMITY Many years ago, there were many restrictions placed on a young athlete with scoliosis or kyphosis, especially with respect to the heavycontact sports. Cobb,13 Keim,30 Kuprian,32 and others49 have written that because no exercise is benecial to inhibiting the development of scoliosis, it was not to be encouraged. In 1941, the American Orthopaedic Association actually came to the conclusion that in idiopathic scoliosis, exercise should be avoided. Currently, however, knowledge and experience has taught us that scoliosis or kyphosis itself is not a contraindication to participation in most sports. There are some exceptions in the literature, however. Williams,59 has suggested that the developing child with scoliosis should not play volleyball at the professional level, citing the loads placed on the spine by the extreme rotations. There are no objective controlled studies, however, to support this contention. Becker,5 wrote that the role of swimming as a therapeutic exercise in the treatment of scoliosis is denitely contraindicated, because it has little effect on reversing the curvature. It was assumed that competitive swimming would have a progressive effect on the curvature if between the ages of 10 and 15. Our centers experience has been otherwise, however. We actively encourage the adolescents participation in any and all sports, including swimming and contact sports. We have not seen, nor is there any objective evidence in the literature to suggest, that active participation in any of these sports is directly associated with worsening of scoliotic or kyphotic curvatures above and beyond that of the natural history of the disease process. We feel that the aquatic activity helps maintain exibility, strength, and endurance and thus minimizes compressive and shear forces on the spine. We realize that swimming or any other exercise is not expected to reverse or correct any pathologic spinal deformity, but it does not mean that there are not therapeutic and psychological benets to such participation. ATHLETIC PARTICIPATION AFTER TREATMENT FOR SPINAL DEFORMITY Patients receiving treatment for scoliosis or kyphosis will typically wear a brace if the severity of the curve has increased and continued growth remains. For both scoliosis and kyphosis, the Milwaukee brace was the rst successful method of nonoperative treatment for spinal deformities rst introduced in the late 1940s (Fig. 3).1, 8 Before that, the principle means of nonoperatively affecting spinal growth was with a cast. Casting is still used occasionally in the treatment of some rigid

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Figure 3. Anterior (A) and posterior views (B) of a Milwaukee brace. Posterior view (C) of brace on an adolescent female with idiopathic scoliosis. (From Roach JW: Adolescent idiopathic scoliosis. In Weinstein SL [ed]: The Pediatric Spine: Principles and Practice. Raven Press, New York, 1994; with permission.)

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deformities, especially kyphosis. The Milwaukee brace consists of pads around the hips (the girdle) connected to pads against the spinal protrusion and a neck ring from which the patient actively pulls away, effecting correction of the curvature (Fig. 4). Historically, it was worn at least 23 out of 24 hours, although as skeletal maturity approached, time spent in the brace diminished. It was used for both kyphosis and scoliosis (Fig. 5). In fact, in part because of the development of the plastic thoracolumbarsacral corset, its use today is principally for that of kyphosis. Even with near continuous wear, an active exercise program has been considered a necessary part of a successful bracing program. Patients were encouraged, not discouraged, from participating in regular physical education, and sport even while wearing the brace, if possible, such as bicycling, horseback riding, or cheerleading. Swimming (during the hour out of the brace) was especially encouraged. The feeling was that swimming would remove the deforming effects of gravity on the

Figure 4. The application of a Milwaukee brace detailing the pad and force application. (From Ogilvie JW: Spinal orthotics. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

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Figure 5. Lateral view of a Milwaukee brace and pad application for the treatment of Scheuermanns kyphosis. (From Ogilvie JW: Spinal orthotics. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

spinal curvature while enhancing muscular conditioning and improve vital capacity as well as overall tness. The buttery stroke, however, continues to be discouraged by some because of a fear that overdevelopment of the pectoral muscles might worsen a kyphotic deformity.41, 60 Contact sports were denitely discouraged. Sport participation at the most concentrated levels, i.e., multiple hours, multiple sessions per day, makes wearing this orthosis impractical. In the 1970s, Benson et al,6 began extending the time out of the brace in a small series of competitive athletes (up to 5 hours) and showed no worsening of the radiographic measurements or the rib hump deformities. This ultimately was duplicated by other authors, and wearing the Milwaukee brace only 16 to 18 hours out of the day in selected patients became quite common.20, 28 In the 1980s, a new type of underarm orthosis was developed that consisted of a molded plastic shell with padding on the prominences, the thoracolumbosacral orthosis (Figs. 6 and 7).11, 34 It relies more on passive correction of the deformity rather than the active correction of a patients posture via the neck collar. It is custom molded to the patient in the lying position with padding added interiorly for curve correction.

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Figure 6. Anterior view of a Boston underarm thoracolumbarsacral orthosis (TLSO). (From Roach JW: Adolescent idiopathic scoliosis. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

Corrective forced can be adjusted by adding to or reducing the thickness of the pads. Initially, this too was to be worn 23 of 24 hours for patients with worsening curvatures; however, experience came to show that in many selected individuals, the success rates were similar wearing the orthosis 16 to 18 hours of the day.20, 28, 58 In 1989, Charles Price et al introduced the Charleston night-time bending brace42 (Fig. 8). This was a plastic orthosis similar to the thoracolumbosacral orthosis, yet it was molded with the patient bent to the side of the spinal deformity so as to correct the curve and was intended for night-time bed use only, i.e., 8 to 10 hours a day. There are certain curvatures where this type of bracing as been shown to be equally as efcacious as the more standard thoracolumbarsacral orthosis.42, 29 What advancement in the knowledge of brace-wear has allowed is more and more time for the athlete with spinal deformity to compete in his or her sport with and without the brace. Some institutions continue to discourage vigorous contact sports or heavy, upright weight lifting46, 38; however, their experience is mostly anecdotal and conjectural, because no study exists to date showing actual deleterious effects of contact sports on the curve of a braced individual. Our current practice and

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Figure 7. Boston underarm TLSO for the treatment of idiopathic scoliosis. (From Roach JW: Adolescent idiopathic scoliosis. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

others38, 25 is to encourage any and all athletic participation during the hours out of the brace (although certain sports may still lend themselves to in-brace participation in the newer lower prole orthoses), not only for its physical benet but also for the psychological and social wellbeing of the adolescent as well. In instances where the spinal deformity is too advanced to be effectively controlled with brace treatment or when the current bracing has been unsuccessful in halting the progression of the deformity, surgery is indicated. In the 1960s, the principle method for surgical correction of scoliosis and kyphosis was with a Harrington rod (or two) consisting of hooks inserted into the bones of the spinal at the top and bottom of the curvature, which were then extended to correct the deformity, which was then fused using bone typically grafted from the patients hip. Curve correction was signicant; however, because of the limited strength of the rods and its xation, patients typically spent weeks in bed and months in a body cast, excluding them virtually from all athletic participation. Modern techniques of surgical correction of spinal deformity typically employ much more rigid instrumentation xed to the spine with hooks and screws at multiple sites, with parallel rods on both sides

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Figure 8. Charleston night-time bending brace. Shown is the application of the brace which bends the spine so as to correct the principle scoliosis. (From Gavin TM, et al: Orthotic treatment for spinal disorders. In Weinstein SL [ed]: The pediatric spine: Principles and practice. Raven Press, New York, 1994; with permission.)

of the spine, allowing tremendous three-dimensional correction of the deformity, often without the need for postoperative immobilization7, 14, 45 (Fig. 9). Still, it generally takes 1 to 2 years for a fusion mass to become completely mature and solid. In the past, it was suggested that after scoliosis fusion, participation in certain sports such as gymnastics, diving, and contact sports should be contraindicated.2, 38, 37, 52 This was for fear of disruption of the instrumentation or the fusion mass and to avoid concentration of forces above or below the rigid fusion mass. Biomechanical studies do show increased stress at spinal levels adjacent to a rigid fusion, which could theoretically risk increased degenerative changes over time. In addition, there have been isolated reports of spinal injury adjacent to a fusion mass,5, 2, 46, 37, 19 but there remains no evidence to suggest that as a population this type of injury is occurring with any greater frequency than that seen in the general population. In our experience, the rigidity of the new xation and correction techniques has allowed patients to return to sporting activities much earlier than before. Currently, activities such as recreational swimming, bicycling, and hiking can begin as early as 2 months postoperatively. By 4 months, light physical activities such as tennis, playing catch, and shooting basketballs is allowed. By 6 months, if the fusion appears solid and the instrumentation appears stable, and the patient is without pain, we currently allow resumption of full activities, including contact and twisting sports. The treating physician must take into account, however,

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Figure 9. AP radiograph showing scoliosis corrected with multiple hooks, screws and wires, allowing participation in vigorous sports 4 months following surgery.

exactly how much of the spine has been fused, especially how low into the lumbar spine it extends as well as the expected demands the unfused spine will see. We think that on a recreational level, and even fulltime, participation as an adolescent in all activities is possible. At the Orthopadische Klinik in Hanover, Germany,17 they reported on 10 patients treated with surgical correction and spinal fusion with instrumentation for Scheuermanns kyphosis, all of whom returned to sport, including swimming bicycling and gymnastics, none of whom reported any complications. In fact, almost all found that their physical load capacity and behavior in relation to back pain were better than before the operation. Our experience has been similar. However, with long fusions into the lower part of the lumbar spine, L3 or below, we would caution the adolescent against taking up heavy twisting or contact sports as a career. With this approach, we have had no instances of instrumentation dislodgment or other sequelae during the 10 years we have employed this philosophy. The reader should be aware, however, that others are somewhat more conservative and still

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keep patients out of activities such as football and wrestling on a permanent basis.9 SUMMARY Today more and more children with diagnoses of adolescent spinal deformity are participating in athletic competitions. Certain sports appear to have an increased association with spinal deformity, especially in the adolescent female population. Modern treatment techniques including bracing will allow participation in most athletic endeavors. Those treated with surgery need to have their postoperative care individualized. However, modern surgical techniques still allow continued participation in most activities. References
1. Andrews G, MacEwen GD: Idiopathic scoliosis. An 11-year follow-up study of the role of the Milwaukee brace in curve control and trunco-pelvic alignment. Orthop 12: 809, 1989 2. Arvidson EB, Micheli LJ: Spine and trunk problems in athletes. Curr Opin Orthopaed 1:361, 1990 3. Ascani E, Giglio GC, Salsano V: Scoliosis screening in Rome. In Zorab PA, Siegler D (eds): Scoliosis. London, Academic Press, 1980, p 39 4. Ascani E, La Rosa G: Scheuermanns kyphosis. In Weinstein SL (ed): The Pediatric Spine: Principles and Practice, vol. 1. New York, Raven Press, 1994, p 557 5. Becker TJ: Scoliosis in swimmers. Clin Sports Med 5:149, 1986 6. Benson DR, Wolf AW, Shoji H: Can the Milwaukee brace patient participate in competitive athletics? Am J Sports Med 5:7, 1977 7. Birch JG, Herring JA, Roach JW, Johnston CE: Cotrel-Dubousset instrumentation in idiopathic scoliosis. A preliminary report. Clin Orthop 227:24, 1988 8. Blount WP, Schmidt AC, Bidwell RG: Making the Milwaukee brace. J Bone Joint Surg (Am) 40:526, 1958 9. Bridwell K: Adolescent idiopathic scoliosis. In Weinstein SL (ed): The Pediatric Spine: Principles and Practice., vol 1. New York, Raven Press, 1994, p 511 10. Burwell RG, James NJ, Johnson F, et al: Standardized trunk asymmetry scores. J Bone Joint Surg (Br) 65:452, 1983 11. Carman DL, Browne RH, Birch JG: Measurement of scoliosis and kyphosis radiographs. Intraobserver and interobserver variation. J Bone Joint Surg (Am) 72:328, 1990 12. Carter DR: Mechanical loading histories and cortical bone remodeling. Calc Tissue Int 36(suppl 1):S19, 1984 13. Cobb JR: Scoliosis. J Bone Joint Surg (Am) 40:510, 1958 14. Cotrel Y, Dubousset J, Guillaumat M: New universal instrumentation in spinal surgery. Clin Orthop 227:10, 1988 15. Cowell HR, Hall JN, MacEwen GD: Familial patters of idiopathic scoliosis. J Bone Joint Surg (Am) 51:1236, 1969 16. Cowell HR, Hall JN, MacEwen GD: Genetic aspects of idiopathic scoliosis. Clin Orthop 86:121, 1972 17. Daentzer D, Scholz M, von Strempel A: Sport und korperliche belastbarkeit nach aufrichtungsspondylodese bei patienten mit Scheueermann-kyphose. Sportverl Sportschad 13:22, 1999 18. Drummond DS, Rogala EJ: Growth and maturation of adolescents with idiopathic scoliosis. Spine 5:507, 1980

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19. Friedman RJ, Micheli LJ: Aquired spondylolisthesis following scoliosis surgery. Clin Orthop 190:132, 1984 20. Green NE: Part-time bracing of adolescent idiopathic scoliosis. J Bone Joint Surg (Am) 68:738, 1986 21. Gussbacher A, Rompe G: Die dynamische und statische beanspruchung der Wirbelsaule und ihre moglichen auswirkungen bei verschiedenen sportarten. Schweiz Z Sportmed 31:119, 1983 22. Hauser E: Scoliosis. Physiother Rev 17:234, 1937 23. Hellstrom M, Jacobsson B, Sward L: Radiologic abnormalities of the thoraco-lumbar spine in athletes. Acta Radiol 31:127, 1990 24. Hou JC, Salem GJ, Zernicke RF: Structural and mechanical adaptations of immature trabecular bone to strenuous exercise. J Appl Physiol 63:1309, 1990 25. Hunter LY, Andrews JR, Clancy WG, Funk FJ: Common orthopaedic problems of female athletes. Instr Course Lect 31:126, 1982 26. Jantz RL, Brehme H: Directional and uctuating asymmetry in the palmar interdigital ridge-counts. Anthropol Anz 51:59, 1993 27. Jensen RK, Bellow DG: Upper extremity contraction moments and their relationship to swimming training. J Biomechanics 9:219, 1976 28. Kahanovitz N, Levine DB, Lardone J: The part-time Milwaukee brace treatment of juvenile idiopathic scoliosis. Clin Orthop 167:145, 1982 29. Katz DE, Richards BS, Browne RH, Herring JA: A comparison between the Boston brace and the Charleston bending brace in adolescent idiopathic scoliosis. Spine 22: 1302, 1997 30. Keim HA: The Adolescent Spine. New York, Springer-Verlag, 1982 31. Krahl H, Steinbruck K: Sportsachaden and sportverletzungen and der wirbelsaule artztebl deutsch. 12:19, 1978 32. Kuprian W: Physical Therapy for Sports. Philadelphia, WB Saunders, 1982 33. Kuprian W, Ork H, Meissner L: Spinal column and torso. In Kuprian W (ed): Physical Therapy for Sports. Philadelphia, WB Saunders, 1982, p 262 34. Labelle H, Dansereau J, Belleeur C, Poitra SB: Three-dimensional effect of the Boston brace on the thoracic spine and rib cage. Spine 21:5964, 1996 35. Lowe TG: Scheuermann Disease. J Bone Joint Surg (Am) 72:940, 1990 36. Mente PL, Stokes IA, Spence H: Progression of vertebral wedging in an asymmetrically loaded rat tail model. Spine 22:1290, 1997 37. Micheli LJ: Sports following spinal surgery in the young athlete. Clin Orthop Rel Res 198:152, 1985 38. Moe JH: Back problems in the young athlete. Journal of the American College Heath Association 17:126, 1968 39. Ogden JA, Ganey TM, Sasse J, et al: Development and maturation of the axial skeleton. In Weinstein SL (ed): The Pediatric Spine., vol. 1. New York, Raven Press, 1994, p 3 40. Ohlen G, Wredmark T, Spangfort E: Spinal sagittal conguration and mobility related to low-back pain in the female gymnast. Spine 14:847, 1989 41. Omey ML, Micheli LJ, Gerbino PG: Idiopathic scoliosis and spondylolysis in the female athlete: Tips for treatment. Clin Orthop Rel Res 372:74, 2000 42. Price CT, Scott DS, Reed FE, Riddick MF: Nighttime bracing for adolescent idiopathic scoliosis with the Charleston bending brace: Preliminary report. Spine 15:1294, 1990 43. Scheuermann HW: Kyphosis dorsalis juvenalis. Ugeskr Laeger 82:385, 1920 44. Scoles PV, Latimer BM, DiGiovanni BF, et al: Vertebral alterations in Scheuermanns kyphosis. Spine 16:509, 1991 45. Shufebarger HL, Ellis RD, Clark CE: Cotrel-Dubousset instrumentation (CDI) in adolescent idiopathic scoliosis: Minimum two year follow-up. Orthop Trans 3:79, 1989 46. Slack CM: The spine in sports. Comprehensive Therapy 6:68, 1980 47. Solomon R, Brown T, Gerbino PG, Micheli LJ: The young dancer. Clin Sports Med 19: 717, 2000 48. Stokes IA, Aronsson DD, Spence H: Mechanical modulation of intervertebral disc thickness in growing rats. J Spinal Disord 11:261, 1998 49. Stone B, Beekman C, Hall V, et al: The effect of an exercise program on change in curve in adolescents with minimal idiopathic scoliosis. Phys Ther 59:759, 1979

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50. Tall RL: Spinal injury in sport: Epidemiologic considerations. Clin Sport Med 12: 441, 1993 51. Tanchev PI, Dzherov AD, Parushev AD, et al: Scoliosis in rhythmic gymnasts. Spine 25:1367, 2000 52. Von Strempel A, Scholz M, Daentzer M: Sports capacity of patients with scoliosis. Sportverletzung Sportschaden 7:58, 1993 53. Warren MP: The effects of exercise on pubertal progression and reproduction in girls. J Clin Endocrinol Metab 51:1150, 1980 54. Warren MP, Brooks-Gunn J, Hamilton LH, et al: Scoliosis and fractures in young ballet dancers. Relation to delayed menarche and secondary amenorrhea. N Engl J Med 314: 1348, 1986 55. Watson AWS: Posture and participation in sports. J Sports Med Phys Fitness 23: 231, 1983 56. Weinstein SL: Adolescent idiopathic scoliosis: Prevalence and natural history. Instr Course Lect 38:115, 1989 57. Weinstein SL: Idiopathic scoliosis. Natural history. Spine 11:780, 1986 58. Willers U, Normelli H, Aaro S, et al: Long-term results of Boston brace treatment on vertebral rotation in idiopathic scoliosis. Spine 18:432, 1993 59. Williams L: Volleyball. In Watkins RG (ed): The Spine in Sports. St. Louis, MosbyYear Book, 1996, p 522 60. Wilson FD, Lindseth RE: The adolescent swimmers back. Am J Sports Med 10: 174, 1982 61. Wojtys EM, Ashton-Miller JA, Huston LJ, Moga PJ: The association between athletic training time and the sagittal curvature of the immature spine. Am J Sports Med 28: 490, 2000 Address reprint requests to Kirkham B. Wood, MD University of Minnesota 420 Delaware St. SE, #492 Minneapolis, MN 55455 e-mail: woodx003@tc.umn.edu

THE SPINE AND SPORTS

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EPIDEMIOLOGY OF BACK PAIN IN THE ATHLETE


Timothy J. Trainor, MD, and Sam W. Wiesel, MD

Back pain affects millions of people and is one of the most common maladies prompting patients to seek medical attention. The lifetime prevalence of low back pain in the general population approaches 85% with 2% to 5% of people affected yearly. Back pain is the most common cause of disability in persons younger than age 45.3 The average patient who suffers spine trauma in the general population is a 30-year-old male. A sport-related mechanism occurs in 6% to 13% of these injuries.3 With so many of the general population affected by back pain, the athlete cannot escape the pervasive nature of this ailment. In addition, many sporting activities place the athlete at greater risk of sustaining a back injury than the nonathlete. Numerous authors have estimated that approximately 10% to 15% of sports injuries are related to the spine.22, 32, 34, 35 Tall and Devault reported spinal injuries with associated neurologic compromise occur in .6% to 1% of all sports injuries.35 Certain sports, both contact and noncontact, are associated with particular injuries and incidences of back pain. Dreisinger and Nelson reported the incidence of back pain varies between 1.1% to 30%, depending on the specic sport involved.8 Similar to the back pain and injuries that occur in the general population, the vast majority of these ailments in the athletic population are self-limiting processes that respond well to modied activities, mild analgesics, and physical therapy. However, many unique differences exist between the athletic and nonathletic populations that affect the specic epidemiologic patterns of back pain and the individuals re-

From the Department of Orthopaedic Surgery, Georgetown University Medical Center, Washington, DC

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sponse to it. Furthermore, within the athletic population itself there exist differences in regard to adolescent and adult subgroups. The distinctions between these groups will briey be reviewed with a focus on how they affect the epidemiology of back pain in the athlete. The specic etiologies of back pain and injury in the athlete will then be outlined with a discussion of appropriate strategies for imaging and treatment. ATHLETES AND NONATHLETES When examining the epidemiology of back pain in the athlete, it is important to recognize certain distinctions between the athletic and nonathletic populations. Furthermore, epidemiologic data gathered in relation to nonathletic populations should not be applied to the athletic population for many reasons. The specic etiology of back pain in the general population is often elusive and may not be diagnosed with conventional diagnostic tests. The Orthopaedic Knowledge Update 6 (OKU 6) reports that up to 97% of back problems in the general adult population result from soft-tissue strains or sprains with fewer than 5% caused by a more serious underlying condition.3 Epidemiologic studies suggest that most back injuries in athletes are also soft-tissue related. Dreisinger and Nelson reported that a specic pain generator could not be identied in up to 85% of cases.8 Harvey and Tanner claim that the correct diagnosis of acute low back pain is established only 2% of the time at presentation.17 However, numerous epidemiologic studies have been conducted in an attempt to identify injury risk patterns associated with particular sports. These studies have been helpful in identifying certain high-risk sports and activities that predispose athletes to specic injuries. Nonetheless, these epidemiologic reports must be viewed with the unique characteristics of the athletic population in mind. Remember that an overwhelming majority of sports-related back injuries are selflimited and resolve before reported. In addition, many athletes may be reluctant to report back problems for fear of losing playing time or, in the case of professional athletes, monetary compensation; therefore, the incidence and types of various back ailments may be underestimated in the athletic population. In stark contrast, members of the general population may be motivated to report even minor injuries to receive workers compensation. In addition, the motivation of a general laborer to return to work may be quite different than the desire of an athlete to return to a sporting activity. This fact may have a considerable impact on the effort a patient expends in the rehabilitation process. Furthermore, the typical 4 to 6 weeks of treatment that is usually required for resolution of a back problem in the general population may be an unacceptable length of time to the scholarship athlete. The physiological and biochemical composition of the athletes back is the same as that of the nonathletes. Studies have not demonstrated that athletes have stronger back muscles than nonathletes do. This has important implications for both the treatment and prevention of back

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pain in athletes and stresses the importance of consciously working to strengthen the back muscles before returning to athletic competition. Although athletes and nonathletes have the same back anatomy, the forces that the athletes back is subjected to are often much greater than those seen by nonathletes. Moreover, these forces are usually sustained for long periods of time. The spine is vulnerable to injury in both contact and noncontact sports because the spine acts to absorb and transmit force between the upper and lower extremities. In addition, it maintains support and balance throughout the activity. Specic movements and body positions are required in different sports that will predispose the athlete to specic injury. For example, the increased incidence of spondylolysis is well documented in gymnasts who are constantly hyperextending their lower backs.13, 16, 27, 29, 35 Back pain in athletes typically results from one of two mechanisms, either an acute traumatic event or a repetitive activity that causes fatigue injuries. Overuse injuries are far more common than acute traumatic injuries. The specic etiology of these stress-type injuries is also much more difcult to identify. A nal distinction that should be made between athletes and nonathletes concerns the much higher incidence of degenerative and arthritic conditions seen in the nonathlete group. This fact is related to the much younger population that comprises the athletic group.14, 17, 24 Stenosis and spondylosis are exceedingly rare in the athletic population and are not generally discussed in reference to athletes except when referring to congenital stenosis. This is not to say that the athletic population is immune to the degenerative process that affects the general population; however, they are typically not affected appreciably until the conclusion of their athletic pursuits. Micheli and Wood examined the various causes of back pain affecting young athletes and members of the general population and found signicant differences in the etiologies between the two groups. They reported a 47% incidence of spondylolysis in young athletes compared with only a 5% incidence in the general adult population. They also cited an 11% incidence of disc-related back pain in adolescent athletes compared to a 48% incidence of discogenic back pain in the nonathletic adult population.24 ADOLESCENT AND ADULT ATHLETES The athletic population itself can be further divided between adolescent and adult groups. This is an important distinction to make because the adolescent group is prone to some unique causes of back pain that are related to the growth process itself.17 During the adolescent growth spurt, the paraspinal muscles and soft tissue do not grow at the same rate as the bone. As a result, the lumbodorsal fascia may become excessively tight, stressing the spine and causing back pain. Additionally, hamstring tightness encountered with growth of the lower extremities may lead to back discomfort. In the adolescent, the cartilaginous endplate is weaker than the nucleus pulposis; therefore, excessive compres-

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sive forces can cause the end plate to fracture. Fractures of the growth plate at the vertebral endplate allow the nucleus to herniate into the vertebral body. Acute stress fractures of the pars interarticularis are commonly encountered in the younger athlete. Spondylolysis generally develops between the ages of 6 and 10, with a reported prevalence of 4%. These injuries should be suspected in the adolescent athlete involved in sports requiring hyperextension motions such as diving and gymnastics. Awareness of the possibility of an acute pars fracture has important implications for the correct diagnostic evaluation of the adolescent athlete. The fracture often occurs without a specic traumatic event. Oftentimes, radiographic evaluation is unnecessary at the time of initial assessment in the older athlete with an acute episode of low back pain. By contrast, adolescent athletes may benet from obtaining an x-ray at their initial presentation because, if the pars defect is identied early, measures may be taken to allow the fracture to heal before it develops into a nonunion or a brous union. PREDISPOSING FACTORS TO BACK PAIN AND INJURY IN THE ATHLETE There are a number of factors that predispose the athlete to back pain and injury.17 One of the most common causes of pain is a recent change in the athletes training regimen. A sudden increase in the intensity or frequency of a training program will often initiate a painful back problem. This situation is often encountered at the start of a new season or before a particularly important sporting event for which the athlete has heightened his or her training schedule. This intense increase in activity most commonly will injure muscles, tendons, and ligaments, resulting in back pain. Poor conditioning can predispose the athlete to back pain. Athletes returning from the off season without maintaining a proper conditioning program are likely to suffer from back injuries. The abdominal musculature together with the erector spinae muscles act to stabilize the spine during sports activities. The normal ratio of trunk-exion strength to trunk-extensor strength is 1 : 1.3. Foster and Fulton showed this ratio to be substantially reduced in athletes with low back pain.11 As has been mentioned, athletes do not have stronger back muscles than nonathletes do; therefore, the importance of proper back strengthening exercises cannot be overemphasized. Hamstring tightness increases lumbar lordosis, whereas inexibility of the hip extensors acts to limit the lumbar lordotic curve. A proper balance between the two affords the spine better resistance to the stresses of axial loading. Muscular activity is transferred from the upper to lower extremities via the spine and pelvis. Decreased pelvic mobility will increase the strain felt by the low back. The athlete must maintain exibility to avoid undue stress to the spine.

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Improper technique and poor equipment may also contribute to low back pain in the athlete. Down linemen in football who block from an erect stance may sustain hyperextension injuries.10, 28, 30 Excessive lordosis in a weightlifter performing a military press will place extreme strain on the low back. Micheli reported a similar mechanism in male ballet dancers who were lifting their partners during performances.23 Unsuitable equipment can also play a role in back injury in athletes. Hochschuller reported on cyclists sustaining back pain secondary to excessively high bicycle seats.18 A very common type of athletic equipment that is often overlooked is proper footwear. The physician must be mindful of both technique and equipment when evaluating the athlete with a back complaint. GENERAL DIAGNOSTIC AND TREATMENT PRINCIPLES A review of multiple previous epidemiologic studies reveals that most sports-related spinal injuries are self-limited soft-tissue insults. Furthermore, multiple studies have shown that 80% to 90% of back problems resolve in 4 to 6 weeks; therefore, in most situations, an extensive work up is neither warranted nor economically feasible. An extensive history and a thorough physical examination remain the most important steps in attaining the proper diagnosis in the athlete with back pain. Plain radiographs and other imaging modalities are often unnecessary tests that should be reserved for specic scenarios. Imaging tests should be considered in an athlete whose back pain is severe, was caused by an acute, identiable traumatic event, or fails to improve after several weeks of appropriate conservative treatment. Obviously, patients with any neurologic compromise need further radiographic evaluation. Additionally, the very young adolescent athlete may benet from early radiographs as previously mentioned. Bone scan is helpful in detecting inammatory or malignant processes or in diagnosing an acute spondylolysis. Computed tomography scan is most useful to assess for fractures. Magnetic resonance imaging (MRI) allows for excellent visualization of disc abnormalities; however, a high incidence of asymptomatic patients has abnormal MRI scans, and this fact must be recognized. The immediate consequence of an athletic back injury is a decrease in functional mobility with a resultant deconditioning of the athlete. Immediate treatment is aimed at avoiding long periods of bedrest that will perpetuate a deconditioning cycle. Bedrest should be limited to 24 to 36 hours in most situations, and walking should be encouraged. Spasms may be treated acutely with ice. Nonsteroidal anti-inammatory drugs (NSAIDS) should be used to reduce the inammatory response. Narcotic medication should be avoided except to allow the athlete to sleep. Rehabilitation should be initiated as soon as the spasm and pain is subsiding, preferably at approximately 48 hours. Again, the goal is to avoid the deconditioning that occurs as the athlete remains inactive.

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Williams exion and McKenzie extension exercises are a mainstay of rehabilitation. Rehab should focus on strengthening both exors and extensors unless specically contraindicated. Specically, extension should be avoided in spondylolysis, spondylolisthesis, and facet joint disorders. Flexion is contraindicated in an acute herniated nucleus pulposis. The rehabilitation process progresses as symptoms dictate, with more aggressive therapy initiated as symptoms abate. Return to athletic competition may be allowed when the athlete demonstrates normal strength and exibility and the functional skills required of the specic sport involved. Approximately 40% to 60% of back pain recurs at some point; therefore, maintenance of a back program is an important step in preventing future problems. SPORT-SPECIFIC BACK PAIN Many epidemiologic studies have been conducted to identify specic injuries associated with certain sports. Some authors argue that analyzing the precise mechanism of injury is more useful than examining the individual sporting event during which it occurs. They claim the back injury is more closely related to the magnitude and point of force rather than to the specic sport involved. Any mechanism can occur in any sport; however, certain mechanisms are more commonly encountered in specic sports activities. Therefore, it is useful to recognize the forces involved in certain sports that predispose the athlete to specic injury. As has been mentioned, the incidence of spinal injuries related to sporting events has been reported to be between 10% and 15%. Fortunately, neurologic involvement occurs in less than 1%.35 Neorologic injury is most commonly associated with football, water sports, gymnastics, rugby, and ice hockey. These injuries occur almost exclusively in the setting of a specic traumatic event. Noncontact Sports Back pain is a common complaint of many noncontact athletes. Tall and Devault found 29% of professional golfers reported a history of low back pain.35 At any given time, 10% to 30% of tour players experience back pain. Spencer and Jackson reported that 90% of tournament golfers have sustained back injuries.32 Low back pain is not as common in runners and is rarely encountered in the age group younger than 25 years old. Glick reviewed 120 middle-aged runners and found a 9% history of back pain.15 Jackson reported a 1.1% incidence of low back pain in adult runners.21 Rossi found a 22.5% incidence of spondylolysis in track and eld athletes.27 Weight lifting places tremendous forces on the spine. Disc failure has been reported to occur at 220 kg.35 Disc degeneration is quite com-

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mon in weightlifters, with a reported incidence of 80% in male lifters older than age 40. Females older than 40 have a 65% incidence of disc degeneration.35 Rossi reported a 36.2% incidence of spondylolysis in weightlifters.27 Racquet sports require extensive twisting and rotational movements; therefore, back pain is commonly seen in these sports. Haas reported 3.8% of professional tennis players missed a tournament secondary to low back pain. Chard and Lachmann reviewed 631 injuries sustained in racquet sports. They reported a 12% incidence of back injury, with 59% related to squash, 21% related to tennis, and 20% related to badminton.5 The majority of these injuries were in athletes older than the age of 25. Back pain and injury occurs frequently in gymnasts and divers because both athletes commonly perform hyperextension types of activities.16 Garrick reported 12.2% of injuries in gymnasts were related to the spine.13 Tall and Devault reported a rate of spondylolysis of up to 11% in gymnasts.35 Rossi reported an incidence of 32% in gymnasts and 63% in divers.27 More than 15 hours of training per week has been associated with a higher incidence of back injury in these athletes. Contact Sports Back pain has been reported in basketball, wrestling, and rugby; however, by far the most extensive research has examined back pain in ice hockey and football. Tall and Devault reported that during the 1980s more than 15 hockey-related major spinal injuries occurred per year in Canada.35 These injuries typically resulted after a check sustained in the back that catapulted the player forward into the boards. The high speed attained by the players contributes to the tremendous forces the neck and back experience during competition. Football-related back pain and injury has been studied more extensively than injury sustained in any other individual sport. Saal reported in 1988 that up to 30% of football players miss games because of back pain.28 Semon and Spengler found 27% of 506 collegiate football players complained of lumbar back pain.30 In a review of 1097 injuries sustained at the professional level, 6% were back injuries. Approximately 50% of lineman report having a history of back pain. Back pain in football players is associated with both the cervical and lumbar spine. Alley reviewed more than 19,000 high school football players and found a .6% incidence of cervical spine injury.1 Another review of high school football players found 4% of players lost playing time because of cervical injury. Burners and even transient quadriparesis are not uncommon. Torg and Reiley studied college football teams and found a 52% incidence of stingers in one calendar year despite only 10% of these players being examined by the team physician. Congenital cervical stenosis has been implicated as a risk factor for sustaining neurologic insult after an injury. Multiple studies have examined lumbar spondylolytic defects and spondylolisthesis. Shaffer et al reported a .9%

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prevalence of spondylolisthesis among college football players and 1.5% among professionals.31 When analyzed by position, 48% in college and 50% in professional football were lineman. McCarroll et al reported a 4% prevalence of listhesis among incoming freshman football players. SPECIFIC DIAGNOSTIC ENTITIES The vast majority of back pain in the athlete occurs as a result of soft-tissue sprain or strain with only a small percentage of injuries resulting from more serious conditions. Other diagnoses that must be considered include herniated nucleus pulposis, fractures, spondylolysis and spondylolisthesis, stingers, transient quadriparesis, tumors, infection, primary inammatory conditions, and nonspine-related conditions such as shoulder or hip pathology. Sprains involve injuries to ligaments. Strains are insults of muscle or musculotendinous units. These are by far the most common injuries associated with back pain in the athlete. These injuries are readily diagnosed based on history and physical examination. The athlete may not recall a specic episode in which the injury occurred. At times the player will remember a twisting type of injury. The patient experiences point tenderness and may suffer from paraspinal spasm. Radiographs are not necessary as long as the athlete is neurologically intact and did not sustain the injury with an excessive amount of force. These conditions generally respond quite well to conservative treatment with rest, a short period of activity restriction, ice for the spasms, NSAIDS for acute pain relief, and physical therapy to strengthen the spinal muscles. Bed rest should be avoided, and walking is encouraged. Symptoms usually resolve in 2 to 6 weeks. Depending on the severity of symptoms, the athlete may need to be restricted from competition for a short time. When the spasm has subsided, the pain is tolerable, and the athlete has full exibility, return to competition is permitted. If symptoms do not resolve in 2 to 4 weeks, a more thorough diagnostic evaluation should be pursued. The intervertebral disc is most at risk with lateral bending and axial rotation. Repetitive torsional forces and lumbar exion can stress the annulus bers and result in tears. The posterolateral annulus is the weakest area and is where most herniations occur. HNP in the athlete may not present with true sciatic symptoms, but rather may appear with nonspecic buttock pain. MRI imaging allows excellent evaluation of the disc; however, many asymptomatic patients will have abnormal MRI studies and this test should be used with this fact in mind. The natural history of herniated nucleuspulposus (HNP) is quite favorable with most herniations even in the presence of neurologic compromise. Several studies have shown that most herniated discs resorb over time. HNP most often responds well to conservative therapy. Rest and NSAIDS should be employed along with extension exercises. Unlike soft-tissue injuries, the athlete is usually restricted from competition for a longer period of time. Motor strength should be normal before return to compe-

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tition. With severe symptoms, an epidural injection may be used early in treatment. If the athlete does not respond to 6 weeks of appropriate conservative treatment or in the setting of progressive neurologic decit, surgical options may need to be explored. An extensive discussion of spine fractures is beyond the scope of this review; however, a brief mention of some common minor injuries is warranted. Anterior compression fractures may be seen in the setting of forced exion. Direct blows can cause fractures of the spinous or transverse processes. Adolescent athletes are susceptible to fractures of the growth plate at the vertebral endplates. These injuries are diagnosed on plain x-ray. These injuries are treated with rest, pain medication, and modied activity. As symptoms abate, the athlete can be returned to activity in a phased continuum. Spondylolysis and spondylolisthesis may be diagnosed as an incidental nding on plain radiographs. However, lysis and listhesis must be considered in the athlete performing repetitive hyperextension motions such as gymnastics, diving, football, and wrestling. These conditions are diagnosed on plain x-rays most of the time. It is important to obtain anteroposterior (AP), lateral, and both right and left oblique views. Approximately 20% of defects are unilateral and will be missed if both oblique views are not obtained. If spondylolysis is not seen on the plain radiographs but is still suspected in the acute injury setting, a bone scan should be obtained. A brace may be used in the acute setting along with appropriate analgesia. The athlete is restricted from participation with the hope that the defect may unite. Stingers or burners are frequently seen in contact sports such as football and rugby. The incidence has been reported to be between 49% and 65% in college football players.3 A stinger is a temporary episode of a unilateral upper extremity burning dysesthesia accompanied by motor weakness. The painful sensation usually radiates from the neck down to the ngertips. The spinatus, deltoid, and biceps are the most commonly involved muscles. The mechanism of injury is usually a direct blow to the neck or shoulder causing a traction type of injury to the brachial plexus, cervical nerve roots or both. The diagnosis is made by history and physical exam. Immediately after the injury, the player is watched closely on the sideline. If the dysesthesias disappear, the athlete has return of normal motor strength, and it is the rst time he or she has sustained this injury, he or she may be permitted to return to the game. Transient quadriparesis is a neuropraxia of the cervical spinal cord. An incidence of approximately 7 per 10,000 has been reported in collegiate football players.3 Both sensory and motor abnormalities are present bilaterally. The symptoms usually last for approximately 15 minutes but may remain for up to 48 hours. The motor dysfunction ranges from bilateral upper and lower extremity weakness to complete paralysis. Developmental cervical stenosis, the presence of a congenital cervical fusion, and cervical instability are predisposing factors. The diagnosis made by clinical exam, and the athlete will need to undergo further work up with plain x-rays and MRI scan.

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The athlete is not immune to other diagnostic entities that afict the general population such as tumor, infection, or primary inammatory conditions. These possibilities must be considered in the setting of unusual presentations or in situations where the other more common diagnoses do not seem plausible. Athletes with these conditions will typically have nonmechanical pain, night pain, and other constitutional symptoms. After a thorough history and physical, x-rays and laboratory studies are obtained, and the need for more extensive imaging studies is reviewed. Treatment is then tailored to the specic diagnosis. Finally, pain may be referred to the back from other areas of pathology, including, but not limited to, the hip, the shoulder, and the viscera. Again, a complete history plays a key role in drawing the physicians attention to these other diagnostic possibilities. A thorough physical examination of the patient will prove invaluable in narrowing the scope of diagnostic possibilities.

SUMMARY Back pain and injuries are common complaints of athletes. The nature of the sport involved with the specic stresses that it places on the athletes spine may play a role in the injuries incurred. These injuries may limit an athletes function and hinder performance; however, the majority of these insults are self-limiting and respond well to conservative measures. Based on the epidemiologic data, it appears that possibly the single most important step in reducing the back pain experienced by athletes would involve the performance of a structured back-strengthening program. Such a plan might reduce the most common diagnostic entities encountered by the athlete with back pain.

References
1. Alley RH: Head and neck injuries in high school football. JAMA 188:418, 1976 2. Birney J, Hanley E: Traumatic cervical spine injuries in children and adolescents. Spine 14:1277, 1989 3. Beaty JH, ed.: Orthopaedic Knowledge Update Six, 1999 4. Cannon SR, James SE: Back pain in athletes. Br J Sports Med 18:159164, 1984 5. Chard MD, Lachmann MA: Racquet sports-patterns of injury presenting to a sports injury clinic. BR Sports 21:150, 1987 6. Commandre FA, Gagnerie G, Zakarian M, et al: The child, the spine in sport. J Sports Med 28:11, 1988 7. Deusinger RH: Biomechanical considerations for clinical applications in athletes with low back pain. Clin Sports Med 8:703715, 1989 8. Dreisinger TE, Nelson B: Management of back pain in athletes. Sports Med 21:313 320, 1996 9. Feeler L: Racquet Sports: The Spine in Sports. Philadelphia, Hanley and Belfus, 1990, pp 143151 10. Ferguson RJ, McMaster JH, Staniski CZ: Low back pain in college football linemen. J Sports Med 2:63, 1974

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11. Foster DN, Fulton MN: Back pain and the exercise prescription. Clin Sports Med 10: 197209, 1991 12. Fredrickson BE, Baker D, McHolick WJ, et al: The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg (Am) 66:699707, 1984 13. Garrick JG, Requa RK: Epidemiology of women gymnast injuries. Am J Sports Med 8: 261, 1980 14. Gerbino PG, Micheli LJ: Back injuries in the young athlete. Clin Sports Med 14: 571590, 1995 15. Glick J, Katch V: Musculoskeletal injuries in jogging. Arch Phys Med Rehabil 51: 123, 1970 16. Goldstein JD, Berger PE, Windler GE, Jackson DW: Spine injuries in gymnasts and swimmers: An epidemiologic investigation. Am J Sports Med 19:463468, 1991 17. Harvey J, Tanner S: Low back pain in young athletes. Sports Medicine 12:395406, 1991 18. Hochschuler SH: The Spine and Sports. Philadelphia, Hanley and Belfus, pp 267275, 1990 19. Jackson D, Forman W, Benson B: Patterns of injuries in college athletes: A retrospective study of injuries sustained in intercollegiate athletics in two colleges in a two year period. Mt Sinai J Med 47:423, 1980 20. Jackson DW, Spencer CW: Back injuries in the athlete: Symposium on Olympic sports medicine. CIRN Sports Med 2:291, 1983 21. Jackson DW, Pagliano J: The ultimate study of running injuries. Runners World, November 1980, p. 42 22. Maxwell C, Spiegel A: The rehabilitation of athletes following spinal injuries. In Hochschuler SH: The Spine in Sports. Philadelphia, Hanley and Belfus, 1990, pp. 281 292 23. Micheli LJ: Back injuries in dancers. Clin Sports Med 2:473484, 1983 24. Micheli LJ, Wood R: Back pain in young athletes: Signicant differences from adults in causes and patterns. Arch Pediatr Adolesc Med 149:1518, 1995 25. Osterman K, Schlenzka D, Poussa M, et al: Isthmic spondylolisthesis in symptomatic and asymptomatic subjects, epidemiology, and natural history with special reference to disk abnormality and mode of treatment. CORR 297:6570, 1993 26. Riley T, Leatt D, Troup JG: Spinal loading during circuit weight training and running. Br J Sports Med 20:119, 1986 27. Rossi F: Spondylolysis, spondylolisthesis and sports. J Sports Med Phys Fitness 18: 317340, 1988 28. Saal JA: Rehabilitation of football players with lumbar spine injury. Phys Sport Med 16:61, 117, 1988 29. Saal JA: Lumbar injuries in gymnastics. In Hochschuler SH: The Spine in Sports. Philadelphia, Hanley and Belfus, 1990, pp. 192206 30. Semon RL, Spengler D: Signicance of lumbar spondylolysis in college football players. Spine 6:172, 1981 31. Shaffer B, Wiesel S, Lauerman W: Spondylolisthesis in the elite football player: An epidemiologic study in the NCAA and NFL. J Spinal Disorders 10:365370, 1997 32. Spencer CW, Jackson DW: Back injuries in the athlete. Clin Sports Med 2:191216, 1983 33. Stanish W: Low back pain in athletes: An overuse syndrome. Clin Sports Med 6: 321344, 1987 34. Stinson JT: Spine problems in the athlete. Md Med J 45:655658, 1996 35. Tall RL, DeVault W: Spinal injury in sport: Epidemiologic considerations. Clin Sports Med 12:441448 36. Weiker GG: Evaluation and treatment of common spine and trunk problems. Clin Sports Med 8:399417, 1989 Address reprint requests to Timothy J. Trainor, MD Georgetown University Hospital Department of Orthopaedic Surgery 3800 Reservoir Rd; Ground PHC Bldg. Washington, DC

THE SPINE AND SPORTS

02785919/02 $15.00 .00

MANAGEMENT OF THE ATHLETE WITH LOW BACK PAIN


Steven Z. George, MS, PT, and Anthony Delitto, PhD, PT, FAPTA

Low back pain (LBP) is a common experience for the general population, and, unfortunately, athletes are not immune to the effects of LBP.9 The elite athlete losing signicant playing time because of a back injury is a familiar but anecdotal story. A brief review of the literature indicates that LBP is a common cause of limited play and practice time for a variety of sports, including rowing,42 swimming,24, 48 gymnastics,24, 38, 44 football,26, 45 weightlifting,1, 43 racquet sports,8 and triathlon.32 In addition to affecting many different types of sports, LBP is found at all levels of athletics.10, 28, 39, 46 For these reasons, clinicians working with athletes should be familiar with the evaluation and treatment of LBP. The clinician evaluating an athlete with low back pain must consider a management dichotomy. The majority of athletes with low back injuries are likely to have pain from a benign source.46 These athletes will be expected to respond well to nonoperative treatment and return to their sport in a timely manner. A minority of athletes, however, may experience pain from a different source (e.g., spinal stress fracture or nerve root compression).5, 17, 23, 29, 30 In these cases, different management may be indicated. The clinician evaluating athletes with LBP must be able to effectively distinguish between these two scenarios.46 After making the determination that an athlete is appropriate for nonoperative treatment, additional decisions are to be made. For example, the clinician must consider the severity of the disease process. The clinician cannot be expected to manage the athlete with acute LBP in the same manner as the athlete with chronic low back pain. After the

From the School of Health and Rehabilitation Sciences (SZG, AD); and the Department of Physical Therapy (AD), University of Pittsburgh, Pittsburgh, Pennsylvania

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severity of the disease is considered, a treatment that is specic to the athlete must be employed. In making these decisions, the clinician must consider factors that are unique to the athletes clinical presentation. Delitto et al12 have proposed a treatment-based classication system (TBC) for the management of LBP. This system provides a framework for clinicians to determine whether a patient is appropriate for nonoperative management, to determine the severity of the disease, and to apply a specic, matched treatment. The clinician makes these decisions using historical information, self-report questionnaires, and clinical examination ndings. The purpose of this article is to discuss the evaluation and treatment of the athlete using TBC as proposed by Delitto et al.12 FIRST-ORDER CLASSIFICATION: DOES THE ATHLETE NEED ADDITIONAL DIAGNOSTIC TESTING? The question to be answered during rst-order classication is: Is this athlete appropriate for physical therapy? With athletes, the primary concern at this level of classication is the identication of situations that require the clinician to consult with surgical or medical specialists. This is accomplished by recognizing signs of serious pathology that are not musculoskeletal in nature or by identifying lumbar pathology that is commonly misdiagnosed in athletes. Examples of such pathology include Scheuermanns disease, lumbar stress fractures, spondylolytic defects, nerve-compression disorders, infection, and metastatic diseases.5, 23, 30, 46, 48 For athletes, a lesser concern at this level of classication is the identication of signs and symptoms that are associated with magniedillness behavior. Because of its relative importance to the athletic population, this discussion will focus on the identication of suspected lumbar pathology. Athletes are screened for the presence of serious pathology by using a medical questionnaire, a disability questionnaire, and a pain-intensity scale.12, 19 The clinician then reviews these forms so any issues can be further reviewed with the athlete during the examination. The medical questionnaire includes questions that are intended to identify serious pathology that is not musculoskeletal in origin. These questions focus on unexplained weight loss, history of cancer, night pain, history of immunosuppression, vascular insufciency, and alterations of bowel and bladder function.4, 49 Any positive response on this questionnaire should be reviewed with the athlete, and, if appropriate, a full screen of the body system in question should be performed.12 The Oswestry Disability Questionnaire (ODQ)15, 16 and the painintensity scale are used to screen athletes for the presence of serious pathology. For the ODQ, athletes rate their function in 10 different areas by using a 05 scoring system. The total score is then expressed as a percentage, with 100% indicating total disability and 0% indicating no disability.15, 16 In the absence of magnied illness behavior, ODQ scores greater than 75% raise the suspicion that serious pathology may be

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present.12 For the pain-intensity scale, athletes rate their pain from 0 to 10 under three different conditions. The rst condition is the athletes present pain, the second condition is the athletes best pain rating in the past 24 hours, and the third condition is the athletes worst pain rating in the past 24 hours. Because mechanical LBP is often associated with a posture that reduces pain intensity, very high levels of pain (810) on all three conditions also increase the suspicion of serious pathology.12 In addition to considering the presence of more serious pathology, the clinician evaluating athletes with LBP must be aware of situations that are unique to athletes. A high level of suspicion for pars interarticularis pathology is needed for athletes involved in sports involving frequent collisions, loading of the lumbar spine in hyperextension, or repetitive, combined extension and rotation movements of the lumbar spine (e.g., gymnastics, ballet, football, diving, lacrosse, soccer, or hockey).3, 18, 47 Because stress reaction is often not detected during radiographic examination, additional diagnostic testing is often indicated to resolve the suspicion of pars interarticularis pathology.3, 47 In addition to lumbar spine defects, Featherstone17 recommends the evaluation of sacral stress fracture through magnetic resonance imaging in athletes with persistent LBP. Special attention must also be given to the adolescent and younger athlete. Micheli recommends that a high level of suspicion should be maintained to diagnose stress fractures and spondolytic defects in these athletes.38 To ensure proper evaluation of these defects, Libson30 suggests the use of oblique lumbar spine views. To detect rare conditions that may mimic LBP, Watkins and Dillen46 recommend bone scans in adolescent athletes having signicant LBP for more than 3 weeks. Signs of serious pathology and indications of lumbar pathology that are sometimes misdiagnosed need to be thoroughly investigated by the evaluating clinician. If appropriate, additional diagnostic testing should be requested before a decision regarding rehabilitation is made. Clinicians taking this approach are ensured that the athletes under their care are receiving the most appropriate treatment. SECOND-ORDER CLASSIFICATION: STAGING THE ATHLETE WITH REGARD TO ACUITY The question to be answered during second-order classication is: What stage in the disease process is this athlete? This is similar to determining whether the patient has symptoms that are consistent with acute, subacute, or chronic LBP. In TBC, there are three possible stages: Stage I, Stage II, and Stage III. This staging decision is not solely based on the amount of time that has elapsed since the initial injury. Instead, the athletes ability to perform basic activities and the athletes amount of disability (via ODQ score) are also considered when determining the severity of the disease process. Athletes who are unable to stand for 15 minutes, sit for 30 minutes,

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or walk 14 of a mile because of LBP would be considered appropriate for Stage I treatment.12 In our clinical experience, these athletes are expected to have an ODQ score that ranges between 40% and 60%. The treatment goal of Stage I is pain modulation, and specic treatment for patients in this stage will be discussed in detail in the section on thirdorder classcation. Athletes are considered appropriate for Stage II treatment when they exceed the requirements of Stage I but still have limitations in performing daily activities that are more advanced than standing, sitting, and walking (e.g., jogging).12 In our clinical experience, these athletes are expected to have an ODQ score that ranges between 20% and 40%. Athletes may progress from Stage I to Stage II with treatment, or athletes may have symptoms that are consistent with Stage II during the initial examination session. Pain modulation continues to be a treatment goal, and the additional goal of addressing signs of physical impairment is added in this stage. Treatment in this stage will be geared toward the athletes specic physical impairments and may include strength training, exibility training, aerobic training, and postural/body mechanics training. Athletes are considered appropriate for Stage III treatment when they can perform all daily activities but cannot resume full participation in sport.12 Stage III treatment is also appropriate for athletes with minimal disability who continue to have recurrent episodes of LBP. In our clinical experience, these athletes are relatively asymptomatic and are expected to have an ODQ that is below 20%. The ODQ is most helpful in documenting disability in Stage I and Stage II. Athletes in stage III will often have very low ODQ scores and will still not be able to return to their sport. This is because the ODQ is not as sensitive in rating disability among individuals who return to activities with a high physical demand. The treatment goal for patients in this stage is to return to full athletic participation and to prevent recurrence of LBP. This is accomplished through trunk-strengthening exercises, functional training, and sport-specic training. Stage III treatment represents the most important component of managing the athlete because it results in the athlete returning to sport and instructs the athlete in an exercise program that may prevent future episodes of LBP. THIRD-ORDER CLASSIFICATION: MANAGING THE ACUTE CONDITION Third-order classication is reserved for athletes who are appropriate for Stage I treatment. The question to be answered at this level of classication is: What specic treatment is most appropriate for this athlete? This question is best answered by having the clinician form an initial hypothesis as to what treatment would most likely benet the patient.13 Examination ndings then inuence the clinician to alter the hypothesis if appropriate.13

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Table 1. SUMMARY OF TREATMENT-BASED CLASSIFICATION SYSTEM12 Classication Extension syndrome Key Examination Findings Flexion activities increase pain Status improves with extension testing Status worsens with exion testing Recommended Treatment Extension exercises Restriction of exion activities

Flexion syndrome Mobilization syndrome (lumbar) Mobilization syndrome (sacroiliac)

Extension activities increase pain Flexion exercises Status improves with exion testing Restriction of extension activities Status worsens with extension testing Local, unilateral LBP Patterned, restricted range of motion Local pain at PSIS Positive sacroiliac tests Mobilization techniques Manipulation techniques Mobilization techniques Manipulation techniques Avoidance of sustained posture Trunk strengthening exercises Pelvic translocation exercises Extension exercises Mechanical traction Autotraction

Immobilization Frequent episodes of LBP syndrome Increased pain with static posture Lateral shift syndrome Traction syndrome Visible deformity Unilateral sidebending restriction Radicular symptoms Status worsens with lumbar movements

Components of the clinical examination used to formulate and test treatment hypotheses include the patient history, the observation of posture, the assessment of pelvic landmarks, and the examination of lumbar movements.12 The clinician identies clusters of key examination ndings that are unique to the appropriate treatment classication. Refer to Table 1 for a list of Stage I treatment syndromes and the corresponding key examination ndings. Seven individual treatment classications, broken down into four classication categories, have been described by Delitto et al (Fig. 1).12, 22 The rst treatment classication is specic exercise, containing the extension syndrome and exion syndrome. The specic exercise classication is based on examination and treatment principles rst described by Robin McKenzie.37 Athletes appropriate for this treatment category frequently note a postural preference and often have symptoms radiating into the lower extremity. Age is also an important consideration in this treatment classication. Athletes who are younger than age 40 should be considered more likely to be extension syndrome candidates, and athletes who are older than age 50 should be considered more likely to be exion syndrome candidates.22 The key examination nding that conrms this treatment classication is the ability of the athlete to improve (centralize37) or worsen (peripheralize) the status of his symptoms by performing repeated lumbar movements.12, 37 This treatment classication also consists of patients

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Figure 1. Original treatment classications collapsed into classication categories. (From Delitto A, Erhard RE, Bowling RW: A treatment-based classication approach to low back syndrome: Identifying and staging patients for conservative treatment. Phys Ther 75: 470485, 1995; and Fritz JM, George S: The use of a classication approach to identify subgroups of patients with acute low back pain: Interrater reliability and short-term treatment outcomes. Spine 25:106114, 2000; with permission.)

who were originally classied for lateral shift treatment and were able to improve their symptoms with lumbar movements. The lumbar movement associated with an improvment of symptoms is reinforced through therapeutic exercise, and the lumbar movement associated with a worsening of symptoms is discouraged through education or bracing. The second treatment classication is mobilization, containing sacroiliac mobilization and lumbar mobilization. Athletes in this treatment classication typically have symptoms that are unilateral and localized to the low back or sacroiliac region. The key examination ndings for the sacroiliac mobilization treatment syndrome are based on pelvic landmark testing and sacroiliac tests. If the clinician notes multiple positive ndings during these tests, sacroiliac mobilization is conrmed as the appropriate treatment. Treatment consists of a sacroiliac manipulation technique, which is typically followed by lumbar range of motion exercises. The key examination nding for lumbar mobilization treatment classication is the presence of an opening or closing lumbar movement pattern. An opening pattern is consistent with limited lumbar exion and limited lumbar sidebending opposite the side of pain. A closing pattern is consistent with limited lumbar extension and limited lumbar sidebending toward the side of pain. After the movement pattern is detected, the clinician conrms the location of the limitation through passive intervertebral joint testing. Treatment consists of the appropriate lumbar mobilization/manipulation technique (i.e., closing mobilization technique for a closing pattern), which is typically followed by lumbar range of motion exercises. When determining whether an athlete is appropriate for mobilization/manipulation for LBP, the absolute and relative contraindications of the manual techniques must be considered. In the athletic population,

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absolute contraindications for these techniques are signs/symptoms of nerve root compression and the presence of spondylolisthesis.25 In addition, mobilization or manipulation treatment is contraindicated for any athlete with a high level of suspicion (regardless of diagnostic ndings) of spinal stress fracture. Relative contraindications to consider in the athletic population are the training of the clinician, and the apprehension level of the athlete with the proposed technique. Mobilization/manipulation of the athlete with suspected lumbar segmental instability is also viewed as a relative contraindication. The third treatment classication is immobilization. Athletes in this treatment category will have a history of frequent episodes of LBP, often from minimal spinal perturbations. In addition, a history of increased pain with prolonged static postures is associated with this treatment syndrome. The key examination nding that conrms the immobilization classication is the worsening of symptoms with sustained lumbar movement testing and the improvement of symptoms with repeated movement testing. Treatment focuses on the avoidance of end-range spinal postures through education and bracing. Trunk-strengthening exercises and motor-control exercises are also prescribed for this treatment classication. The fourth treatment classication is traction. Athletes in this treatment category will have symptoms radiating into the lower extremity. The key examination nding that conrms the traction classication is that the athlete is not able to improve his or her symptoms with any lumbar movements. In fact, the athlete may experience a worsening of his or her symptoms with most lumbar movements. This treatment category also includes athletes who were originally classied for lateral shift treatment but were unable to improve their symptoms with lumbar movements. Treatment for the traction classiciation consists of mechanical traction or autotraction. During treatment, the clinician must carefully monitor the athletes neurologic status through reex, strength, and sensory testing. Any deterioration in neurologic status should be communicated to the referring physician so the appropriate medical and/or surgical decisions can be promptly made.

CLINICAL SCENARIOS The management of the athlete using TBC will be highlighted in the three clinical scenarios presented below. For each example, assume that the clinician has already determined that the athlete is appropriate for physical therapy treatment. Because acute injuries are thought to be of common occurrence in athletic populations,28, 32 the rst two scenarios demonstrate the determination of appropriate Stage I treatment. The last scenario provides the rationale used to determine a Stage II and Stage III exercise prescription for an athlete with recurring LBP and suspected lumbar segmental instability.

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Scenario 1 This athlete is a 20-year-old female tennis player without any previous episodes of LBP. She experienced a sudden onset of LBP 5 days ago in practice while reaching for an opponents drop shot. Since then she has treated her back pain with ice, but the pain has worsened during the past 5 days. The team physician has referred her to physical therapy for evaluation and treatment of LBP. Figure 2 is a pain diagram identifying the location of this athletes symptoms. The clinicians initial hypothesis is that this patient is appropriate for the mobilization classication. This decision was based on two factors: the symptoms are local to her low back, and this is the athletes rst episode of LBP. To test his hypothesis, the clinician decides to focus the clinical examination on the athletes response to lumbar movements, pelvic landmark tests, and sacroiliac tests. During the single lumbar movement testing, the clinician detects a decrease in lumbar exion but

Figure 2. Pain diagram depicting location of symptoms for scenario No. 1. The X used by the athlete corresponds with a burning symptom descriptor.

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Figure 3. Demonstration of sacroiliac manipulation technique used to treat athlete No. 1.

does not detect an opening or closing pattern. In addition, the clinician notes that the athlete cannot improve or worsen her symptoms with repeated lumbar movements. The clinician does detect an elevated iliac crest on the right side, a positive seated exion test, and a positive prone knee bend test for this athlete. The clinician feels that he has conrmed his initial hypothesis and that sacroiliac mobilization is the most appropriate treatment. This is because of the lack of a lumbar movement pattern and the presence of positive sacroiliac joint tests. The clinician decides to initiate treatment by performing a sacroiliac joint manipulation (Fig. 3). After the manipulation is performed, the athletes pain intensity and lumbar range of motion are reassessed by the clinician. The athlete notes a slight decrease in pain intensity, and the clinician observes an improvement in lumbar exion range of motion. At this point, the athlete is prescribed lumbar range-of-motion exercise for her home program and instructed to return to physical therapy in 2 days. Scenario 2 The second clinical scenario involves an 18-year-old male high school football player who experienced a sudden onset of symptoms after a tackling drill in which he was forced into a exed position. He reports that the LBP radiates into his lower extremity and limits his sitting time to 10 minutes. His leg pain improves with standing, but his low back pain does not. His family physician has evaluated him and performed radiographs, which were unremarkable. The athlete is being referred to physical therapy for evaluation and treatment of lumbar radiculopathy. Refer to Figure 4 for a pain diagram that represents the location of this athletes symptoms. The clinicians initial hypothesis is that this athlete is appropriate

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Figure 4. Pain diagram depicting location of symptoms for scenario No. 2. The / used by the athlete corresponds with a stabbing symptom descriptor.

for the specic exercise classication. This decision was based on the following factor: the presence of symptoms in the lower extremity. The clinician further hypothesizes that the extension syndrome will be appropriate because of the athletes postural preference and age. To test his hypothesis, the clinician decides to focus the clinical examination on pelvic landmark testing and lumbar movements. The clinician does not detect any asymmetries during pelvic landmark testing. With single lumbar movement testing, the clinician detects a signicant limitation in exion and extension. With repeated lumbar movement testing, the athlete is unable to improve his symptoms with exion or extension. During repeated exion, the athlete notes that the symptoms go below his knee after the fth repetition. Attempts at repeated extension do not alter this change in status. At this point, the clinician decides to alter his hypothesis and feels this athlete may be appropriate for the traction classication. This decision was made because the athlete failed to improve his symptoms with

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Figure 5. Autotraction machine used for treatment of athlete No. 2.

lumbar movements. Before initiating treatment, the clinician performs a neurologic examination that reveals weakness in the great-toe extensors. The clinician decides that treatment will consist of autotraction (Fig. 5) in an attempt to have the athlete improve his symptoms. In addition, the clinician initiates communication with the referring physician regarding the athletes neurologic status. The clinician indicates that without improvement in neurologic status within 1 week, the athlete will be referred back to the physician for the consideration of additional diagnostic testing. Scenario 3 The third clinical scenario involves a 22-year-old gymnast with recurrent episodes of LBP. During the initial examination, the clinician detected several clinical signs thought to be associated with lumbar segmental instability. These signs and the athletes history were used to conrm the immobilization classication. The athlete responded well to her Stage I treatment and has now progressed to Stage II treatment. Because of the athletes history of recurrent episodes of LBP and presumed segmental lumbar instability, the clinician decided to focus Stage II treatment on trunk-strengthening exercises. In selecting an exercise prescription for trunk strengthening, the clinician must consider several

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Figure 6. Exercise to strengthen the erector spinae muscle group. The athlete is instructed to prevent excessive lumbar lordosis while performing this exercise.

factors, including the amount of lumbar compressive forces generated by the exercise, the amount of lumbar shear forces generated by the exercise, the appropriate muscle groups that are targeted, and the parameters of the exercise prescription that are appropriate.21, 36 Clinicians should prescribe trunk-strengthening exercises that generate minimal lumbar compressive and lumbar shear forces.36 For example, McGill2, 34, 35 has suggested that bent- and straight-knee curl ups are to be avoided because of the excessive compressive and shear forces generated. In addition, excessive compressive forces may be generated with exercises that emphasize the lumbar erector spinae muscles.6, 7 The clinician should also prescribe trunk-strengthening exercises that activate

Figure 7. Exercise to strengthen the transversus abdominis. The athlete is instructed to pull the navel toward the spine and hold this contraction while moving the lower extremities.

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muscles that stabilize the spine. A consensus has not been reached, but evidence in the literature exists to support the role of the transversus abdominis,40, 41 the oblique abdominals,40 the multidus,27, 40 the erector spinae,6 and the quadratus lumborum33 as spinal stabilizers. Lastly, the clinician must consider the manner in which the trunk muscles are trained. A recent review indicates that more evidence exists for exercise prescription that trains trunk muscles for endurance parameters, rather than strength parameters.36 In this scenario, the clinician decided to initiate trunk strengthening by training the athletes transversus abdominis, oblique abdominals, and erector spinae muscle groups. A randomized trial reported that patients with chronic LBP performing exercises similar to these had less pain and disability at short-term (10 weeks) and long-term (30 months) followup periods.40 In addition, the authors of this article hypothesize that performance of trunk-strengthening exercises is an important component in preventing recurrence of LBP. The clinician selected exercises that have been documented in the literature as generating acceptable amounts of lumbar compressive forces. The clinician selected exercise parameters that had the athlete perform high-repetition, low-load tasks on a daily basis. The exercises performed by the athlete are pictured in Figures 68. As the athlete with suspected segmental instability progresses through a rehabilitation program (i.e., to Stage III), it has been proposed that the motor-control system should also be trained.31, 41 One way to do this is to perform the trunk-strengthening exercises during sport-specic activities or on unstable surfaces (Fig. 9).

Figure 8. Exercise to strengthen oblique abdominal muscles. The athlete is instructed to hold trunk in this position. To decrease difculty, exercise can be performed with legs bent.

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Figure 9. Exercise to promote motor control of trunk muscles. Athlete is instructed to prevent excessive lumbar lordosis while performing this exercise.

SUMMARY The evaluation of an athlete with LBP using the classication system proposed by Delitto et al12 has been outlined. For outpatient orthopaedic practice, evidence in the literature is available documenting the reliability22 and the effectiveness of treatment guided by TBC.11, 14, 20 This classication system provides framework for the clinician to evaluate athletes with LBP because it investigates the presence of serious pathology, considers the severity of the disease process, and provides matched treatment based on the athletes clinical presentation. When treating athletes with episodes of acute LBP, pain modulation and return to daily function are the primary treatment goals. When treating athletes with episodes of chronic LBP, return to sport and prevention of recurrence are the primary treatment goals.

References
1. Aggrawal ND, Kaur R, Kumar S: A study of changes in weight lifters and other athletes. Br J Sports Med 13:5861, 1979 2. Axler CT, McGill SM: Low back loads over a variety of abdominal exercises: Searching for the safest abdominal challenge. Med Sci Sports Exerc 29:804811, 1997 3. Bellah RD, Summerville DA, Treves ST, Micheli LJ: Low-back pain in adolescent athletes: Detection of stress injury to the pars interarticularis with SPECT. Radiology 180:509512, 1991 4. Bigos S, Bowyer O, Braen G: Acute low back problems in adults. Clinical Practice Guideline No. 14 ed. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services, 1994 5. Brukner P, Bradshaw C, Khan KM, et al: Stress fractures: A review of 180 cases. Clin J Sport Med 6:8589, 1996 6. Callaghan JP, Gunning JL, McGill SM: The relationship between lumbar spine load and muscle activity during extensor exercises. Phys Ther 78:818, 1998

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7. Callaghan JP, McGill SM: Muscle activity and low back loads under external shear and compressive loading. Spine 20:992998, 1995 8. Chard MD, Lachman SM: Racquet sportsPatterns of injury presenting to a sports injury clinic. Br J Sports Med 21:150153, 1987 9. Croteau LL: Managing sports-related low back pain. Nurse Pract Forum 7:141147, 1996 10. Davies JE: The spine in sportInjuries, prevention and treatment. Br J Sports Med 14: 1821, 1980 11. Delitto A, Cibulka MT, Erhard RE, et al: Evidence for use of an extension-mobilization category in acute low back syndrome: A prescriptive validation pilot study. Phys Ther 73:216222, 1993 12. Delitto A, Erhard RE, Bowling RW: A treatment-based classication approach to low back syndrome: Identifying and staging patients for conservative treatment. Phys Ther 75:470485, 1995 13. Delitto A, Synder-Mackler L: The diagnostic process: Examples in orthopedic physical therapy. Phys Ther 75:203211, 1995 14. Erhard RE, Delitto A, Cibulka MT: Relative effectiveness of an extension program and a combined program of manipulation and exion and extension exercises in patients with acute low back syndrome. Phys Ther 74:10931100, 1994 15. Fairbank JC, Couper J, Davies JB, OBrien JP: The Oswestry low back pain disability questionnaire. Physiotherapy 66:271273, 1980 16. Fairbank JC, Pynsent PB: The Oswestry Disability Index. Spine 25:29402953, 2000 17. Featherstone T: Magnetic resonance imaging in the diagnosis of sacral stress fracture. Br J Sports Med 33:276277, 1999 18. Fehlandt AF Jr, Micheli LJ: Lumbar facet stress fracture in a ballet dancer. Spine 18: 25372539, 1993 19. Fritz JM: Use of a classication approach to the treatment of 3 patients with low back syndrome. Phys Ther 78:766767, 1998 20. Fritz JM, Delitto A, Erhard RE: Comparison of a classication based approach to physical therapy and therapy based on the AHCPR clinical practice guidelines for patients with acute low back pain: A randomized clinical trial. Spine 2001; In review. 21. Fritz JM, Erhard RE, Hagen BF: Segmental instability of the lumbar spine. Phys Ther 78:889896, 1998 22. Fritz JM, George S: The use of a classication approach to identify subgroups of patients with acute low back pain. Interrater reliability and short-term treatment outcomes. Spine 25:106114, 2000 23. Garces GL, Gonzalez-Montoro I, Rasines JL, Santonja F: Early diagnosis of stress fracture of the lumbar spine in athletes. Int Orthop 23:213215, 1999 24. Goldstein JD, Berger PE, Windler GE, Jackson DW: Spine injuries in gymnasts and swimmers. An epidemiologic investigation. Am J Sports Med 19:463468, 1991 25. Grieve GP: Mobilisation of the spine. In A Primary Handbook of Clinical Method, 5th ed. London, Churchill Livingstone, 1991 26. Halpern B, Thompson N, Curl WW, et al: High school football injuries: Identifying the risk factors. Am J Sports Med 15:316320, 1987 27. Hides JA, Richardson CA, Jull GA: Multidus muscle recovery is not automatic after resolution of acute, rst-episode low back pain. Spine 21:27632769, 1996 28. Keene JS, Albert MJ, Springer SL: Back injuries in college athletes. J Spinal Disord 2: 190195, 1986 29. Kujala UM, Kinnunen J, Helenius P, et al: Prolonged low-back pain in young athletes: A prospective case series study of ndings and prognosis. Eur Spine J 8:480484, 1999 30. Libson E, Bloom RA, Dinari G, Robin CG: Oblique lumbar spine radiographs: Importance in young patients. Radiology 151:8990, 1984 31. Luoto S, Taimela S, Hurri H, et al: Psychomotor speed and postural control in chronic low back pain patients. A controlled follow-up study. Spine 21:26212627, 1996 32. Manninen JS, Kallinen M: Low back pain and other overuse injuries in a group of Japanese triathletes. Br J Sports Med 30:134139, 1996 33. McGill S, Juker D, Kropf P: Quantitative intramuscular myoelectric activity of quadra-

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34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49.

tus lumborum during a wide variety of tasks. Clin Biomech (Bristol, Avon) 11:170 172, 1996 McGill SM: The mechanics of torso exion: Situps and standing dynamic exion manoeuvres. Clin Biomech (Bristol, Avon) 10:184192, 1995 McGill SM: Distribution of tissue loads in the low back during a variety of daily and rehabilitation tasks. J Rehabil Res Dev 34:448458, 1997 McGill SM: Low back exercises: Evidence for improving exercise regimens. Phys Ther 78:754765, 1998 McKenzie RA: The Lumbar Spine: Mechanical Diagnosis and Therapy. Waikanaie, New Zealand, Spinal Publications Limited, 1989 Micheli LJ: Back injuries in gymnastics. Clin Sports Med 4:8593, 1985 Micheli LJ: Sports injuries in children and adolescents: Questions and controversies. Clin Sports Med 14:727745, 1995 OSullivan PB, Phyty GD, Twomey LT, Allison GT: Evaluation of specic stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine 22:29592967, 1997 OSullivan PB, Twomey L, Allison GT: Altered abdominal muscle recruitment in patients with chronic back pain following a specic exercise intervention. J Orthop Sports Phys Ther 27:114124, 1998 Reid DA, McNair PJ: Factors contributing to low back pain in rowers. Br J Sports Med 34:321322, 2000 Risser WL: Musculoskeletal injuries caused by weight training: Guidelines for prevention. Clin Pediatr 29:305310, 1990 Sward L: The thoracolumbar spine in young elite athletes. Current concepts on the effects of physical training. Sports Med 13:357364, 1992 Thompson N, Halpern B, Curl WW, et al: High school football injuries: Evaluation. Am J Sports Med 15:117124, 1987 Watkins RG, Dillin WM: Lumbar spine injuries. In Fu FF, Stone DA (eds): Sports Injuries: Mechanisms, Prevention, Treatment, ed 1. Baltimore, MD, Williams & Wilkins, 1994, pp 877948 Weir MR, Smith DS: Stress reaction of the pars interarticularis leading to spondylolysis. A cause of adolescent low back pain. J Adolesc Health Care 10:573577, 1987 Wilson FD, Lindseth RE: The adolescent swimmers back. Am J Sports Med 10: 174176, 1982 Wipf JE, Deyo RA: Low back pain. Med Clin North Am 79:231246, 1995 Address reprint requests to Steven Z. George, MS, PT 6035 Forbes Tower Physical Therapy Department University of Pittsburgh Pittsburgh, PA 15260 e-mail: georgesz@msx.upmc.edu

THE SPINE AND SPORTS

02785919/02 $15.00 .00

BACK PAIN IN THE YOUNG ATHLETE


Greg Sassmannshausen, MD, and Brian G. Smith, MD

For the orthopedist, the patient presenting with low back pain is often approached apprehensively. Within the general population, the prevalence of low back pain ranks second only to the common cold as a cause of all physician visits.4 The ubiquitous nature of this complaint can arise from multiple causes that can make attaining positive treatment outcomes very difcult. However, in the pediatric and adolescent athletic population, any complaint of low back pain must be taken seriously and assumed to be a signicant problem until proved otherwise.17, 19 Back injuries and back pain in the young athlete occur in 10% to 15% of participants, with up to 75% of high performance athletes having had back pain.9, 15, 22 This prevalence does vary between sports and positions played.28 A full and comprehensive evaluation is usually recommended for any athlete with low back pain rendering him or her unable to participate or continuing for more than 10 days.39 Accurate diagnosis of back pain in the young athlete requires a complete and thorough history and physical examination of the patient. The treating physician must be aware that injuries occurring in the adolescent are different from those occurring in adults.10 In the adult, 48% of patients with low back pain had discogenic etiologies, whereas 47% of low back pain in adolescents was from spondylolysis and 25% from hyperlordosis.25 Knowledge of this statistical data facilitates accurate diagnosis and thereby promotes prompt treatment in this population. The purpose of this article is to identify the likely causes of back pain in the young athlete and provide an overview on diagnosis and

From the Connecticut Childrens Medical Center Hartford, Connecticut; and DartmouthHitchcock Medical Center, Lebanon, New Hampshire

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treatment. Armed with this information, the clinician should be able to develop a thorough, efcient, and economical diagnostic and treatment approach for management of this problem in this patient population. HISTORY As with any complaint, a thorough history is paramount in diagnosing the etiology of the young athletes back pain. The physician should specically seek to determine the quality and duration of the pain. Focus must be directed to the mechanism of injury distinguishing an atraumatic or traumatic cause. The sport and position played must be identied as well as any associated repetitive motions. The location of the pain and associated radiation of the pain, or bowel and bladder involvement, should be discussed. The physician should inquire about aggravating or alleviating factors, the presence of night pain, and the effects of taking medications (aspirin, nonsteroidal anti-inammatory drugs [NSAIDs]). Specic questions about weight loss, diet, malaise, or other constitutional symptoms must be included. A complete family history regarding spinal disorders should be obtained. Finally, the physician should try to delineate any psychosocial factors contributing to the patients complaint. PHYSICAL EXAMINATION The physical examination should be performed with the patient disrobed wearing an examination gown. Observation of the patient should evaluate body habitus. Cachexia or pallor may indicate underlying malignant or nutritional disorders. Examination of the skin should include observation of any cutaneous anomalies overlying the spine. Gait should be evaluated, including walking on toes and heels, as well a presence of a waddling-type gait. The spine should be examined for scoliosis and kyphosis. A heartshaped buttocks may indicate spondylolisthesis. The Trendelenburg sign and pelvic obliquity should be noted. If lumbar exion or extension elicit pain, the provocative hyperextension test may help determine the presence of posterior element injury. A complete neurologic exam including formal manual motor and sensory testing and deep tendon reexes is essential. Tension signs including femoral nerve stretch test and straight-leg raising will elicit reproducible symptoms if a herniated nucleus pulposus (HNP) or apophyseal fracture is present. Assessment for hamstring tightness, which is often associated with spondylolysis, should also be performed. Abnormal abdominal reexes and long-tract signs may indicate an upper motor neuron problem. If the history indicates possible genitourinary or abdominal pathology, a careful abdominal, pelvic, and rectal exam is indicated.

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DIAGNOSTIC STUDIES A systematic approach to the evaluation of the young athlete with back pain is required to implement the most cost-effective use of diagnostic studies. This systematic approach has been proposed by Wenger.40 With a history of minor trauma with a negative exam, further work-up is postponed. If the child has pain that persists for 3 to 4 weeks and has an inconclusive exam, work-up includes standing anterior-posterior and lateral spine lms. If the lumbosacral region is involved, oblique views should be obtained. If pain persists for 3 to 4 weeks after original lms, further evaluation with a bone scan or single-photon emission computed tomography (SPECT) scan is indicated. For the patient presenting with severe pain, neurologic decit, tight hamstrings, or positive straight leg raise, work-up should include plain radiographs, an urgent CT scan and/or magnetic resonance imaging (MRI) study. Based on these results, the patient may require biopsy, drainage, or other surgical intervention. If the patient has systemic complaints including fever, chills, malaise, and weight loss, laboratory studies including complete blood count (CBC), sedimentation rate and C-reactive protein are indicated. Based on examination and radiographic results, further laboratory studies may be required. DIFFERENTIAL DIAGNOSIS As previously mentioned, the differential diagnosis for back pain in the young athlete differs that of the adult population. In evaluating 100 adolescent athletes presenting with back pain, Micheli found nearly 50% were from spondylolysis and another 25% were from lordotic back pain.25 The age of the patient may guide the physicians differential diagnoses. For the child under 10 years of age, discitis, vertebral osteomyelitis, leukemia, eosinophilic granuloma, neuroblastoma, and astrocytoma are more common.11 For children older than age 10, disorders involving repetitive trauma such as spondylolysis and spondylolisthesis, as well as Scheuermanns kyphosis, HNP, and apophyseal ring fractures occur more frequently.11 Osteosarcoma and osteoblastoma are more common in this age group. Psychogenic back pain is customarily seen in the adolescent and pubescent athlete. Spondylolysis Spondylolysis represents a pars interarticularis defect frequently causing mechanical low back pain. In the athletic population, the majority of spondylolytic lesions are related to pars interarticularis stress fracture.43 Risk factors include positive family history,14 indigenous Alas-

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kan ancestry,35 and coincident spinal anomalies.26 Repetitive hyperextension has routinely been shown to be a major risk factor particularly in gymnastics, the football lineman, gure skating, and dance.2, 16, 2224 The patient generally complains of low-grade back pain with intermittent episodes of increased severity. This pain is exacerbated by hyperextension activities such as the back walkover in gymnastics or the blocking by offensive linemen. Rarely are there concomitant neurologic symptoms. Symptoms tend to improve or resolve by avoiding hyperextension activities and with rest. Physical examination reveals normal gait. There is rarely tenderness to palpation. Forward exion is full, but pain on hyperextension is common. If pain exists, the provocative hyperextension test will demonstrate reproducible symptoms. Generally, the neurologic exam will be normal. Often the patient will have tight hamstrings. Completion of the evaluation includes standing lumbosacral radiographs with oblique views looking for the so-called Scotty dog lesion. If radiographs are nondiagnostic, a bone scan may demonstrate an increased uptake in the pairs indicating a stress reaction. SPECT is useful in the absence of radiographic and scintigraphic ndings. SPECT has been shown to be the most sensitive method of diagnosing spondylolysis.1 Treatment for symptomatic patients includes activity modication and rest. As pain diminishes, strengthening exercises targeting the back and abdominal musculature are recommended. In the setting of acute spondylysis, immobilization in a thoracolumbosacral orthosis is indicated. Nearly a 75% healing rate of early defects has been shown with the use of orthotic device only.27 For persistently symptomatic spondylytic defects, open reduction internal xation (ORIF) and bone grafting across the defect may be indicated. Spondylolisthesis Spondylolisthesis in the young athlete is usually associated with either a pars interarticularis defect or elongation.2, 42 Most of the slip progression occurs during the preadolescent growth spurt.43 The patient may present complaining of low back pain or altered gait and postural abnormalities depending on the level of the slip. Diagnostic focus again should include risk factors similar to spondylolysis. Physical examination may show a characteristic stiff-legged, short stride gait. This so-called pelvic waddle is caused by tight hamstrings.31 If the slip is severe, a step-off may be appreciated at the lumbosacral junction. The buttocks may have a heart-shaped conguration secondary to the vertical position of the sacrum. Radiographs including a spot lateral of the lumbosacral junction allow for determination of the slip percentage and slip angle. Based on the slip percentage, treatment can be instituted. For the symptomatic athlete with slips ranging from 25% to 50%,

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treatment includes observation followed closely with spot lateral radiographs. Slippage is associated with rapid growth and with slip angles of more than 50 degrees.26 Therefore, observation must continue to the end of growth. The patient and family must be cautioned that participation in contact sports may have to be restricted if progression occurs.11 If progression occurs, pain persists, neurologic decits develop, or the spondylolysthesis is more than 50%, posterolateral in situ fusion is the treatment of choice. After successful fusion, pain, gait abnormalities, and tight hamstrings resolve in 90% of patients.12 Controversy remains regarding techniques for reduction with instrumentation of high-grade spondylolisthesis. Postoperative neurologic decits after reduction and/ or instrumentation have been shown to be a very infrequent occurrence.29 Hyperlordosis/Lordotic Low Back Pain The second most common etiology of back pain in the adolescent athlete is lordotic low back pain.25 As growth becomes more rapid during the adolescent growth spurt, the thoracolumbar facsia becomes tight as the axial skeleton grows. When skeletal growth exceeds the capacity of the soft tissues to remain limber, pathologic tightness occurs.10 This tightness may cause traction apophysitis at the iliac crest, spinous process, or impingement of adjacent spinous processes forming a pseudarthrosis.14 The patient presents with activity-related low back pain. Risk factors include rapid growth and sports that require strong hamstrings, which could exacerbate tightness.10 On examination, there may be hyperlordosis of the lumbar spine. Pain with forward exion may be elicited. Tight hamstrings may exist. Plain radiographs may reveal apophyseal avulsions. However, lordotic low back pain is often a diagnosis of exclusion after evaluation with a bone scan reveals increased activity in the area of the injured apophysis.14 Treatment for hyperlordotic back pain focuses on increasing mobility of the thoracolumbar spine, pelvis, and hamstrings.34 Relative rest is also indicated. Rarely, temporary antilordotic bracing may be required.14 The patient may return to activities as tolerated as symptoms subside, although exibility must be preserved to prevent recurrence.10 Scheuermanns Kyphosis Sheuermanns kyphosis is thoracic kyphosis with anterior wedging of at least 5 degrees of three consecutive vertebra. There are also typical vertebral end plate changes, Schmorls nodes, and apophyseal ring fractures. An increased prevalence is associated with sports such as water skiing, particularly if started before age six.38 The patient presents complaining of back pain aggrevated by prolonged sitting, standing, or activity. Typically, there is no traumatic event leading to the development of pain. Examination reveals a round back

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posture with possibly a gibbus deformity worsened with forward exion. The kyphos does not resolve with hyperextension or lying supine. Radiographs are diagnostic. Treatment includes upper trunk and postural exercises. If the kyphosis is greater than 60 degrees, thoracolumbosacral is indicated. Surgical treatment with anterior discectomy and fusion of the apical segment along with posterior fusion of the entire kyphotic segment may be indicated with a kyphos of more than 75 degrees or a rigid curve with marked anterior wedging. Atypical Sheuermanns kyphosis involves the area of the thoracolumbar junction. End-plate changes, Schmorls nodes, and apophyseal ring fractures may occur, but frequently involve only one vertebra. This is frequently seen in sports with repetitive exion and extension such as gymnastics and wrestling.36, 39 The patient again presents with low back pain exacerbated with forward exion. Examination may show a at thoracic spine with a tight thoracolumbar fascia. Occasionally, a palpable bump or gibbus may be felt at the affected level.39 Radiographs again may be diagnostic. A SPECT scan will show increased activity at one or two levels. Treatment addresses stretching the tight thoracolumbar fascia, abdominal strengthening, and rest from athletics. A hyperextension lordotic brace is useful in returning the athlete back to sports in 1 to 2 months.14 Acute Disc Herniation Unlike adults, acute HNP in the adolescent or child is quite uncommon. Nevertheless, 10% of back pain in the adolescent athlete arises from a discogenic etiology.25 Athletes at risk are weight lifters and those participating in collision sports.9 The patient often presents lacking sciatica because the herniation tends to be more central and the volume of extruded annulus is less than that for adults. Rather, the patient complains of low back, buttock, or posterior thigh pain. The pain is exacerbated by sitting, sports activities, coughing, or sneezing. The acute onset of symptoms is precipitated by a traumatic event in more than half of the cases.6, 7 Examination may reveal an abnormal gait secondary to paraspinal muscle spasm. There may be decreased lumbar motion. Tension signs including the straight-leg raise or femoral stretch test may be present in 80% to 90% of patients.11 Neurologic ndings have been reported in fewer than 40% of adolescents with HNP, most commonly extensor hallucis longus weakness or decreased reexes.6 Plain radiographs are often normal but should be obtained to rule out other pathology. Occasionally, a transitional vertebra at L5 or S1 may be identied and is considered to be associated with the development of HNP.11 An MRI is the imaging study of choice for evaluating HNP. A multidisciplinary approach to treatment exists for disk herniation in the young athlete. These include NSAIDs, short-term bed rest, and physical therapy exercises. Rigid bracing in hyperlordosis for 3 to 4

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months is typically required to prevent recurrence and allow healing.10 Rarely epidural steroid injections may be required. The patient may return to sports when he or she has attained full range of motion and strength. Persistent symptoms, cauda equina syndrome, progressive neurologic decit, or reinjury are indications for discectomy. Excellent to good results in more than 90% of patients undergoing discectomy have been reported.6 Apophyseal Ring Fractures Unique to the adolescent patient population are apophyseal ring fractures. These occur at the junction between the vertebral body and the apophysis attached to the outer annulus brosus before they completely fuse at approximately age 18 years old. Injury to the apophyseal ring produces avulsions displaced posteriorly into the canal attached to the intervertebral disc. This produces signs and symptoms similar to a central HNP. Approximately 50% of these injuries occur secondary to acute trauma, and repetitive microtrauma accounts for another signicant number of apophyseal ring fractures.35 Most patients are involved in sports such as weight lifting or that require repetitive hyperexion of the lumbar spine.8, 21 The inferior apophysis of L4 is most commonly involved.37 The patient usually presents with complaints similar to those seen with HNP: back, buttock, and posterior thigh pain. Sciatica may or may not be present. Symptoms are worsened with prolonged sitting, coughing, sneezing, and sports activities. Neurologic symptoms are rare. On examination, lumbar tenderness and paraspinal muscle spasm may be found. Other physical ndings are similar to those with HNP. However, in the patient with an apophyseal ring fracture, contralateral straight leg raise test is more frequently positive than in the patient with a herniated disc.13 Lateral radiographs may show a small avulsion fracture off of the vertebral body. CT is the imaging study of choice because MRI does not distinguish between bone and disc material well. Treatment for an apophyseal ring fracture without neurologic decits is similar to that of a herniated disc. Nonoperative treatment with rest, NSAIDs, physical therapy, and bracing is usually successful. If progressive neurologic decits, cauda equina syndrome, or persistent symptoms exist, surgical excision of the bony fragment and disc material is indicated. Discitis/Vertebral Osteomyelitis Discitis and vertebral osteomyelitis represent a spectrum of the same disease process. This is usually a bacterial infection secondary to hematogenous seeding owing to the unique blood supply of the pediat-

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ric spine. The blood supply traverses the vertebral endplate from body to disc establishing a route for transmission of infection. The patient usually presents with complaints of back pain, irritability, and other constitutional symptoms. If the infection involves the T8-L1 levels, abdominal pain may be the presenting complaint.11 On examination, the patient may be febrile. The patient may appear toxic and irritable. There may be tenderness to palpation of the spine with loss of lumbar lordosis and hamstring tightness. Tension signs may be positive. Laboratory evaluation should include a complete blood cell count with differential, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Although the ESR is usually elevated in 90% of cases, the white blood cell count may only be abnormal in 10% of cases.32 Blood cultures are only positive in 50% of the cases for the causative organism, with Staphylococcus aureus being the most common.41 Radiographs of the spine may be negative if symptoms have only persisted for 2 to 3 weeks. When radiographic abnormalities exist, they include erosion and sclerosis of the end plate with a decrease in disc space height. If radiographs are normal in the presence of abnormal laboratory results, a bone scan or MRI is indicated. MRI allows for differentiating between discitis or vertebral osteomyelitis and an epidural abscess. Treatment of discitis and vertebral osteomyelitis is usually nonoperative. Immobilization along with 1 week of parenteral antibiotics followed by 4 to 6 weeks of oral antibiotics provides symptomatic relief in 85% of patients by 2 to 3 weeks.32 Traditionally, antibiotics are continued until the ESR is normalized.

Neoplasms Neoplastic processes in the spine must always be considered in the differential diagnosis of a young athlete presenting with back pain. These are exceedingly rare with only 0.5% of primary musculoskeletal tumors occurring in spine of a child or adolescent.5 Most of the neoplasms are benign and may involve the anterior or posterior elements. The most common benign neoplasms are osteiod osteoma, osteoblastoma, and anuerysmal bone cysts.5 Primary malignant spinal neoplasms are quite rare. These include osteosarcoma and Ewings Sarcoma. Leukemia and lymphoma have also been reported in the young athlete.3, 33 Skeletal metastasis generally affects children under the age of 10.11 The most prevalent malignancy with spinal metastasis is neuroblastoma, particularly with a predilection for the thoracic spine.20 The patient commonly presents with a complaint of back pain both with activity and rest. Night pain, constitutional symptoms, and an atraumatic etiology of pain should alert the physician to a possible neoplastic source. Occasionally, pain will be relieved with NSAIDs. The

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patient or family may notice abnormalities in gait or assymetry. Rarely, neurologic symptoms caused by compression from the lesions will exist. Examination may include the presence of a nonstructural scoliosis with paraspinal muscle spasm and tenderness. Hamstring tightness may be present, although focal neurologic decits are rare. A soft-tissue mass may be palpated posteriorly. Imaging studies must always include plain radiographs. Radiographic changes suspicious for a malignant process include thinning and destruction of pedicles, vertebral body collapse, and expansile lesions with a soft-tissue mass. Based on history, examination, and plain lms, further imaging may include bone scan, CT, or MRI. Treatment for benign primary spinal lesions include rest, bracing, and resection. Although osteiod osteoma lesions have been reported to be self-limiting, excision of the nidus is the treatment of choice.11 This may include using preoperative radioactive tracer to assist in localization of the mass and to ensure complete excision. If the surgeon suspects a malignant primary neoplasm, the patient should be referred to an orthopedic tumor specialist expeditiously for appropriate staging and treatment. Other Sources The athlete presenting with back pain may many other pain generators. Rheumatologic disorders including juvenile rheumatoid arthritis and ankylosing spondylitis may present with back pain. Appropriate laboratory studies and radiographs may conrm these. Rare metabolic or hematologic disorders may also result in low back pain. Any evidence of psychosocial disturbances must be pursued. Finally, pathology from the abdomen, including hollow and solid viscera, the genitournary system, and the aorta, may only present with the symptom of back pain. The physician must be wary of these nonmusculoskeletal etiologies and pursue further work-up or referral if highly necessary. OVERVIEW OF APPROACH TO THE ADOLESCENT ATHLETE Back pain in the adolescent athlete serious enough to warrant medical attention mandates a careful evaluation. As discussed above, a thorough history and physical examination are essential. The most typical patient presentation scenario is often that of a 10- to 14-year-old girl with a new-onset back pain related to sports or activity, classically a gymnast. The frequency of participation in practice or competition will suggest whether the symptoms are secondary to a chronic repetitive over-use syndrome or strain related to a relatively new onset activity. One approach to managing these patients would be to rst recommend the activity stop for a minimum of 5 to 7 days with a goal of pain

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relief. Imaging studies would not usually be obtained at the time of initial presentation unless indicated by specic ndings. The use of NSAIDS is recommended to decrease pain. After approximately 5 days of rest, if the pain is substantially better, resumption of light activities such as exercises and swimming or biking is allowed. NSAIDs are continued as needed, and light sport-specic activities are resumed in a 10 to 14 day period if pain is minimal or absent. If symptoms recur, activity is restricted, and this cycle is followed at a slower pace. Often, this process of rehabilitation is facilitated and guided by a physical therapist with familiarity of the sport involved. Input obtained from the therapist is helpful for determination of readiness to return to full activity. Sometimes the most difcult issue in managing back pain in the adolescent athlete is the often unrealistic expectations of the parents regarding the childs athletic ability and future prospects. The parents attitudes are driven by the potentially huge sums of money represented by a four-year college scholarship or even the prospect of participation at the professional level. In the authors experience, this attitude is particularly prevalent among parents of gymnasts, a sport in which the coaches themselves have a predisposition for intensive or excessive training in these young athletes. Usually a very frank discussion about the potential risks of further injury from continued participation of an injured athlete is persuasive enough for the parent to permit some time for rest and appropriate rehabilitation. As the adolescent athlete with back pain returns to sport-related activities, a program of graduated performance and/or modications in the training regimen agreed to by the coach are often invaluable in a successful and lasting resumption of the sports activity. For example, not having the athlete do a specic routine or exercise that may risk re-injury as a routine part of training may also be a helpful way to keep the athlete active. In gymnastics, avoidance of the back-walk-over routine would minimize hyperextension stress on the lower back and thus the possibility of a recurrence on pain in this vulnerable area. In a scenario of persistent pain after a period of rest and rehab as the patient returns to activity or even preventing return to sports, workup with imaging studies is warranted. Plain radiographs including anterior-posterior and lateral of the lumbosacral spine are obtained in the patient to rule out an obvious abnormality like a pre-existing spondylolysis of spondylolisthesis. Should these be normal, a Technitium bone scan with SPECT imaging is indicated to assess for an early but otherwise occult spondylolysis, so common as a cause of back pain in young athletes, especially gymnasts. Even with the nding of a positive scan and an acute spondylolysis, appropriate management of the adolescent gymnast with bracing and rest, rehabilitation, and a modied training regimen can still be a successful way to return the patient back to gymnastics.

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SUMMARY Back pain in the pediatric athlete is rare compared to the adult population. However, the diagnosis should be accurate as most have specic etiologies and treatment. Nearly 50% of the time, the cause of the pain is an injury to the pars interarticularis. A thorough history and careful physical examination should guide the physician to a working differential diagnosis. Based on this, appropriate laboratory and imaging work-up is pursued to arrive at a timely diagnosis and subsequent treatment regimen. References
1. Bedner RJ, Heyman S, Drummond DS: The use of single photon emission computed tomography (SPECT) in the diagnosis of low-back pain in young patients. Spine 13: 11551160, 1988 2. Cirillo JV, Jackson DW: Pars interarticularis stress reaction, spondylolysis, and spondylolisthesis in gymnasts. Clin Sports Med 4:95110, 1985 3. Clark A, Stanish WD: An unusual case of back pain in a young athlete. A case report. Am J Sports Med 12:5154, 1985 4. Cypress BK: Characteristics of physician visits for back symptoms: A national perspective. Am J Public Health 73:389395, 1983 5. Delamarter RB, Sachs BL, Thompson GH, et al: Primary neoplasm of the thoracic and lumbar spine: An analysis of 29 consecutive cases. Clin Orthop 256:87100, 1990 6. DeLuca PF, Mason DE, Weiand R: Excision of herniated nucleus pulposus in children and adolescents. J Pediatr Orthop 4:318322, 1994 7. Epstein JA, Epstein NE, Marc J: Lumbar intervertebral disc herniation in teenage children: Recognition and management of associated anomalies. Spine 9:427432, 1984 8. Epstein NE, Epstein JA: Limbus lumbar vertebral fractures in 27 adolescents and adults. Spine 16:962966, 1991 9. Ferguson RJ, McMastor JH, Stanitski CL: Low back pain in college football linemen. Am J Sports Med 2:321327, 1974 10. Gerbino PG, Micheli LJ: Low back pain in the young athlete. Sports Med Arthro Rev 4:122131, 1996 11. Ginsburg GM, Bassett GS: Back pain in children and adolescents: Evaluation and differential diagnosis. J Am Acad Ortho Surg 5:6778, 1997 12. Harris IE, Weinstein SL: Long-term follow-up of patients with grade III and IV spondylolisthesis. Treatment with and without posterior fusion. J Bone Joint Surg 69A: 960969, 1987 13. Hashimoto K, Fujita K, Kojimoto H, et al: Lumbar disc herniation in children. J Pediatr Orthop 10:394396, 1990 14. dHemecourt P, Gerbino II PG, Micheli LJ: Back injuries in the young athlete. Clin Sports Med 19:663679, 2000 15. Hubbard DD: Injuries to the spine in children and adolescents. Clin Orthop 100: 5665, 1974 16. Ireland ML, Micheli LJ: Bilateral stress fracture of lumbar pedicles in a ballet dancer, J Bone Joint Surg 69A:140142, 1987 17. Jackson DW, Wiltse LL: Low back pain in young athletes. Phys Sportsmed 2:53, 1974 18. Jackson DW, Wiltse LL, Cirincoine RJ: Spondylolysis in the female gymnast. Clin Orthop 117:6873, 1976 19. Kraaus DR, Shapiro D: The symptomatic lumbar spine in the athlete. Clin Sports Med 8:5969, 1989 20. Leeson MC, Makley JT, Carter JR: Metastatic skeletal disease in the pediatric population. J Pediatr Orthop 5:261267, 1985

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21. Lundin O, Ekstrom L, Hellstrom M, et al: Injuries in the adolescent spine exposed to mechanical compression. Spine 23:25742579, 1999 22. Micheli LJ: Back injuries in gymnastics. Clin Sports Med 4:8593, 1985 23. Micheli LJ, Kasser JR: Painful spondylolysis in a young football player. In Hochschuler SH (ed): The Spine in Sports. Philadelphia, Hanley and Belfus, 1990, pp 327330 24. Michell LJ, McCarthy C: Figure skating. In Watkins RG (ed): The Spine in Sports. St. Louis, Mosbey-Year book, 1996, pp 557564 25. Micheli LJ, Wood R: Back pain in young athletes. Signicant differences from adults in causes and patterns. Arch Pediatr Adolesc Med 199:1518, 1995 26. Miki T, Tamura T, Senzoku F: Congenital lumbar defect of the upper lumbar spine associated with pars defect. Spine 16:353355, 1991 27. Morita T, Ikata T, Katoh S: Lumbar spondylolysis in children and adolescents. J Bone Joint Surg 77B:620625, 1995 28. Mundt DJ, Kelsey JL, Golden AL: Northeast collaborative group on low back pain. An epidemiologic study of sports and weightlifting as possible risk factors for herniated lumbar and cervical discs. Am J Sports Med 21:854860, 1993 29. OBrien JP, Mehdian H, Jaffrey D: Reduction of severe lumbosacral spondylolisthesis. A report of 22 patients with a ten year follow-up period. Clin Orthop 300:6469, 1994 30. Ohmori K, Ishida Y, Takatsu T: Vertebral slip in spondylolysis and spondylolisthesis. J Bone Joint Surg 77B:771773, 1995 31. Phalen LW, Dickson JA: Spondylolisthesis and tight hamstrings. J Bone Joint Surg 43A: 505512, 1961 32. Ring D, Johnston CE II, Wenger DR: Pyogenic infectious spondylitis in children: The convergence of discitis and vertebral osteomyelitis. J Pediatr Orthop 15:652660, 1995 33. Rogalsky RJ, Black GB, Reed MH: Orthopaedic manifestations of leukemia in children. J Bone Joint Surg 68A:494501, 1986 34. Snyder-Mackler L: Rehabilitation of the athlete with low back dysfunction. Clin Sports Med 8:717729, 1989 35. Stewart TD: The age incidence of neural-arch defects in Alaskan natives. Considered from the standpoint of etiology. J Bone Joint Surg 35A:937950, 1953 36. Swaard L, Hellstrom M, Jacobsonn B: Acute injury to the vertebral ring apophysis and intervertebral disc in adolescent gymnasts. Spine 15:144148, 1990 37. Takada K, Inoue SI, Takahashi K, et al: Fracture of the posterior margin of a lumbar vertebral body. J Bone Joint Surg 70A:589594, 1988 38. Tall RL, DeVault W: Spinal Injury in Sport: Epidemiologic considerations. Clin Sports Med 12:441446, 1993 39. Weiker GG: Evaluation and treatment of common spine and trunk problems. Clin Sports Med 8:399417, 1989 40. Wenger DR: Back pain in children: In Wenger DR, Rang M (eds): The Art and Practice of Childrens Orthopaedics. New York, Raven Press, 1993 pp 455486 41. Wenger DR, Bobechko WP, Gilday DL: The spectrum of intervertebral disc-space infection in children. J Bone Joint Surg 60A:100108, 1978 42. Wiltse LL: Spondylolysis in children. Clin Orthop 21:156163, 1961 43. Wiltse LL, Widell EH, Jackson DW: Fatigue fracture: The basic lesion in isthmic spondylolisthesis. J Bone Joint Surg 57A:17, 1975 44. Wynne-Davies R, Scott JH: Inheritance and spondylolisthesis: A radiographic family survey. J Bone Joint Surg 61B:301305, 1979 Address reprint requests to Brian G. Smith, MD Orthopaedic Department-1H Connecticut Childrens Medical Center 282 Washington Street Hartford, CT 06106

THE SPINE AND SPORTS

02785919/02 $15.00 .00

SPONDYLOLISTHESIS IN THE ATHLETE


R. Lane Wimberly, MD, and William C. Lauerman, MD

The athlete with spondylolysis or spondylolisthesis can be both a diagnostic and a treatment dilemma. The treating physician must recognize and respect the motivation of the athlete to return to competition. Often the athlete has contractual obligations, scholarship opportunities, or a competitive drive that may complicate the situation. The mere diagnosis of spondylolisthesis can at times be detrimental to an athletic career.6, 16, 33, 34 The term spondylolisthesis was rst documented in an article from 1854 by H.F. Kilian19a, and is formed from the Greek word spondylos, meaning spine, and olisthenein, meaning to slip. In this article, it was assumed the entire vertebra shifted on the inferior vertebra; it was later discovered, however, that a fracture of the pars interarticularis was often the inciting event, and the term, spondylolysis, where lysis is also of Greek origin and means to dissolve, came into use.6 Currently, spondylolisthesis is used as an all-encompassing term describing the continuum from the pre-slip spondylolysis to fully dislocated spondyloptosis. Isthmic spondylolisthesis, found in up to 50% of athletes with persistent back pain, has an overall prevalence of 4% to 5% in children at 6 years of age. The prevalence increases by age 18 to approximately 6%. In a longitudinal study by Fredrickson, et al, three-quarters of all individuals with spondylolysis had an identiable pars defect on plain lms by age 6, and approximately 75% of these patients had evidence of a slip at that time.8 Further progression of the slip in adulthood is quite rare.7, 8 Risk factors for spondylolisthesis include an Alaskan Es-

From the Department of Orthopaedic Surgery, Georgetown University Medical Center Washington, DC

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kimo heritage, a history of a rst-degree relative with a slip, the presence of spina bida occulta, and the presence of scoliosis.1, 10, 17, 30, 31 Classication of spondylolisthesis (Fig. 1) is based on the etiology of the slip as follows43: 1. Congenital: caused by insufciency or agenesis of the superior articular facet 2. Isthmic: caused by pars interarticularis defects Lytic Elongation of the pars Acute pars fracture 3. Degenerative: secondary to articular degeneration 4. Traumatic: caused by fracture or dislocation of the lumbar spine, not involving the pars 5. Pathologic: caused by malignancy, infection, or other types of abnormal bone (e.g., osteogenesis imperfecta) 6. Iatrogenic/postsurgical The etiology of an isthmic spondylolisthesis involves a weakened or defective pars interarticularis that is further injured with repetitive hyperextension loading. These fatigue fractures have certain characteristics that separate them from other stress fractures. These include a

Figure 1. Classication of spondylolisthesis

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hereditary predisposition, rare callous formation, young age of onset, relatively minor trauma responsible, and a low incidence of spontaneous bony union.42 The lumbar spine is the link between the torso and lower extremities and as such must support the entire body weight above the pelvis. The greatest forces occur at the L5-S1 articulation.1, 12 The cross-sectional area of the pars interarticularis is merely 0.75 cm2 at the L5 level, making the total area 1.5 cm2 for the neural arch.23 Fractures of the pars have been demonstrated ex vivo with cycling 1536 times at a force of 570 / 190 N in a 14 year old; the normal forces in exion and extension range from 400 to 630 N.23 Anatomically, the position of the sacrum creates anterior shear and compressive forces that increase the tensile forces on the spinal ligaments and shear forces on the neural arch.1, 36, 37 The upright, bipedal stance further exacerbates these stresses.5 The erector spinae musculature places considerable strain on the posterior elements to maintain an upright posture. Finally, during hyperextension motions, complete closure of the facets can be obtained, and any subsequent extension must occur through the neural arch.1 The repetitive motions involved in many sports are thought to be the causative agents in the higher prevalence of slips in athletes. Hyperextension is a common maneuver and the most implicated movement creating a pars injury. Repetitive rotational motion may be the cause of a unilateral defect. The sports with relatively high incidences of such injuries include gymnastics, football linemen, hockey, diving, wrestling, throwing sports, volleyball, pole vaulting, racquet sports, and weightlifting, with gymnastics and football generally considered the highest risk.1, 3, 6, 9, 10, 14, 15, 17, 18, 19, 22, 25, 30, 31, 33, 34, 36, 37, 39 Without a doubt, there has been an increase in the amount and intensity of athletic participation in skeletally immature athletes, often at the elite level. Because there is recognition of an increased risk of spine injury during times of rapid skeletal growth, many of these children are placing themselves at risk.12, 15, 35 Many factors are thought to predispose a young athlete to injury, both in general and to the back. These include improper techniques, abrupt increases in training frequency, unsuitable equipment, improper footwear choices, different playing surfaces, and musculoskeletal weakness and inexibility.5, 12, 15 The athlete with spondylolisthesis tends to present with a dull, occasionally unilateral backache that is exacerbated by hyperextension and rotational movements.10, 12, 16 Only rarely is there a history of a single signicant episode of trauma, whereas a history of similar, subclinical backache is relatively common. The pain is often located at the belt-line and is frequently relieved with extended periods of rest.3, 10, 16 Hamstring spasm is typical, although a exible athlete may mask this tightness.26, 31, 35 Other physical exam ndings include tight hip exors, relative thoracic kyphosis, a palpable step-off with high-grade slips, and a positive oneleg hyperextension test.5, 10, 16, 19, 31 With extremes of slip heart-shaped buttocks, a relatively short torso, low rib cage, and high iliac crests are noted.6

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Neurologic symptoms are rare, and straight leg raising is usually negative. When a decit occurs, the L5 root may be compressed in the foramen, or the cauda equina may be stretched over the dome of the sacrum.38, 39 The diagnosis of spondylolisthesis is usually straightforward on plain radiographs, although occult pars defects can be more difcult to identify. Nonetheless, in most situations, and depending on the athletes age, the severity of the pain, and the presence of radicular symptoms, a delay in radiographic imaging is usually warranted to permit a trial of conservative management.38, 30, 41 Although this is partly economic, the gonadal dose of radiation for lumbar spine lms should also be considered.40 The rst studies to be obtained include plain, standing anteroposterior (AP), and lateral radiographs. The slip is best identied on the lateral lm (Fig. 2), and most pars defects are seen on the lateral view as well. Oblique views, looking for the well-known collar on the neck of the Scotty dog of LaChapelle, will demonstrate most but not all pars defects not seen on the lateral lms (Fig. 3). Often, plain lms are without obvious pathology.10, 12, 39 Multiple methods of further describing the condition have been described using plain lms. Meyerding grades the spondylolisthesis as the percent anterior displacement of the superior vertebra on the lower

Figure 2. A 5-year-old girl with back pain. Her plain lateral radiograph demonstrates spondylolisthesis with a defect in the pars interarticularis at L5.

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Figure 3. A and B, Spondylolysis, as evidenced by disruption of the pars interarticularis (the collar on the neck of the scottie dog).

body. Thus, Grade I slips are displaced from 0% to 25%, Grade II from 26% to 50%, Grade III from 51% to 75%, Grade IV from 76% to 100%, and Grade V more than 100%. The Taillard system gives an exact percentage of the slip. Sacral inclination is the relationship of the plane of the sacrum to the vertical plane. The sacrum tends to a more vertical position with increasing slips. The slip angle, also known as sagittal roll or lumbosacral kyphosis, is the relationship determined by a line along the posterior border of S1 and the inferior endplate of L5 (Fig. 4). The slip angle and percent slip may predict the risk of future slip progression.39, 44 Bone scans are quite sensitive for showing an inammatory response but are relatively nonspecic and poorly localize lesions. Scans may be indicated in patients with negative plain lms but persistent pain and symptoms suggestive of a pars injury.23 Bone scans may aid in dating and identifying the metabolic activity of a fracture because acute and healing fractures will be positive, but chronic or healed nonunions will not illuminate.12 The therapeutic implications of identifying a pars defect that is positive versus negative on a bone scan remain unproven. Single-photon emission computed tomography (SPECT) scanning is more sensitive than conventional bone scans, plain radiography (including oblique views), and computed tomography scanning in showing early lesions and is the test of choice for diagnosing an occult spondylolysis.22 Computed tomography is best to dene bony detail, especially in surgical planning. This study is indicated in the presence of a known defect if repair is being considered and may be used in the rare case

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Figure 4. Measurements, including percent slip, slip angle, and sacral inclination (SI), useful for evaluating and describing L5-S1 spondylolisthesis.

where bony healing of the defect is being pursued.41 Magnetic resonance imaging provides a detailed image of the neural elements, including the exiting nerve root in the foramen and should be ordered in cases associated with neurologic decits.22 It is particularly helpful in adults (Fig. 5). The treatment of spondylolisthesis is dependent on the severity of the symptoms, the age of the patient, and the chronicity of the problem. Certain guidelines have been recommended for the skeletally immature yet asymptomatic patient. It should be noted that after skeletal maturity, activity level and treatment should be based solely on the presence of symptoms. For an asymptomatic patient with a slip of less than 25%, most physicians advocate no restrictions on activity.10, 22, 24, 30 Serial standing lateral radiographs until skeletal maturity are recommended at 6month to 1-year intervals or sooner with symptom progression.6, 21, 30, 40 In the athlete with an asymptomatic slip measuring between 25% and 50%, restriction from collision sports and high-risk activities such as gymnastics are typically recommended, although we advocate judiciously using these guidelines, particularly in the truly asymptomatic athlete.1, 31 For slips of more than 50% or with documented slip progression, even in an asymptomatic patient, surgical stabilization is recommended.24 The symptomatic patient is treated according to the severity of the symptoms and of the slip, the duration of symptoms, and the patients

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Figure 5. A 42-year-old former college football player with back and leg pain. These parasagittal images demonstrate spondylolisthesis at L4-L5, near complete collapse of the disc space, and severe foraminal stenosis with nerve root compression at that level.

response to previous treatment. In individuals with pre- or Grade I slips, a period of conservative management including analgesia and activity restriction is advocated.12 This should continue until the patient is painfree, at which time gradual resumption of activity is allowed. When this regimen is unsuccessful in allowing a full return to activities, the use of a Boston anti-lordotic brace may be helpful. The brace is worn for comfort, not necessarily full-time, and some adolescent athletes even compete in the brace. Once the athlete is pain-free in the brace, weaning begins at a rate of 1 fewer hour per day per week.31 After these conditions are met, the patient may return to all activities without restriction. With Grade II slips, management is again conservative with activity restriction and bracing until pain free; however, with grade II slips the athlete may need to be counseled against returning to high-risk activities. Physical therapy that includes both strengthening and stretching exercises is often recommended but should be delayed until pain with daily activities has subsided.3 Williams exion-type exercises to improve the abdominal musculature are most important.22 In general, the number of repetitions and the resistance used in these exercises must be tailored to the individual athlete.12 Hamstring stretching is also emphasized. It should be noted that continuing with the prescribed therapy is important

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in reducing recurrence of symptoms.5 For a symptomatic athlete with a slip of greater than 50%, surgery is advised.24 The treatment goal should be return to an asymptomatic, pain-free state and the resumption of activity when allowed.10 Stable bony union of the pars defect is rarely achieved, a point that should be stressed to the patient and parents. Healing of a defect may occur, but more often it results in an asymptomatic pseudarthrosis.42 Despite the formation of an apparent brous nonunion, most patients are able to return to activity.16, 35 Anesthetic injections are not indicated to facilitate return to sports.6 In general, the results of conservative management are good in the majority athletes with Grade I or II slips.24 The indications for surgery include pain persisting for more than 6 to 12 months that has been unrelieved by rest and immobilization with any degree of slip, progression of spondylolisthesis, a more than 50% slip, and any signicant neurologic changes.3, 6, 10, 24 In adolescent athletes, pain control with nonoperative treatment can almost always be achieved; it is returning the patient to his or her chosen sport that can be difcult. In this setting, we typically delay surgery for at least 1 year. In the adult, such an extended period of activity restriction, impacting on athletic pursuits and the patients occupation (if they are different), is often impractical, and surgery is often considered earlier. In either case, we are very reluctant to allow a return to previous level of athletic participation to be the major goal of surgical treatment. Fear of progression of a slip in an adult is not an indication for surgery.42 Many surgical procedures have been described for the treatment of spondylolysis and spondylolisthesis. All procedures tend to involve a fusion, with or without decompression, of the involved levels, or repair of the pars defect. It is generally felt that the percent slip and the slip angle are predictors of surgical outcomes.24 In selected patients with spondylolysis, and with slips of less than 10%, direct repair of the defect can be performed.6, 11, 22, 35 Originally reported by Buck in the 1970s using screw xation, success was achieved in 88% of patients3a, although no indication of postoperative activity levels was given. Chen et al have recently described a spondylolysis hook-screw construct and bone grafting procedure for direct repair of the pars interarticularis.4 Selection criteria include a young adult with persistent pain for more than 6 months, failure of conservative management, pure isthmic spondylolysis, and a normal disk. In Chen et als series, all patients had resumed normal activities by 6 months.4 The major benet of pars repair is saving motion that would be lost in a fusion procedure. They also purport to reduce the adjacent segment degeneration caused by a fusion mass. The role for decompression is limited in children and is somewhat controversial in adults. The only absolute indications for decompression are signicant motor decits or bowel or bladder dysfunction. Decompression is rarely performed in the skeletally immature and never without concomitant fusion. Many authors have demonstrated resolution of neurologic signs and symptoms after the establishment of a solid fusion,

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in children and adults. The Gill procedure refers to decompression by removal of the loose neural arch without a concomitant fusion. This method has fallen out of favor because of persistent pain as well as the risk of slip progression, particularly in children. As a result, decompression alone is contraindicated as a treatment of spondylolisthesis in children.22 Although some physicians continue to perform this procedure in adults with neurologic signs and symptoms, we feel that fusion should be performed in all age groups. We reserve decompression, consisting of thorough foraminotomy in addition to removal of the loose arch, for adults with signicant radicular pain or weakness and always perform a concomitant fusion. Most commonly, the procedure of choice is fusion at the involved level. Fusion is selected for patients with persistent back pain from spondylolisthesis, with or without radiculopathy, and after failure of conservative management. Posterolateral, anterior, and combined fusions have been performed with relatively good results reported. The selection of the procedure is at the discretion of the physician. Some advocate selecting a procedure based on the percent slip, whereas others use the patients age and symptoms as a guide.22, 32 Nevertheless, most often a bilateral lateral fusion is performed with extension to the adjacent level with slips of more than 50%.22 The need to extend the fusion is caused by the unusual shear stresses placed on the L5 transverse processes that are below the sacral ala in severe slips.24 The use of instrumentation in fusion procedures is not without controversy. Studies can be found that both advocate and condemn the use of pedicle-screw instrumentation.22, 27, 28 Postoperative immobilization is promoted by many because it may help reduce motion through the fusion mass and improve the fusion rate. In theory, the use of instrumentation obviates the need for external bracing, although even with instrumentation many surgeons use a brace.22, 24 A study by Kim et al showed improved fusion rates in anterior and posterior fusion performed in combination with cast immobilization.20 The use of casts has also been shown to reduce immediate postoperative progression of the slip. Once appropriate fusion has been obtained, there is no indication to continue to restrict the patient from activities.22 In children and adolescents, we perform a bilateral intertransverse fusion, through a muscle-splitting paraspinal approach, usually without instrumentation. A single-pantaloon spica cast is typically used for immobilization. In older teenagers and in adults we favor a transforaminal interbody fusion utilizing interbody cages lled with cancellous autograft placed through a far-lateral posterior approach and pedicle-screw instrumentation. This technique eliminates the need for postoperative immobilization, restores and preserves disk height and the cross-sectional area of the neural foramina, and is associated with an extremely high rate of union (Fig. 6). Anterior lumbar interbody fusion tends to be saved for use as a salvage procedure after failed posterolateral fusion. The advantages of

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Figure 6. A 33-year-old man, a recreational athlete, with an 8-year history of back and right leg pain. His preoperative lateral radiograph (A) demonstrates Grade I isthmic spondylolisthesis. MR imaging (B) shows compression of the L4 root in the L4-L5 foramen. AP (C) and lateral (D) views 6 months following foraminotomy and transforaminal interbody fusion (TLIF). He had complete resolution of his preoperative pain, and returned to full activity.

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interbody fusions include restoration of vertebral body height and improved decompression of the foramena. Fusion rates have been reported of between 70% and 100%.22 Anterior lumbar interbody fusion as a primary procedure without posterior stabilization runs the risk of destabilizing the olisthetic segment. Reduction is controversial in the treatment of severe spondylolytic slips. In general, indications include cauda equina symptoms and unacceptable cosmetic deformity, although the indications are broadening. Some surgeons do not advocate reduction of any slip, whereas others will attempt to improve the slip for anything more than 50%. The longterm consequences of accepting signicant lumbosacral kyphosis are not clear, but we have seen a number of patients many years after fusion in situ with severe degenerative, postural, and stenotic changes above their fusions. Reduction advocates also cite reduced pseudarthrosis rates, reduced incidence of progression, improved cosmetic appearance, and the potential avoidance of the rare case of nerve injury caused by stretch of the roots over the sacrum. No convincing literature supports these claims, and many surgeons have had excellent results with in situ fusion for children with all degrees of slip. With reduction, approximately 20% of patients will experience an L5 nerve root decit, although most are transient.22, 24 For those who wish to perform reduction, multiple methods have been described and include closed casting, staged surgical procedures including L5 vertebrectomy, instrumented fusions, and gradual instrumented reductions.13, 22 In general, the athlete with a spondylolytic defect or spondylolisthesis should be treated in the same manner as the general population with identical pathology. The difculties arise in dealing with the different motivations, goals, and overall physiology of the athletic population. One can be comforted by the relatively good success in patients treated nonoperatively for minor slips and treated surgically for more resistant conditions.

References
1. Alexander MJL: Biomechanical aspects of lumbar spine injuries in athletes: A review. Can J Appl Sport Sci 10:120, 1985 2. Bernicker JP, Kohl HW, Sahni I, et al: Long-term functional and radiographic follow-up of surgically treated isthmic spondylolisthesis. Am J Orthop November:631636, 1999 3. Blanda J, Bethem D, Moats W, et al: Defects of pars interarticularis in athletes: A protocol for nonoperative treatment. J Spinal Disord 6:406411, 1993 3a. Buck JE: Direct repair of the defect in spondylolisthesis. J Bone Joint Surg 61A:479, 1979 4. Chen JF, Lee ST: A physiologic method for the repair of young adult simple isthmic lumbar spondylolysis. Chang Gung Med J 23:9297, 2000 5. Cook PC, Leit ME: Issues in the pediatric athlete. Orthop Clin North Am 26:453464, 1995 6. Ciullo JV, Jackson DW: Pars interarticularis stress reaction, spondylolysis, and spondylolisthesis in gymnasts. Clin Sports Med 4:95110, 1985 7. Floman Y: Progression of lumbosacral isthmic spondylolisthesis in adults. Spine 25: 342347, 2000

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8. Fredrickson BE, Baker D, McHolick WJ, et al: The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg 66:699707, 1984 9. Gainor BJ, Hagen RJ, Allen WC: Biomechanics of the spine in the polevaulter as related to spondylolysis. Am J Sports Med 11:5357, 1983 10. Garry JP, McShane J: Lumbar spondylolysis in the adolescent athlete. J Fam Pract 47: 145149, 1998 11. Gillet P, Petit M: Direct repair of spondylolysis without spondylolisthesis using a rodscrew construct and bone grafting of the pars defect. Spine 24:12521256, 1999 12. Harvey J, Tanner S: Low back pain in young athletes: A practical approach. Sports Med 12:394306, 1991 13. Herkowitz HN, Garn SR, Balderston RA, et al: Iatrogenic lumbar spondylolisthesis: Treatment by anterior and iliac arthrodesis. J Spinal Disord 13:309318, 2000 14. Hellstrom M, Jacobsson B, Sward L, et al: Radiologic abnormalities of the thoracolumbar spine in athletes. Acta Radiol 31:127132, 1990 15. Hutchinson MR: Low back pain in elite rhythmic gymnasts. Med Sci Sports Exerc 31: 16861689, 1999 16. Jackson DW, Wiltse LL, Dingeman RD, et al: Stress reactions involving the pars interarticularis in young athletes. Am J Sports Med 9:304312, 1981 17. Jackson DW, Wiltse LL, Cirincoine RJ: Spondylolysis in the female gymnast. Clin Orthop 117:6873, 1976 18. Jones DM, Tearse DS, El-Khoury GY, et al: Radiographic abnormalities of the lumbar spine in college football players: A comparative analysis. Am J Sports Med 27:335 338, 1999 19. Keene JS, Drummond DS: Mechanical back pain in the athlete. Compr Ther 11: 714, 1985 19a. Kilian HF: Schilderungen never eckenformen und ihres verhaltens in Leven. Mannheim, Verlag von Basserman and Mathy, 1854 20. Kim SS, Denis F, Lonstein JE, et al: Factors affecting fusion rates in adult spondylolisthesis. Spine 15:979984, 1990 21. Kraus DR, Shapiro D: The symptomatic lumbar spine in the athlete. Clin Sports Med 8:5969, 1989 22. Lauerman WC, Cain JE: Isthmic spondylolisthesis in the adult. L Am Acad Orthop Surg 4:201208, 1996 23. Letts M, Smallman T, Afanasiez R, et al: Fracture of the pars interarticularis in adolescent athletes: A clinical-biomechanical analysis. J Pediatr Orthop 6:4046, 1986 24. Lonstein JE: Spondylolisthesis in children: Cause, natural history, and management. Spine 24:26402648, 1999 25. McCarroll JR, Miller JM, Ritter MA: Lumbar spondylolysis and spondylolisthesis in college football players: A prospective study. Am J Sports Med 14:404406, 1986 26. Micheli L: Back injuries in gymnastics. Clin Sports Med 4:8593, 1985 27. Moller H, Hedlund R: Surgery versus conservative management in adult isthmic spondylolisthesis: A prospective randomized study: Part I. Spine 25:17111715, 2000 28. Moller H, Hedlund R: Instrumented and noninstrumented posterolateral fusion in adult spondylolisthesis: A prospective randomized study: Part II. Spine 25:17161721, 2000 29. Moller H, Sundin A, Hedlund R: Symptoms, signs, and functional disability in adult spondylolisthesis. Spine 25:683689, 2000 30. Muschik M, Hahnel H, Robinson PN, et al: Competitive sports and the progression of spondylolisthesis. J Pediatr Orthop 16:364369, 1996 31. Omey ML, Micheli LJ, Gerbino PG: Idiopathic scoliosis and spondylolysis in the female athlete: Tips for treatment. Clin Orthop 372:7484, 2000 32. Osterman K, Schlenzka D, Poussa M, et al: Isthmic spondylolisthesis in symptomatic and asymptomatic subjects: Epidemiology, and natural history with special reference to disk abnormality and mode of treatment. Clin Orthop 297:6570, 1993 33. Semon RL, Spengler D: Signicance of lumbar spondylolysis in college football players. Spine 6:172174, 1981 34. Shaffer B, Wiesel S, Lauerman W: Spondylolisthesis in the elite football player: An epidemiologic study in the NCAA and NFL. J Spinal Disord 10:365370, 1997

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35. Stinson JT: Spine problems in the athlete. Md Med J 45:655658, 1996 36. Sward L: The thoracolumbar spine in young athletes: Current concepts on the effects of physical training. Sports Med 13:357364, 1992 37. Sward L, Hellstrom M, Jacobsson B, et al: Spondylolysis and the sacro-horizontal angle in athletes. Acta Radiolog 30:359364, 1989 38. Teitz CC, Cook DM: Rehabilitation of neck and low back injuries. Clin Sports Med 4:455476 39. Teitz CC, Hu SS, Arendt EA: The female athlete: Evaluation and treatment of sportsrelated problems. J Am Acad Orthop Surg 5:8796, 1997 40. Thomas JC: Plain roentengrams of the spine in the injured athlete. Clin Sports Med 5: 353371, 1986 41. Watkins RG, Dillin WH: Lumbar spine injury in the athlete. Clin Sports Med 9: 419448, 1990 42. Wiltse LL, Hutchinson RH: Surgical treatment of spondylolisthesis. Clin Orthop 35: 116135, 1964 Address reprint requests to William C. Lauerman, MD 3800 Reservoir Rd., NW Washington, DC 20007

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02785919/02 $15.00 .00

LUMBAR DISC INJURY IN THE ATHLETE


Robert G. Watkins, MD

LUMBAR SPINE INJURIES The lumbar spine is a highly vulnerable area for injury in a number of different sports. The incidence varies from 7% to 27%.6, 11, 12 Although the incidence is signicant and the time lost may be signicant, probably the most important problems are related to the fear of spinal injuries and the need for a therapeutic plan. Lumbar pain is signicant in many sports, but an organized diagnostic and therapeutic plan can prevent permanent injury, allowing full function and maximum performance. The sports most often associated with lumbar spine injury are discussed in the following sections. Gymnastics The motions and activities of gymnastics produce tremendous strains on the lumbar spine. The hyperlordotic position used with certain maneuvers, such as back walkovers, requires extreme exibility, and the lumbar exion/extension used during ips and vaulting dismounts requires great strength to support the spine during these extremes of exibility. It is believed that the vigorous lumbar motion in hyperextension in gymnastics produces a fatigue fracture, resulting in spondylolysis. There is also a hereditary predisposition to the stress fracture of spondylolysis, and nding occult spina bida in some of these gymnasts reveals a possible weakness.
From the University of Southern California Center for Orthopedic Spinal, Los Angeles, California

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Ballet Many of the motions used in ballet resemble those in gymnastics, particularly the arabesque position, which requires both extension and rotation of the lumbar spine. Ballet also involves lifting of dancers, especially in awkward positions. Off-balance bending and lifting are hallmarks of back problems in industrial workers and yet ballet, although balanced, is often designed to produce extremely difcult lifts. Resulting spondylolysis and spondylolisthesis often produce severe mechanical back dysfunction.

Water Sports In addition to injuries to the wrist and cervical spine, in diving the lumbar spine is subjected to added strain, both in rapid exion/extension changes and in severe back arching after entering the water. Although swimming and water exercises form a major component of back rehabilitation programs, certain kicks, such as the buttery, produce vigorous exion/extension of the lumbar spine, especially in young swimmers. The swimmer must attain good abdominal tone and strength to protect the back during vigorous kicking motions.

Weight Lifting The incidence of lower back pain and problems in weight lifters is estimated to be 40%. The tremendous forces exerted on the lumbar spine by lifting weights over the head produce extreme lever-arm effects and compressive injury to the spine. Extension forces of the lumbar spine naturally lead to increased risks of spondylolysis and spondylolisthesis. Many newer training techniques in weight lifting emphasize the role of general body conditioning, exibility, aerobic conditioning, speed, and cross training in addition to the ability to lift weight.

Running Low back pain is commonly reported in runners. In achieving the aerobic conditioning that running provides, the runner often experiences stiffness, contractures, and selected areas of muscle weakness. Runners also have a natural tendency to develop isolated abdominal weakness, frequently producing a signicant imbalance between exor and extensor muscles in the legs and in the trunk.

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Golf Golfers have the highest incidence of back injury of all professional athletes. Lumbar spine pain in golfers results from torsional stress on the lumbar spine. Baseball Torsional problems develop in both pitchers and hitters. Pitchers require a rigid cylinder of strength to transfer torque from their legs to their throwing arm. Fatigue reduces the control of the pitching motion and ball location. As the abdominal musculature weakens because of fatigue, lumbar lordosis increases, and the back arches. Attempts to compensate for loss of trunk strength and a slow arm increase the use of the arm musculature and predispose the shoulder to injury. Hitters initiate a violent lumbar rotation based on instantaneous ocular information. Therefore, the head position and maintenance of that position are as critical as acuity and eye focus. Delayed recognition of the ball produces a rotation with hips too far in front of the shoulders, a loss of parallelism of the shoulders and hips, and increased torsional strain on the lumbar spine. In summary, the keys to proper management of lumbar spine problems in athletes include the following: 1. Comprehensive diagnosis 2. Aggressive, effective nonoperative care 3. Pinpointing operations that do as little damage as possible to normal tissue but correct the pathologic lesion CLINICAL ANATOMY AND BIOMECHANICS OF THE LUMBAR SPINE Understanding the basic biomechanics of the lumbar spine begins with an understanding of the forces and stresses applied to the spine in relation to the normal curvatures seen. Because of the lordotic shape of the spine, vectorial forces are usually composed of two vertical axial loading compressive forces (one perpendicular to the surface of the disc and one horizontal to the disc) producing a shear strain. The combination of these two forces produces tensile stresses in the annulus brosis and a shear force on the neural arch.4 The center of gravity of body weight is anterior to the spine. This weight multiplied by the distance back to the spine produces a lever-arm effect of the weight of the body. This is resisted by the erector spinae muscles, the abdominal musculature, the lumbodorsal fascia, and the gluteus maximus.4 When abnormal stresses are applied, the result may be annular tears of the intervertebral discs or stress fractures on the neural arch as a result of

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the excessive resistive force. The most common lace for stress fractures is the pars interarticularis. The basic mechanism of injury is a combined vector of force that may be difcult to analyze in a force diagram.5 Three common mechanisms of injury to consider are: 1. Compression or weight loading to the spine 2. Torque or rotation (may result in various shear forces in a more horizontal plane) 3. Tensile stress produced through excessive motion on the spine The compressive type of stress is more common in sports that require high body weight and massive strengthening, such as football and weight lifting. Torsional stresses occur in athletes participating in sports such as javelin throwing, baseball, and golf. Motion sports that put tremendous tensile stresses on the spine include gymnastics, ballet, dance, pole vaulting, and high jumping. Some injuries result from direct blows. In sports such as football there can be muscle contusions, muscle stretches, and tears of fascia, ligaments, and occasionally muscle. Lumbar fractures can occur from direct blows to the back with fracture of the spinous process or twisting injuries that avulse the transverse process. Vertebral body end-plate fractures from axial compression loading on the disc are a relatively common source of compressive disc injury. Although the annulus is more likely to be injured in rotation, the end plate is more vulnerable to compression than the annulus. Axial loading compression injuries can result from jarring injuries in motor sports or boating. Flexion rotation fracture dislocations of the cervical and lumbar spine are possible. In any sport in which one athlete falls on another, an athlete can suffer an asymmetric loading, rotational injury to the thoracolumbar spine. Any time equipment is involved, such as a motorcycle, board, or automobile, direct translational blows can produce a fracture dislocation. The intervertebral disc is injured predominantly through rotation and shear, producing circumferential tears and radial tears. Initially the layers may actually separate, or the inner layers may break. As the inner layers weaken and are torn, additional stress is placed on the outer layers. This can produce a radial tear of the intervertebral disc. With the outer layers torn, the inner layers of annulus break off and, along with portions of the nucleus, are forced with axial loading to the place of least resistance, the weak area in the annulus. The outer areas of annulus are richly innervated, producing tremendous pain and reex spasm when the annulus tears. The nuclear material can produce a chemical neuritis and inammation. The spasm and pain are mediated through the sinovertebral nerve with anastomosis through the spinal nerve and the posterior primary ramus. As the herniated annular fragment extrudes, producing pain from the traversing or exiting nerve root itself, the patient may develop sciatica or radiculopathy. Intradiscal inltration of the granulation tissue adds increased potential for painful sensation

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in the annulus. The annulus, with time, can heal. Although the healing annulus will not retain the same biomechanical function capability as the original intervertebral disc, it can be completely compatible with pain-free function. Biomechanical functioning of the spinal column and its relationship to the biomechanics of nerve tissue involve several basic concepts: 1. In the spine, exion of the lumbar spine increases the size of the intervertebral canal and the intervertebral foramina.10 2. Extension decreases the size of the intervertebral canal and the intervertebral foramina.10 3. Flexion increases dural sac and nerve root tension.9 4. Extension decreases dural sac and nerve root tension.9 5. Front exion, axial loading, and an upright posture increase intradiscal pressure. 6. With exion the annulus bulges anteriorly.14 7. With extension the annulus bulges posteriorly.14 8. Nuclear shift in an injured disc is poorly documented, but the disc probably shifts in the direction of the annular bulge.10 9. Rotation and torsion produce annular tears and disc herniations.2 These facts indicate that motion does have an effect on the nerves and the neuromotion segments of an injured area. For example, if there is a spinal obstructive problem such as spinal stenosis, extension exercises can further compress the neurologic structures and make them worse; if there is a nerve root tension problem, such as disc herniation, then exion can produce increased tension in an already-tense nerve and increase symptoms.

HISTORY AND PHYSICAL EXAMINATION The key to a proper history and physical examination is to have a standardized form that accomplishes the needed specic objectives, which are: 1. Quantitate the morbidity. Use a value scale of pain, function, and occupation to determine how sick the patient is. Converse with the patient and listen to the inections and manner of pain description. Detail the time of disability and the time of origin of the pain. We use the Oswestry scale and the disability rating. The severity of the morbidity often determines the aggressiveness of the diagnostic and therapeutic plan. 2. Delineate the psychosocial factors. Know what psychologic effect the pain has had on the patient. Know the social, economic, and legal results of the patients disability. We use the pain drawing on the initial visit and a detailed psychologic report in certain instances. Understand what can be gained by the patients being

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sick or well. Derive an understanding of what role these factors are playing in the patients complaints. 3. Eliminate the possibility of tumors, infections, and neurologic crisis because these conditions have a certain urgency that requires immediate attention and a diagnostic therapeutic regimen that is very different from that required for disc disease. Constant, unrelenting pain more at night than during the day is an indication of tumor or infection. Ask about bowel, bladder, and sexual dysfunction, and conduct a thorough examination. 4. Diagnose the clinical syndrome: a. Nonmechanical back and/or leg painInammatory, constant pain; minimally affected by activity; usually worse at night or in early morning b. Mechanical back and/or leg painMade worse by activity; relieved by rest c. SciaticaPredominantly radicular pain; positive stretch signs, with or without neurologic decit d. Neurogenic claudicationRadiating leg or calf pain and negative stretch signs; made worse with ambulation and spinal extension and relieved by exion Pinpoint the pathophysiology causing the syndrome. Three important determinations are: 1. What level? Which neuromotion segment? 2. What nerve (especially in radiculopathy)? 3. What pathology? What is the exact structure or disease process in that neuromotion segment that is causing the pain? Some key factors in the history and physical examination are: 1. 2. 3. 4. What caused the injury The time of day when the pain is worse A comparison of pain levels during walking, sitting, and standing The effects of Valsalvas maneuver, coughing, and sneezing on pain 5. The type of injury and duration of the problem 6. The percentage of back versus leg pain (we insist on getting an accurate estimate of the relative amount of discomfort in the back versus that in the legs. These two numbers must add up to 100%) The physical examination should address: 1. 2. 3. 4. 5. Maneuvers during the examination that reproduces the pain The presence of sciatic stretch signs The neurologic decit Back and lower extremity stiffness and loss of range of motion The exact location of tenderness and radiation of pain or paresthesias

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Diagnosis After completion of the history and physical examination, the diagnosis should certainly be based on the history and physical ndings. If the patient has a profound neurologic disorder, the appropriate neurologic testing should be carried out. For the majority of spine injuries in athletes, especially professional or in adolescent athletes, the diagnostic evaluation in any athlete with longer than 1 month of signicant back pain should begin with a lumbar bone scan and spect scan. This diagnostic evaluation is vital in diagnosing stress and joint injuries that commonly occur in athletes. This will diagnose an acute spondylolytic defect or an impending spondylolysis. If the bone scan is positive, a computed tomography scan should be ordered to determine what is positive in the bone that is being reected in the SPECT scan. We have made the diagnosis of osteoblastomas and osteoidosteomas at this time with the bone scan and CAT scan combination. Usually it will demonstrate whether there is an acute fracture or impending spondolytic defect. If the SPECT scan is negative a magnetic resonance image will reveal the presence of a lumbar disc herniation or other soft-tissue lesions. The appropriate treatment can usually be based on the results of this testing. Most athletic injuries to the lumbar spine fall under the category of mechanical, axial, back, or leg pain. Within this categorization, several different syndromes exist. Annular Tears of the Intervertebral Disc These are usually a loaded compressive rotatory injury to the lumbar spine producing severe, disabling back spasm and pain. The pain is usually worse on exion with coughing, sneezing, straining, an upright posture, sitting, and any other situations that increase intradiscal pressure. There may be referred leg pain, low back pain with straight leg raising and anterior spinal tenderness. Annular tears can be produced with as little as 3 degrees of high-torque rotation. Three-facet joint alignment that protects the disc from rotatory forces may lead to facet joint injuries as the annulus fails in rotation. Facet Joint Syndrome This more typically occurs in extension with rotation reproduced with extension and rotation during the examination. This syndrome may present with pain on rising from exion, with a lateral shift in the extension motion. Point tenderness may occur in the paraspinous area over the facet joint in association with referred leg pain. The facets and the disc are all part of the same joint: three joints of a one-joint complex. If the facet joint injury causes pain and is accompanied by an annular tear of the intervertebral disc, it is the entire joint that is injured.

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Tears of the Lumbodorsal Fascia, Muscle Injuries, and Contusions These are present with muscle spasm, stiffness, and many of the characteristics of facet joint syndrome or annular tears. Sacroiliac Joint Pain and Pain in the Posterior Superior Iliac Spine These are the most common areas of pain referred from the annulus in the intervertebral disc and the neuromotion segment of the spine. Sciatic pain can occur in the sciatic joint area, as well as in the sciatic notch and buttocks. Although injuries can occur to the sacroiliac joint, the vast majority of syndromes presenting with sacroiliac joint pain are believed to be a result of referred pain from a neuromotion segment in the spine. Lumbar Disc Herniation The usual presenting symptoms of lumbar disc herniation are low back pain with radiating leg pain. The severity of the symptoms and the extent of the neurologic decit are major considerations in the election of a nonoperative or an operative course of treatment. The presence of pre-existing lumbar congenital spinal stenosis plays a major role in the patients ability to recover from the symptoms nonoperatively, even with the best of nonoperative programs. Large herniations and tight spinal canals are more likely to require surgery. A nonoperative treatment for a lumbar disc herniation is initially used with strong anti-inammatory medications including epidural injections, Indocin, and Medrol Dosepak, followed by intensive trunkstabilization training. The trunk-stabilization training program should be followed through to the maximum achievable level. Professional athletes need to do the Level 5 exercises, and collegiate athletes need to do Level 45 exercises. After the symptoms have resolved and the patient is doing a Level 4 or 5 stabilization program, he or she can begin sport-specic exercises and return to practicing the sport. Surgical treatment of an extruded disc fragment of the lumbar spine is a microscopic lumbar discectomy. Whatever exact operative technique (whether tubular retractor with endoscope or microscope, the blade spike retractor with microscope, or a foraminal endoscopic approach), the key is to be as minimally invasive as possible, cause as little harm as possible, and damage as little fascia and muscle tissue as possible. The standard microscopic technique involves using lateral paraspinous needles to plan the incision over the disc space. Our recommendation is to plan from the mid portion of the disc space 2 cm caudal. The incision is made though the skin subcutaneous tissue, and the fascia is opened either with a puncture wound and expansion of the fascia of a small knife incision in the fascia. Exposure of the interlaminar area with the

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endoscope and microscope is the step preceding opening the roof of the spinal canal. For a caudal extruded fragment, the ligamenta avum can be carefully detached off the cephalad edge of the caudal lamina, the epidural space entered, and the fragment removed. Additionally, the cephalad portion of the ligamenta avum can be approached by doing a small laminotomy with the drill in the cephalad lateral position, opening the ligamenta avum or detaching it laterally, and approaching the more cephalad portion of the intervertebral disc. Remove the fragment of the disc; go into the disc space, removing any other loose fragments; avoid a large annular resection; obtain hemostasis; and carefully close the fascia. The exception to this is during cases of a localized acquired or congenital stenosis. Unfortunately, a more generous cephalad and caudal laminotomy is performed under those circumstances in consideration for total laminectomies if the congenital stenosis is extensive and severe. There is risk of a postoperative epidural hematoma in doing a microscopic fragment excision in the face of severe congenital stenosis. It takes very little postoperative epidural hematoma to produce a signicant neurologic decit and need for total laminectomy. My postoperative recommendations are for the patient to walk as much as he or she wants to from the time of the surgery. For 3 weeks, there is to be no bending or lifting anything heavier than a coffee cup; no sitting on low, soft sofas or chairs where one has to throw the body weight forward in order to get up; and no driving. Trunk stabilization training can begin 3 weeks after the surgery. For patients who know the program very well, it can potentially be started at 10 days. The limiting factor is still the hole in the posterior annulus. To prevent a recurrent herniation, it is better not to overly stress the spine until the annular disruption has a chance to begin healing. This is regardless of the technique of opening the skin or the fascia. Regardless of whether an endoscope or a microscope is used, there is still the annulus disruption resulting from the fragmentation and from removal of the tissue from the disc space that is the limiting factor in allowing one to return without an increase risk of recurrent herniation. The postoperative care consists of trunk stabilization training to a Level 4 or 5, sport-specic training, returning to full weight-lifting regimen, aerobic conditioning program before beginning practice, starting practice on a limited basis, and continuing the rehabilitation program. This will put the player in the best position for safe return to play. Disc herniations in atheletes are treated similar to disc herniations in nonathletes. The severity of the pain, the extent of the neurologic decit, and the size and location of the herniation are decision making factors. The only exception may be in athletes who only have pain playing their sport or athletes at the end of the season in whom the herniation is still present but the pain has gone away because they are no longer playing the sport. Often a decision is made to perform a disc excision on a currently asymptomatic patient in preparation for his or her return to the sport the next season. This is acceptable surgical

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decision making and often is an important decision in the life of an athlete. Certainly, disc herniations anywhere in the spine can potentially be treated nonoperatively in the athlete, as it can in other people. MANAGEMENT AND REHABILITATION PRINCIPLES Nonoperative Care The objective of the rehabilitation program is to safely return the patient to whatever level of function the patient wants and to allow the patient to safely test the limits of future performance. Patients who are better at a sport (having the proper muscle coordination patterns to perform the sport) nd it easier to return to the sport without injury. When and whether patients can return to a sport (except for a few conditions) are usually based on their ability to perform the rehabilitation program and to apply the program to their sport. The nonoperative treatment plan consists of several basic steps: 1. 2. 3. 4. 5. 6. Stop the inammation. Restore strength. Restore exibility. Restore aerobic conditioning. Restore balance and coordination. Adapt the rehabilitation program to sport-specic training and exercises. 7. Start back into the sport slowly. 8. Return to full function. Stopping inammation of the spine in an injured athlete often requires rest and immobilization. We try to limit the rest and immobilization to a minimum. Bed rest produces stiffness and weakness, which prolong the pain. Every day of rest and immobilization may necessitate weeks of rehabilitation before the athlete can return to performance. As in the treatment of lower extremity injuries (i.e., fracture bracing and postoperative continuous motion machines), rapid rehabilitation of lumbar injuries in athletes requires effective means of mobilizing the patient. Rapid mobilization requires strong anti-inammatory medications, ranging from epidural steroids, oral methylprednisolone (Medrol Dosepak), and indomethacin (Indocin SR) to other nonsteroidal anti-inammatory agents and aspirin. Lots of ice, a transcutaneous electrical nerve stimulation unit, and mobilization with casts, corsets, and braces are required. Strengthening techniques are started when the brace is applied so the brace can be removed as soon as possible because braces cause stiffness and weakness. As a general rule, our patients with acute disc herniations are treated with up to 3 days of bed rest; physical therapy within 1 to 5 days; a corset to be worn for no more than 10 to 14 days; and indomethacin, occasionally methylpredolone, and epidural injections. The therapist begins the neutral-position, isometric trunk-strengthening program, and,

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depending on the response of the patient, procedes to resistive strengthening, motion, and aerobic conditioning as tolerated. Concern has been raised about the risk of increasing neurologic decit or producing a neurologic decit through nonoperative care. As a result, nonoperative care for neurologic decit has consisted of no care. Today, a short period of bed rest is the usual, initial stage of treatment of the athlete with a disc herniation and neurologic decit. It is believed that bed rest protects the patient from increasing injury to the spine and therefore increasing neurologic decit. However, bed rest can actually increase the risk of injury, and other methods should be used, depending on the goal. If the purpose of bed rest is to decrease inammation, the logical substitute is aggressive anti-inammatory medication. If the objective of bed rest is to prevent motion, braces and casts can be substituted. If the objective of bed rest is to prevent abnormal motion that could injure the spine, it is with the understanding that certain mechanical functions must take place, such as getting on and off bed pans, getting up to go to the bathroom, rolling over in bed, coughing, sneezing, and eventually walking. An exercise program should prevent abnormal motion while restoring strength and exibility in a biomechanically sound fashion to protect the spine from abnormal motions that produce injury and to enhance healing. Lumbar spine injuries in athletes demand prevention of atrophy and stiffness and restoration to maximum function as early as possible. The key to the nonoperative program lies in safety and effectiveness. Rehabilitation begins with the concept of neutral-position isometric strengthening for the spine, emphasizing trunk isometric control and strength, followed by extremity strengthening, extremity stretching, and, nally, trunk mobility. Neck and upper extremity strengthening can be added after trunk stability for neck problems. Trunk Stabilization Rehabilitation Program The principles for the trunk stabilization rehabilitation program outlined here are derived from work by Michael Schlink, RPT, Gayle Hazletine, RPT, Randy Bower, the Folsom Physical Therapy Ofce, Jeff Saal, MD, Arthur White, MD, and others, including Celeste Randolph, Gary Souza and Scott Alstadt. The exercise program concentrates on trunk strength, balance, coordination, exibility and aerobic conditioning. It is a practical application of the use of trunk strengthening in back treatment, injury prevention, and improved performance in athletes. The role of muscle coordination in athletic function cannot be underestimated. Coordinated muscle activity produces the athletic activity necessary for a sport. In our study of the dynamic electromyographic (EMG) analysis of the trunk muscles in professional baseball pitchers, we demonstrated three signicant facts: (1) the opposite side of the abdominal oblique muscle is probably the most important muscle in the throwing athlete; (2) trunk strength is important in any torsional athlete (power must be transferred from the legs and hips and through the

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trunk to the ne control of the arms); and (3) it is coordinated trunk muscle activity that distinguishes higher performance, more effective performance, and pain-free performance. In an EMG study of professional baseball hitters, the role of coordinated trunk activity was demonstrated clearly, and, based on discussions with Ben Hines, hitting coach for the Dodgers, and a number of other sources on baseball hitting, it can be concluded that the general trunk activity of a baseball hitter consists of a coiling-up mechanism followed by uncoiling in which the hips rotate quickly toward the pitcher; getting the hips through the swing quickly is necessary for proper bat speed. This maneuver is followed by a tightly controlled derotation of the upper body that demands a synchrony of upper body and lower body function to transmit the power of the thighs and hips through the end of the bat. The ratio of upper body derotation to lower body derotation is controlled through coordinated muscle function of the trunk. Any adjustment in the speed of derotation of the upper body must involve rapid, coordinated trunk muscle function and occurs in less than a second. Another important aspect of muscle coordination is the role of eye function and muscle coordination. Eye focus on the ball is necessary for coordinated muscle function. For example, the tightrope walker is not looking around at the audience, or walking the rope with the eyes closed. This performer focuses on a point, and it is this focus that produces maximum muscle coordination. Although seeing the ball clearly in maximum focus is certainly important for seeing the rotation on the ball and other aspects, it also produces maximum muscle coordination. At the heart of the trunk stabilization rehabilitation program is coordinated trunk strength. Therefore, an ideal muscle-strengthening program begins trunk muscle coordination exercises as early as possible. All the trunk strengthening is done in response to proprioceptive stimulation and incorporates balance and coordination into the trunk-strengthening exercises. This is why, with the trunk stabilization rehabilitation program, we would rather have a participant do 50 sit-ups while balancing on a green exercise ball than 500 sit-ups on the oor. The program teaches trunk control while teaching trunk strength. The neutral, pain-free position is used because it is the same position a normal lumbar spine assumes when a person walks a tightrope, balances on a slide board, or attempts to lift 150 pounds at waist level. It is the position of power, the position of balance. It is not an exaggerated at-back position. In a patient with back pain, it may involve a slight degree of exion or extension, depending on the painful structures, but as the pain resolves this position of power and balance becomes the neutral position for the strengthening exercises. In patients with back pain, this has the added advantage of the patients nding and maintaining a pain-free position and thus being able to make faster progress in reestablishing isometric muscle control. The program has the added benet of producing back strength

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without having to use unprotected back motion; back motion without ne muscle control and without the proper strength in coordinated trunk muscle function can produce injury to joints whose vector forces are distributed across the joint surface without proper muscle control. Injury to joints is more likely to occur when trunk motion is used for trunk strengthening than when a neutral, pain-free position is used for trunk strengthening. What role does the neutral position play in the actual performance of a sport? Using baseball as an example, when a shortstop sprints for a ball and bends over to catch it, his trunk muscles re to protect his back because they have been trained to do so in response to off-balance peripheral septal stimuli and in response to extremity motion. When the shortstop puts his arm out for the ball, the trunk muscles almost return the spine to the neutral position of balance and power. A program of this type differs from one wherein back strengthening is done with a back-strengthening machine. The ability to bend forward or backward against increasing resistance can be benecial (it is better than no strength), and it is a factor that can be measured objectively. The disadvantages of using a back strengthening machine are that (1) back motion is used for back strength (abnormal forces are more likely to be transmitted through injured joints with resisted back motion than with maintenance of the neutral, pain-free position), and (2) the ability to perform the function on the machine may not translate to the proper muscle coordination necessary to perform the tasks the athlete must perform. For example, the ability to bend forward against resistance on the back machine is not the ability needed to throw a javelin. If coordinated muscle strength can be taught from day one in the program, we believe the program will be more comprehensive and effective. The rehabilitation program in a patient with an injured lumbar spine, with or without neurologic decit, begins with the patient nding a neutral, pain-free position with isometric muscle control; lying supine on the ground with the knees exed and the feet on the ground is the position generally used. This is as atraumatic a beginning to rehabilitation as possible. Also, it forms the basis of an important concept, not only in athletic function but also in activities of daily living for everyone. We retrain muscles to work to support the spine while the patient is using the arms and legs. This is not only theoretically ideal but also practically possible. Teaching muscle control with tight, rigid contraction of the trunk muscles and controlling the spine through muscle control of the lumbodorsal fascia not only results in protection of the lumbar spine but also can improve athletic performance. The power and strength of any throwing athlete come from his trunk. Lifting weight requires functioning of the muscles attached to the lumbodorsal fascia. Trunk strength is an important treatment method for back pain and can prevent back injuries. Although treatment plans for symptomatic patients with back pain may include similar exercises, each treatment plan should be designed to match the examination ndings and the symptoms. Any trunk-strengthening plan puts strain on the spine and

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can produce back pain because of overload. Therefore, it should be conducted in a controlled, progressive manner. The key to safe strengthening is the ability to maintain the spine in a safe, neutral position during the strengthening exercises. For upper body strengthening, the spine must be well aligned, with the chestout posture. Doing isometric trunk exercises and upper body exercises emphasizing this chest-out posture strengthens the support for the cervical spine, builds up the postural muscles needed for maintaining proper body alignment, and prevents neck pain caused by bad postural alignment. The neutral pain-free position obtained in the stability program is one of relative exion. The patient learns to tighten muscles around that position. Just as a patient who has had knee surgery starts with the rst quadriceps set, the patient feels and learns the proprioception for trunk muscles from this position. The patient, feeling (sometimes for the rst time) the abdominal oblique muscles, the gluteal muscles, and other muscles contracting, squeezes to hold that position. The program progresses through a series of balancing and resistive exercises while the patient maintains that position. The muscles are strengthened during balancing. They are trained to maintain or restore that position while attempts are made through resistive maneuvers to move that position. There is an actual time in which the spine is loaded in position or moving under maximum muscle control that not only delivers the maximum torque transfer and performance but also delivers maximum protection from overload injuries to the spine. Aerobic Conditioning Numerous methods are available for aerobic conditioning. Our current interest lies in using aerobic conditioning programs in treating patients with low back pain. Potential benets if aerobic exercises for patients with low back pain include strengthening bone, tendons, ligaments and muscles as well as enhanced oxidation capacity of skeletal muscles, cartilage, and intervertebral discs. The CSF of patients with postoperative chronic low back pain shows decreased b-En (beta endorphin) levels. This decreased b-En level can be elevated, at least in theory, by aerobic exercising and could account for some decreased perception of pain. An analysis of the relationship among tness, low back pain, and depression reported that stronger persons with low back pain are less limited by their pain and higher aerobic work capacity was generally observed in more active patients. The exercise prescription in aerobic conditioning is adequate only if the patient is motivated to comply with the regimen. We make every effort to educate the patient to the exact mode of exercise in terms of duration, frequency, intensity, and potential benets of the regimen. Great care is taken to set realistic goals for the patient. Several methods of aerobic exercises are available to our patients.

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An age-appropriate maximal target heart rate of 80% for 10 to 15 minutes optimizes cardiopulmonary benets and b-En elevation. In certain patients, this involves simple, brisk walking or running. In patients aficted with various arthritides, we have considerable success with water running. This involves wearing a life vest and running in place in the deeper end of the pool. Treadmills vary in their options, but the underlying goal is maintenance of 80% maximal heart rate for 10 to 15 minutes. Appropriate conditioning can be accomplished with a stair climber. Although synchronous recruitment of large muscle groups tend to be inefcient, continuous climbing at 75 degrees on the machine will promote higher oxygen consumption at submaximal work and elevated blood lactate levels at just 5 minutes of exercise (anaerobic exercise). However, this mode of conditioning is associated with a higher injury rate than more aerobic modes such as the treadmill. A ski machine allows aerobic conditioning without the repetitive loading of knee or ankle joint. The maximal oxygen consumption is equivalent to the traditional bicycle ergometer and treadmill. This mode of exercise must be tailored to the patients acceptance, availability to the patient and associated physical limitations. The various kinds of commercially available equipment have the same basic criterion: to maintain a target heart rate for a set time. Restoration of Balance and Coordination Restoration of balance and coordination is vital to an effective return to full activity and sports. Incorporation of balancing techniques into the strengthening program, as is done in the spinal stabilization and rehabilitation program, begins the process of retraining muscles to re at the right time with the proper strength. Balance and coordination are the key to friction-free performance, which is safer and more effective. Coordination is the key to swinging the golf club, throwing a baseball, or even lifting weights. Using the Swiss exercise ball, balance beam, standing positions for resistive exercises, exercises bands, and such techniques as one-legged squats while resisting an exercise band pulling on the waist are methods that use balance with strengthening. Balance and coordination need to be incorporated into all the strengthening, stretching, and aerobic conditioning aspects of a rehabilitation program. Sport-Specic Exercise The physical therapist, trainer, physician, and coach all come together in the rehabilitation program in relation to the sport-specic exercise. After relief of inammation and pain, and restoration of strength, exibility, conditioning, and coordination from doing the rehabilitation exercises, these techniques must be incorporated into the sport. Much will be lost and injury is likely to recur if this does not take place properly. New exercises in addition to the old ones are added that more

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closely simulates the sport. Proprioceptive neuromuscular facilitationtype techniques of resistive rotation and other techniques blend in with the old techniques and are done by the athlete to prepare for the sport. The coach may be able to change certain techniques, such as using a slight external rotation of the lead foot in golf or a different foot plant in baseball. Sport-specic training incorporates certain things that coaches have taught for years. One should be innovative. Being able to understand the sport and design ways to simulate that sports activity in the rehabilitation program will facilitate transfer of the principles of the rehabilitation program to the sport. The athlete should start slowly back into the sport, taking time to test out the new techniques, the new awareness of trunk muscle function, and body alignment. Too fast a return means returning too quickly to the same old rut that often led to the injury. One should build up to the maximum performance. Operative Care The chief indications for surgery in the athlete are the indications for surgery in any patient. The basic principles of dealing with any patient are also of major importance in the athlete: 1. Sufcient morbidity to warrant surgery 2. Failure of conservative care 3. An anatomic lesion that can be corrected with a safe, effective operation 4. A proper, fully developed postoperative rehabilitation program Not enough emphasis can be placed on the last mentioned principle: a proper postoperative rehabilitation program. Failure to do postoperative spinal rehabilitation would be equivalent to failure to do postoperative knee strengthening after reconstruction of the knee or failure to do postoperative strengthening and range-of-motion exercises after surgery on a shoulder. The patient wants restoration of function. The surgeon should be able to guide the patient through the restoration process. The morbidity of the patient, amount of pain, loss of function, and occupation are the critical factors. Spinal operations to enhance performance rather than relieve disabling pain are a part of managing the care of athletes, a part that requires a great deal of experience, not only in spinal surgery but also in dealing with athletes. There are numerous factors to consider. One must always keep in mind the longevity of the patient. Young players can stay out a year after signicant spinal surgery and still return to play. Older players are less likely to return to play after a major spinal reconstructive operation. What the player will be like after retiring from the sportthe condition of the spine at that timeshould be of major importance in decision making early in the players career.

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A major factor involves calculating the odds of the operation being successful. In many sports, after a spinal fusion for example, or a major resection of a supporting structure in a decompression, the chance of returning to the sport may be no greater with the operation than without it. A surgeon must carefully question the use of surgery if the surgeon does not have a proper alternative to the surgery in good, effective nonoperative care. If all one knows is the surgical technique, and if one does not have a proper understanding of and delivery system for a rehabilitation program, then that person should not advise surgery for the athlete. An appropriate team approach among specialists in rehabilitation and specialists in operative care can be worked out so that the decision for surgery is well founded, but the surgeon must understand and participate in all aspects of the decision-making process. The surgeon must understand spinal rehabilitation to understand whether the patient has had a sufcient nonoperative treatment program and whether there is a proper postoperative plan for return to full function. The anatomic lesion is critical to the simple extruded disc herniation, of course, amenable to a single-level microscopic lumbar discectomy, but an annular tear of the intervertebral disc with mild nerve root irritation will not be made better by a decompressive laminectomy and usually will be worse because of abnormal motion (segmental instability), now with a nerve scarred to the back of the annulus. The microscopic discectomy is a standard treatment for removing an extruded disc fragment. A small skin incision is used because that is all that is needed with a microscope. The subcutaneous tissue is gently opened to nd the fascia. The fascia is opened just off the spinous process to allow a tight fascial closure. Muscle is gently elevated and protected. The ligamentum avum is detached, and only the minimum necessary for exposing the fragment and nerve is resected. The microscope, proper positioning, and relative hypotensive anesthesia may allow the surgeon to avoid bleeding and having to use the bipolar electric cautery and cottonoids. The annulus should be handled with care to enhance healing. A blunt puncture with a No. 4 micro-Peneld dissector, expanding the hole with a regular Peneld dissector and a micropituitary rongeur, produces less annular damage than a cruciate incision, which is better than a square incision. Every operation is not necessarily done exactly this way, but an important principle in surgery on athletes is to protect the normal tissue. Tissue-handling techniques should be designed to enhance postoperative healing with a minimum of scar formation. The microendoscopic discectomy is an effective means of performing much the same operation as the microlumbar discectomy. The microendoscopic discectomy allows a 1-cm relative percutaneous approach through the interlaminar area. With detachment of the ligamentum avum the disc fragment can be removed safely. The Microendoscopic discectomy may also be used as well as the microscope, for a paraspinous approach to a foraminal disc herniation. Obviously, this is a proper mandate for all surgery. The extent of the surgery is also

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determined by the need to fully correct the pathologic condition. The skill is in being able to fully correct the pathologic condition with a minimum of surgery. In spondylolisthesis the obvious solution may be a spinal fusion, as it is in the majority of the patients facing surgery for spondylolisthesis. Some athletes can return to their sport after a successful spinal fusion, and some cannot. Part of the danger lies in curing the x-ray results, and not the patient. Another possibility is to cure the patient with a successful operation and leave the player without a job. As with everyone, an absolute indication for surgery for lumbar disc disease is progressive cauda equina syndrome or progressive neurologic decit. Relative indications include static signicant neurologic decit, unrelenting night pain, major loss of functional capability, and inability to play the sport because of spinal pain. There will always be patients who could live the way they are but who cannot perform the way they are. This is a relative indication for surgery, but it must be a frequent consideration in lumbar spine injuries in athletes. A simple question often asked is, how long does one wait before doing surgery for a disc herniation? The key word is wait. A vulture waits until the victim quits moving. A spinal surgeon is not waiting; the surgeon is aggressively treating the patient, judging the response to treatment, listening to the patients expectation of the sport and of life outside of the sport, understanding the patients concern about timing or surgery relative to the start of spring training, and understanding the patients fears concerning the sport and the patients life. The number one factor in when or whether to recommend surgery is what is in the patients best interest.

References
1. Aggrawal ND, et al: A study of changes in weight lifters and other athletes. Br J Sports Med 13:58, 1979 2. Farfan HF: Mechanical Disorders of the Low Back. Philadelphia, Lea & Febiger, 1973. 3. Farfan HF: Muscular mechanism of the lumbar spine and the position of power and efciency. Orthop Clin North Am 6:135, 1975 4. Farfan HF: The biomechanical advantage of lordosis and hip extension for upright activity. Spine 3:336, 1978 5. Keene JS, Drummond DS: Mechanical back in the athlete. Comp Ther 11:7, 1985 6. Keene JS, et al: Back injuries in college athletes. J Spinal Dis 2:190, 1986 7. Kotani PT, et al: Studies of spondylolisthesis found among weight lifters. Br J Sports Med 9:4, 1981 8. Saal JA: Common American football injuries. Sports Med 24:42, 1991 9. Schnebel BE, Watkins RG, Willin WH: The role of spinal exion and extension in changing nerve root compression in disc herniations. Spine 14:835, 1989 10. Schnebel BE, et al: A digitizing technique for the study of movement of intradiscal dye in response to exion and extension of the lumbar spine. Spine 12:309, 1988 11. Sieman RL, Spangler D: The signicance of lumbar spondylolysis in college football players. Spine 6:174, 1981 12. Spencer CW, Jackson DW: Back injuries in the athlete. Clin Sports Med 2:191, 1983 13. Watkins RG: Trunk stretching and strengthening program. Pamphlet prepared for the Professional Baseball Athletic Trainers Society (PBATS), 1987; revised 1989, 1991, 1993.

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14. White AA, Panjabi MM: Clinical Biomechanics of the Spine. Philadelphia, JB Lippincott, 1978 Address reprint requests to Robert G. Watkins, MD University of Southern California Center for Orthopedic Spinal 1500 San Pablo Street Los Angeles, CA 90033

SPECIAL ARTICLE

02785919/02 $15.00 .00

INTRADISCAL ELECTROTHERMAL THERAPY FOR THE TREATMENT OF CHRONIC DISCOGENIC LOW BACK PAIN
Jeffrey A. Saal, MD, and Joel S. Saal, MD

The treatment of chronic low back pain presents a formidable challenge to the spine specialist. There is a discogenic etiology of low back pain in a subgroup of these chronic patients.43 Nonoperative measures are frequently unable to reduce pain and improve function in this patient sub-group.5, 46 Surgical treatment of these patients, including interbody fusion techniques, has yielded mixed results.49, 50 An alternative therapy to address this problem is therefore desirable. The SpineCATH (Oratec Interventions, Inc, Menlo Park, CA) system (Fig. 1) to perform intradiscal electrothermal therapy (IDET) was developed to address this difcult to treat group of patients. Patients with chronic lumbar pain fall into 2 clinical categories: chronic recurrent and chronic persistent. Chronic recurrent patients have multiple pain ares with varying durations of 2 weeks to 3 months. Many patients within this group will begin to have more frequent recurrences with fewer pain-free intervals as time passes. Chronic persistent patients have persistent symptoms that do not abate and last longer than 3 months. The disc has been shown to be the pain source in the

This article originally appeared in the book, Operative Techniques In Orthopaedics, edited by Fu FH, WB Saunders, 2000

From the SOAR Physiatry Medical Group, Menlo Park, California

CLINICS IN SPORTS MEDICINE


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Figure 1. Spine CATH intradiscal catheter (ORATEC Interventions, Inc., Menlo Park, CA).

vast majority of patients with chronic symptoms.43 Carey et al recently reported that patients who do not experience a resolution of their back pain within 3 months of onset had a poor prognosis for further recovery. When assessed at 22 months, patients continued to complain of low back pain and were dissatised with their outcomes.5 Von Korff reported that although 80% of patients had resolution of their acute low back pain in 12 weeks 60% of the patients experienced recurrent symptoms.46 These recent studies underline the fact that chronic low back pain does not necessarily have a favorable prognosis and that the long-held belief that 90% of patients will experience resolution of their back pain within 6 to 12 weeks is incorrect and misleading. A combination of complex interactions is thought to be the underlying basis for chronic discogenic pain. The disc is an innervated structure that is capable of pain generation.4 The posterior longitudinal ligament is the most densely innervated structure in the lumbar spine.4 Nociceptors are present in the outer posterolateral portion of the lumbar disc (Fig. 2). Nociceptor afferent transmission is relayed through the dorsal root ganglion (DRG). Substance P release is triggered by provocative discography.3, 48 In-growth of granulation tissue and small unmyelinated nerve bers has been shown to occur in the degenerative and disrupted disc.6, 12 DISC PATHOLOGY Degenerative Disc The natural history of the degenerating disc includes the loss of nuclear hydrostatic pressure, which leads to buckling of the annular lamellae. This phenomenon leads to increased focal segment mobility and increased shear stress to the annular wall. This process continues to delamination and ssuring of the annular wall. Annular delamination

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Figure 2. Neovascularization through convecting annular tears.

has been shown to occur as a separate and distinct event from annular ssures.31 Fissures can be radial or concentric. In addition, electron microscopy has shown microscopic fractures of collagen brils with disc degeneration. The progressive degeneration of the disc manifested by any of these morphologic changes, has been shown to alter disc mechanics.42 Tearing and delamination of the annulus can cause chronic pain. Mechano-receptors in the disc wall have been shown to discharge with disc mobilization.38 Nociceptive tissue has been shown to be sensitized, resulting in a decrease in their ring threshold after treatment with inammatory enzymes and mediators.36, 37, 47 A scenario for chronic discogenic pain is created when any combination of annular ssures, delamination, or microfractures of collagen brils leads to mechanical distortion of annular lamellae and subsequent sensitization of nociceptors that may have also been presensitized by phospholipase A2 (PLA2),11 nitrous oxide,22, 24 interleukin 1,24 and metallo-proteinase enzyme activity.25 Afferent stimuli create the release of substance P and nociception. Repetitive stimulation of the DRG has been shown to create prolonged neural activity from the dorsal horn receptor elds.9, 36, 45 As the patient continues to load the disc, the neuronal activity continues. This disrupted disc can cause referral pain into the buttocks and leg caused either by DRG stimulation or from direct chemical irritation of the nerve roots. A combination of mechanical and neural properties creates an interplay that leads to chronic discogenic pain. A high intensity zone (HIZ) on T2-weighted magnetic resonance imaging (MRI) scans has been shown to correlate to a pain-producing ssured disc 65% to 95% of the time.2, 20, 94 However, MRI predicts the presence of annular ssures less

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than 50% of the time.20, 30, 35, 44 Therefore, a patient may have a painful annular tear without concomitant MRI ndings. Disc bulging is always associated with annular degeneration and ssures; however, this phenomenon does not always create clinically signicant low back pain.30

Herniated Disc Lumbar disc herniation is a distinct pathologic entity. Lumbar intervertebral disc herniation typically occurs as a result of annular degeneration leading to weakening of the annulus brosis, leaving it susceptible to annular ssuring and tearing. Nuclear migration caused by annular disruption leads to the most common forms of clinically recognized lumbar disc herniation (LDH) (ie, contained, extruded, and sequestered). The spinal canal location of disc trespass will determine the type of neural compromise and clinical pain pattern. The degree of neural compromise can not be judged accurately by the size, type, or location of the disc material.39 Large, free fragments may cause no neurologic decit. However, it is distinctly unusual for a small, contained LDH to create a profound neurologic decit. Pain production from types and locations of disc also varies considerably. Small, contained LDHs may frequently create severe pain, and large extrusions and sequestrations can be painful or painless. The factors that determine the pain-producing capability of an LDH are unclear and may be related more to its chemical potential than to its anatomic characteristics.11, 39 Classic disc herniation predominantly creates leg pain. Some contained disc herniations, especially central herniations, create a mixed pattern of both back and leg pain without true radiculopathy. There are 3 general types of disc pathologies: (1) the leg pain disc, which is the classic disc herniation with nuclear migration and sciatica accompanied by true dural tension sign; (2) the back pain disc, which is the internally disrupted disc (discogenic pain) with annular pathology creating back pain, and variable amounts of leg and buttocks pain referral without frank radiculopathy (although it can cause a chemical radiculitis); and (3) a mixed pattern, such as with small contained disc herniations and central herniations. In addition, the postoperative disc can be a source of pain that mimics internal disc derangement (Table 1). Certainly not all chronic lumbar pain is discogenic. It is estimated, however, that more than 50% of patients with chronic low back pain have the disc as the primary source of pain.43 Screening for patients with facet problems, sacroiliac joint dysfunction, psychosocial problems, systemic disease, neoplasm, and infection should be undertaken when appropriate. A chronic pain syndrome with primarily soft tissue pain and somatization often occurs in the low back pain population. Practitioners must be aware of the potential existence of these phenomenons.

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Table 1. DISC PATHOLOGIES Type Classical disc herniation Discogenic pain Central disc herniation Postoperative painful disc Pain Pattern Leg pain Mixed Mixed Mixed Pathologic Anatomy Nuclear migration Annular ssures Annular ssure, Nuclear migration Annular incompetency Diagnostic Imaging Test MRI Discography MRI, Discography Discography

ELECTROTHERMAL THERAPY OVERVIEW The concept of using heat to affect tissue has been understood for many years. Necrotic lesioning, cutting, ablation, coagulation, and even physical therapy are some of the areas in which heat has been applied in medical care. Recently, the use of heat therapy has expanded to controlled contraction, or shrinkage, of collagenous tissues.15, 32 In arthroscopic applications, the prominent modes of thermal energy used in surgical applications are laser and radiofrequency. Thermal energy can not only precisely target tissue, but it can also be accurately measured with temperature control technology. The disc itself is a virtually avascular structure, and heat does not travel as easily in it as in other soft tissues. This environment allows heat to be held in the tissue with relatively little uctuation during treatment. Adjacent structures are protected from thermal injury by the vascular circulation outside the disc, which quickly dissipates any heat escaping from the disc.40 Temperature and power control gives the SpineCath system the ability to deliver focused energy at the point of contact. Heat is transferred by conduction from the catheter to the adjacent tissue. Temperature sensors deliver feedback to the generator, which adjusts power levels as necessary to reach and maintain set target temperatures. Identifying the precise temperatures needed to affect the disc tissue and having the power to produce the required temperature in the disc offers a high degree of accuracy and consistency to this treatment. EFFECT ON NERVE TISSUE Innervation of the intervertebral disc has been progressively well documented by researchers since the 1930s. Bogduk et als work illustrated the sources of lumbar disc innervation.4 Coppes et al found nociceptive properties in the nerves of the outer annular wall. In fact, they observed nerve bers deeper than the outer third of the annulus brosus.6 Freemont et al also discovered signicant neovascularization with neural expression of substance P and linked that growth to disc degeneration and back pain. They identied nerve bers as deep as the

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inner third of the annulus brosus and into the nucleus pulposus in several disc samples.12 Letcher et al established that irreversible nerve blocks occur at 45C in the brain,26 and Cosman et al7 used radio frequency (RF) lesioning to produce 45C isotherms for neural tissue lesioning. The intradiscal temperatures generated by the SpineCATH, which are 50C to 75C, are in the range necessary to create thermocoagulation of neural tissue. EFFECT ON COLLAGEN Collagen contraction, or shrinkage, has been well documented in the use of nonablative laser energy on joint capsular tissue and, more recently, in RF application in the glenohumeral joint capsule.10, 18 Research has shown that there is a direct correlation between the amount and duration of heat applied to tissue and the resulting collagen contraction.14, 16, 17, 28, 33 The breaking apart of the heat-sensitive bonds of the collagen brils causes tissue shrinkage. The framework of the intervertebral disc is composed primarily of type I and type II collagen, which have a similar molecular structure. The tensile strength of these collagen bers is derived from the extended conformation of the triple helix molecule, which is cross-linked with hydrogen bonds. A portion of these bonds has been shown to be heat-sensitive, breaking apart when exposed to a range of temperatures over time. The disruption of these stabilizing hydrogen bonds releases the molecular strands, which collapse (Fig. 3). This collapse, like the release of a tautly held spring, results in a new contracted state called the denatured or random coil conformation of the collagen ber. Electronmicroscopy images of extended and collapsed collagen are shown in Figures 4 and 5. The optimal temperature for collagen contraction is reported to be 65C. The lowest practical temperature at which heat-sensitive hydrogen bonds will start to break is 60C. As the temperature increases, more bonds break. It is unclear whether there is an additional shrinkage effect over 75C. The typical treatment regimens with the SpineCATH system will target this temperature range of 60C to 75C for collagen contraction. Thermal shrinkage of collagen is also dependent on the duration of the application of heat. Lower temperatures over a longer period of time result in shrinkage comparable with that achieved with a higher temperature over a shorter period of time. Under these parameters, IDET is capable of causing shrinkage of the collagenous bers of the disc annulus. Intradiscal applications of other available thermal energy sources have limitations when compared with temperature-controlled thermal resistive heating (Table 2). Radiofrequency delivered by an intradiscal needle electrode can not transfer the necessary range of thermal energy to achieve the desired effects, and a needle delivery system cannot access the broad expanse of the posterior annular wall.19, 40 Intradiscal laser

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Figure 3. Type I and type II collagen triple helix molecule in normal (A) and contracted (B) states.

Figure 4. Bovine patellar tendon with (A) and without (B) treatment.

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Figure 5. Bovine patellar tendon collagen bers at 10% (A) and 35% (B) contraction rates. Note the loss of clearly dened bril borders and striations as tissue contraction increases.

energy is potentially hazardous to bone and nerve tissue because of the lack of temperature control and extent of tissues heated.16, 17 ACCESS AND TEMPERATURE MAPPING STUDIES A series of experiments were conducted to develop the necessary technology to accomplish posterior annular access and to safely deliver targeted thermal energy to the annulus without damaging the end plates or extradiscal neural structures. A thermal-mapping model was developed with the use of a fresh never frozen cadaveric disc embedded with an array of 14 thermocouples placed in the nuclear cavity (Fig. 6),

Figure 6. In vitro temperature-mapping sensory location. It should be noted that in actuality the catheter is placed into the substance of the annulus.

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Table 2. THERMAL DELIVERY SYSTEMS Delivery System Oratec Energy source: TRC Delivery method: Navigable catheter Benets Good access to pathologic tissue Safety temperature feedback low power use Temperature control allows precise treatment Broad target zone (2-in heater length) No tissue impediance limitations with TRC Easy to place in disc Cost-effective Minimally invasive Safety low power use Cost-effective Minimally invasive Limitations Smaller decompression effect than laser discectomy Not intended for purely radicular symptoms Limited access to severely collapsed discs and postdiscectomy discs

Radiofrequency needle Energy source: Radiofrequency Delivery method: Straight needle

Laser ber Energy source: KTP, Ho-Yag Delivery method: Straight or sidering beroptic

Signicant decompression effect. Good for relief of radiculopathy. Moderate access to pathologic tissue

Tissue impedance limitations, resulting in ineffective heating of disc tissue. Radio frequency heats better in a uid environment. Insignicant decompression effectshort treatment time is insufcient for collagen contraction. Small treatment area Poor accessibility to pathologic tissue. Straight needle cant reach posterior wall. Few nerves can be destroyed if heat cant reach target. Cost prohibitive High energy use No temperature control collagen tissue necrosis Technique sensitive with noncontact lasers.

Abbreviations: TRC, thermal resistive coil; KTP, potassium titanyle phosphate frequency doubled ND: yag laser; Ho-Yag, holmium-yag laser.

the posterior annulus, and extradiscal tissue. The discs were placed in a water bath that had a constant temperature of 37C. The initial temperature-mapping studies were performed by using a radiofrequency needle (Radionics, Inc, Burlington, MA). The results duplicated Houpt et als results, demonstrating poor temperature dispersion from the heat source.19 The RF needle was unable to heat thermocouples that were more than 1 mm from the heat source. Additionally, needles could not be navigated to the posterior aspect of the disc wall (the 4-oclock to 8-oclock position). On the basis of these ndings, a

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navigable catheter was developed that could be navigated into the annulus (Fig. 1). The disc access studies progressed from cadaveric discs under plexiglass plates with direct visualization, to cadaver torsos punctured under the guidance of computed tomography (CT), to patients under CT guidance. To improve heat dispersion and avoid the pitfalls of RF, a 2-inch thermal resistive coil (TRC) was placed into the catheter as the heat source. The catheter was then placed in the posterior annular wall of cadaveric discs by using the thermal-mapping model discussed previously. A typical heating protocol was applied to each disc, gradually raising the internal catheter temperature to 90C or until the tissue temperature achieved steady state. The data recorded from each thermocouple showed that the maximum disc temperature for the samples was 76.8C. The maximum temperature of the peripheral annular lamellae was 49.8C, with an average maximum of 44.8C. The maximum temperature, measured outside the wall of the disc, was recorded at 42.9C and averaged 41.7C. After performing the cadaveric bench studies, live pig studies and perioperative mapping was undertaken during anterior lumbar fusion cases. These studies reproduced similar ndings demonstrating adequate temperature rise in the annulus with fall-off to safe temperature ranges in the epidural space. Temperature mapping was also performed in patients to investigate replication of the cadaveric study results and conrm safety. Fifteen discs were tested in 10 patients. All discs were treated for 15 minutes, with the SpineCATH positioned along the posterior annular wall. A 22gauge needle with a thermocouple embedded in the tip was inserted into the contralateral disc wall, and temperature was measured at 3 positions: inner annular wall within 3 mm of the catheter, 2 mm inside the outer annular wall, and in the foraminal space adjacent to the disc. The maximum disc temperature recorded was 79C. The maximum outer annular temperature measured was 47.5C, with an average maximum temperature of 43.2C for all discs. The maximum epidural temperature measured was 40.6C, with an average maximum temperature of 38C for all discs. The epidural and outer annulus temperatures were lower than in the in vitro studies, indicating the strong convective cooling effect of blood ow outside the disc and an even larger margin that observed in the cadaver discs. These mapping studies indicate that optimal temperature levels are reached by the SpineCATHs resistive heating system to achieve collagen modulation and nociceptor destruction in the outer annular wall. In addition, the low epidural measurements show temperature levels that are well within the parameters needed to avoid damage to unmyelinated nerves. Figure 7 illustrates a typical SpineCATH and outer annulus temperature prole from in vivo temperature measurement of 15.5 minutes of heating with a target temperature of 90C. Note that there is approximately a 15 difference between the catheter temperature and the tem-

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Figure 7. Temperature distribution through annular wall. When the catheter temperature is 90C, the temperature of the tissue adjacent to the catheter is 75C (A), the center of the annulus wall is 60C (B), the outer annulus wall is 42C (C), and the epidural space is 38C (D).

perature of tissue immediately adjacent to the catheter. This initial data was presented at the annual meeting of the International Society for the Study of the Lumbar Spine in Brussels in 1997.

MECHANISMS OF ACTION The precise mechanism of action of the observed positive clinical effect is currently under investigation. The proposed mechanism of action is a combination of annular collagen shrinkage stabilizing annular ssures and thermocoagulation of native nociceptors and ingrown unmyelinated nerve bers. Impact on inammatory and degradory enzymes may play a role as well as tissue regeneration in response to thermal injury. Obviously, controlled, blinded placebo trials, which are currently under way, are necessary to determine the potential impact of the placebo effect. The pathophysiology of chronic discogenic pain48 is complex. The disc is a nociceptively innervated structure that is capable of pain generation.4 Ingrowth of granulation tissue and small unmyelinated nerve bers occurs in degenerative and disrupted discs.6, 12, 13 Increased shear stress across the annular wall1, 13, 21, 34 can lead to pain generation by chronic mechanical stimulation of annular nociceptors.3, 4, 6, 12 Nociceptors exposed to inammagenic substances have been shown to have a lowered threshold or ring.25, 27, 36, 37, 47 Chronic discogenic pain may occur as a result of mechanical stimulation of annulus ssures or delamination of annular lamellae repetitively stimulates nociceptors that may have been presensitized by the intradiscal biochemical milieu, in-

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cluding PLA2,11 nitrous oxide,22 interleukin 1,29 or metallo-proteinase activity.22 The intradiscal thermal catheter system can generate sufcient annular heating to modify collagen and thermocoagulate nociceptors within the annulus.40 The symptomatic improvement patients have achieved is consistent with these phenomenons. The level of intradiscal heat generated is insufcient to cause tissue charring or destruction of collagen. Temperatures between 55C and 65C are sufcient to modify collagen and coagulate nerve tissue. Studies of animal and human collagen have shown that collagen thickening and remodeling occurs after treatment with this level of heat without the development of scar tissue.1618, 28 CLINICAL RESEARCH REVIEW Recently we published the outcome results for 25 patients with chronic low back pain of documented discogenic origin with mean duration of preoperative symptoms of 58.5 months who failed to adequately improve with a comprehensively applied nonoperative care program and elected IDET instead of chronic pain management or spinal fusion.41 Inclusion Criteria The inclusion criteria for our study are, as follows: Function-limiting low back pain of at least 6 months duration. Lack of satisfactory improvement with a comprehensively applied nonoperative care program, including progressive intensive exercise, at least 1 uoroscopically guided epidural corticosteroid injection, a trial of manual therapy, oral anti-inammatory medication, and activity modication. A normal neurologic examination. Negative straight leg raise (SLR). An MRI scan that did not show a neural compressive lesion. Concordant pain reproduction with provocative discography at low pressurization (i.e., at less than 1 mL dye volume) at 1 or more levels. (Concordant pain reproduction was dened as reproduction of the patients typical symptoms.) The demonstration of a control painless level. Exclusion Criteria The following are the exclusion criteria for our study: Inammatory arthritides

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Nonspinal conditions that could mimic lumbar pain Medical or metabolic disorder that would preclude appropriate follow-up and participation

Results The results showed a statistically signicant improvement in functional outcome as measured by visual analog pain scale score (VAS), SF36 Health Survey scores, sitting tolerance times (Table 3), and use of narcotic analgesic medication (Table 4). In 1999, at the Annual Meeting of the North American Spine Society (NASS), we presented the outcome of a group of 62 patients who met our inclusion and exclusion criteria who were treated with IDET and followed up for a minimum of 1 year (mean, 16 months; range, 12 to 23 months) after the procedure. The outcome evaluation scores did not statistically vary from the 6-month group. The mean group change for the SF-36 bodily pain was 17 and for physical function was 20. This study was submitted to Spine for consideration of publication in November 1999. Other researchers have presented their results to NASS in 1998 and 1999. Derby found a 53% improvement in pain scores and 73% satisfaction in the treated group (n 20).8 Karasek et al presented 12-month data on a controlled trial of IDET patients.23 They treated 53 patients who met the criteria for discogenic pain and did not treat 17 patients with the same diagnosis who had failed to receive insurance authorization for care. The treated group achieved statistically signicant improvement in VAS scores, whereas the untreated group had no signicant change in their pain scores. The Karasek study has been accepted for publication in Spine. Maurer presented 6-month outcome data on 19 patients with 86% improvement rate.29 Randomized, blinded trials of IDET are currently underway as well as animal histology studies evaluating the effect of thermal disc treatment in a sheep annular tear model. Our review of MRI studies taken 1 year after IDET (n20) has not shown any signicant disc space collapse or end plate abnormalities after IDET. An independent study by two radiologists, who are blinded to the treated levels and outcome of IDET-treated patients, is currently underway to more precisely evaluate MRI ndings after IDET.

Table 3. SF-36 DATA: PRE- AND POSTTREATMENT COMPARISONS Subsets Physical function subscale Bodily pain subscale Pretreatment Posttreatment Mean Score Mean Score 40.12 5.46 28.48 3.26 55.2 5.38 42.24 3.63 % Change 38 48 Signicance (P value) P .001 P .004

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Table 4. VAS AND SITTING TOLERANCE RESULTS: PRE- AND POSTTREATMENT COMPARISONS Pretreatment Mean VAS (010) Sitting tolerance (min) 7.32 23.6 Posttreatment Mean 3.58 47.2 Change in Mean 3.74 23.6 Signicance (P value) P 0.0001 P 0.0002

Diagnosis and Patient Selection for IDET Based upon our research47 and experience of more than 600 cases to date, we understand that clinical circumstances are rarely ideal and that individualized decisions must be made for each patient. Nonetheless, our present criteria for ideal candidacy for IDET are, as follows: 1. Chronic low back pain for more than 3 months. 2. Failure to adequately improve with a comprehensively applied, aggressive, nonoperative treatment program, consisting of stabilization exercise training, back education, activity modication, and when appropriate, uoroscopically guided, selective, epidural cortisone injections, and in some circumstances, facet injections. 3. A duration of 3 months for the nonoperative care program is recommended. (This would bring the total duration of symptoms to a minimum of 6 months before IDET.) 4. A normal neurologic examination. 5. A negative SLR (i.e., no reproduction of true sciatica). 6. An MRI scan that does not show neural compressive disease. 7. Preservation of disc height at the symptomatic level ( 30% disc space collapse). 8. No measurable segmental instability. 9. A discogram that reproduces concordant pain at 1 or more levels at an injection volume of less than 1.5 mL, with a documented negative control level. However, there are cases where a skilled specialist may not obtain a discogram, when the clinical ndings and MRI ndings are unequivocal and correlate precisely with the clinical scenario. 10. No irreversible psychosocial barriers to recovery. 11. A patient who is motivated to improve with realistic expectations of outcome. In 1999, we presented outcome data on 52 patients treated with IDET with a minimum follow-up of 1 year. This article has been accepted for publication in Spine. The 1-year outcome data did not show a statistically signicant difference in outcome between single level and multilevel treated patients. The overall outcome for the treatment group was not statistically different from the 6- to 8-month group. Patients with

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multilevel disease and disc space narrowing of more than 30% at one or more of the symptomatic levels had a less favorable outcome, but still many patients (66%) reported themselves as improved after IDET. A selected group of patients with 3-level symptomatic lumbar disc derangement were treated in the original study group, 62.5% rated themselves as improved. The extent of disease in the three-level group makes this a difcult group to treat effectively. If these cases are carefully selected, however, gratifying results can be attained to improve this groups functional outcome. Disc space narrowing of more than 30% as an independent criterion requires further study. Although we have seen excellent outcomes in some of these patients, the results have been mixed. Severe disc space narrowing will often permit catheter navigation. This may explain the variability in results attained in this group. To date, insufcient data exists to statistically determine the effectiveness of IDET on the previously operated segment. However, we have seen favorable results in this group of patients as long as the other criteria are met. IDET is intended for patients with chronic low back pain with a documented discogenic source of pain who have failed to improve with an aggressive, exercise-based rehabilitation program. When we choose to perform discography, we use the criteria of low volume concordant pain provocation in an attempt to subset patients with focal annular lesions who will experience pain reproduction at low volumes versus patients with global annular degeneration who will often only experience pain reproduction at 2-mL volumes or more. TECHNIQUE Overview Local anesthesia and conscious monitored sedation is applied to the patient in an outpatient surgical or radiologic setting. A 17-gauge procedure needle is introduced into the symptomatic disc under multiplane uoroscopic guidance. The SpineCATH is introduced through the procedure needle and navigated to the offending portion of the annulus. Care must be undertaken to avoid kinking the catheter because this may lead to catheter breakage. Treatment may be achieved with unilateral catheter deployment, but about 40% of the time bilateral deployment is necessary to cover the entire posterior annular wall. The ORA-50 (Oratec Interventions, Inc) auto-temperature heat generator controls the catheter heat delivery system. Typically, a maximum catheter temperature of 90C is attained (corresponding to tissue temperature of approximately 75C). There are occasions when the temperature prole must be modied to maximum temperatures of 85C to 90C to achieve patient comfort. The patient must be alert enough to be observed for the development of radicular pain during the procedure. If this occurs, the catheter is repositioned or removed. Most patients will experience their

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typical back pain and referral leg pain during the procedure. However, this must be differentiated from radicular pain, especially if the patient experiences it early in the heating cycle (i.e., when the catheter temperature is 65C to 80C). If this occurs, it is usually indicative of an extremely attenuated posterolateral annulus or a catheter that is extradiscal. We prefer to inject 2 to 5 mg of cefazolin sodium into the disc after treatment and removal of the SpineCATH. Course of Recovery Most patients will experience an increase in their typical pain (back, or back and leg) after the procedure. The postoperative pain gradually subsides over 1 to 7 days. Typically, most patients will return to at least their preoperative pain level between the 7th and 14th postoperative day. We have noted that patients often have resolution of their preoperative leg pain symptoms in the rst 4 weeks, whereas the improvement in back pain often requires 6 to 12 weeks to occur (Fig. 8). Postoperative Management Experience has taught us to proceed slowly in the postoperative period. Table 5 outlines our current postoperative guidelines for our patients. The most important principle appears to be allowing time for a

Figure 8. Typical recovery curve represents the authors experience in the rst 100 treated patients. Variation in this recovery curve can be expected based on the number of discs treated and the preoperative physical and emotional status of the patient.

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Table 5. POSTOPERATIVE GUIDELINES FOR PATIENTS Plan to rest for 1 to 3 days after your IDET in a comfortable position (ie, lying down or reclining), limit sitting or walking to 10 to 20 minutes at a time. Return to work: Sedentary work: You may return in roughly 1 week; however, you may still be sore after your IDET. Be aware of sitting restrictions listed below. For other jobs, the decision will be made by your physician. Driving: None for the rst 1 to 5 days, then limit your driving to 20 to 30 minutes for the rst 6 weeks after your IDET. Make sure your vehicle has good lumbar support. You may need a pillow to help maintain your lumbar lordosis (normal low back curve). As a passenger, recline the seat and try to limit driving times to less than 45 minutes for the rst 6 weeks. It is okay to recline and be driven home the day of your procedure or lie down in the back seat. Sitting: Limit to 30 to 45 minutes at any one time in a chair with good support for the rst 6 weeks. Avoid sitting on soft couches or chairs. Use a pillow or towel to maintain your lumbar curve when sitting. Standing and walking about in between sitting periods or short periods of lying down are helpful. Lifting: Limit 5 to 10 lb for the rst 6 weeks. No bending or twisting of the low back. Housework: No bending or twisting for the rst 6 weeks. No chiropractic, manipulation, massage (unless otherwise instructed), inversion traction, or traction for the rst 12 weeks. Exercise Walk daily, beginning at the end of the rst week, for approximately 20 minutes. Increase to 20 minutes twice per day, if tolerated, then progressively increase to 1 hour a day by the end of the fourth week. If back or leg symptoms increase at any point, back down on the duration of walking. You may do gentle leg stretches (hamstring, pyriformis) with your back at on the oor (be sure you know how to do these properly). Abdominal brace exercises can be begun at 2 to 3 weeks, with your back at on the oor. No swimming for the rst 6 weeks. Formal physical therapy will usually begin at 6 to 8 weeks after IDET. Do not use a treadmill or a stairmaster for the rst 6 weeks, unless otherwise instructed. You will be wearing a lumbar corset for the rst 6 to 8 weeks after your IDET.

healing reaction and delaying aggressive exercise training for at least 3 months after the procedure. This time frame may correlate with the timetable of collagen remodeling. Patients should be able to return to ofce work by 2 weeks and to light lifting duties at 6 weeks, although return to heavy work may require 4 to 6 months. The optimal timing of return to work requires further study. (Fig. 9AE) SUMMARY The early studies on IDET are very promising. IDET offers patients with chronic discogenic low back pain an option other than chronic pain

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Figure 9. A 45-year-old woman with disabling low back pain for 2 years. A, Sagittal MR imaging scan of L5S1 disc protrusion. B, Axial MR imaging scan of L5S1 disc protrusion. C, Low-volume discogram with moderately severe concordant pain reproduction. D, Lateral radiograph of L5S1 with SpineCATH (ORATEC Inter ventions, Inc., Menlo Park, CA) navigated to the posterior annular wall. E, Anteroposterior radiograph of L5S1 with SpineCATH navigated to the posterior annular wall.

management or spinal fusion. Studies currently under way will help answer questions relative to mechanism of action, placebo effect, and biomechanical changes after treatment. The cost, morbidity, and currently observed degree of effectiveness make IDET an attractive alternative to spinal fusion for discogenic pain. This may be especially true for the young patient with preserved disc

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height, and patients with inoperable multilevel disease. The technology was designed to be used for a specic diagnostic subset of disc disorders by specialists skilled in performing intradiscal techniques who possess the ability to accurately diagnose and effectively manage patients with complex spinal disorders. Abuse of this ground-breaking technology can be avoided if patient selection criteria are carefully observed and only skilled, technically procient physicians perform the procedure. References
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49. Wetzel FT, LaRocca SH, Lowery GL, et al: The treatment of lumbar spinal pain syndromes diagnosed by discography: Lumbar arthrodesis. Spine 19:792800, 1994 50. Zdeblick TA: A prospective, randomized study of lumbar fusions: Preliminary results. Spine 18:983991, 1993 Address reprint requests to Jeffrey A. Saal, MD SOAR Physiatry Medical Group 2884 Sand Hill Road, Suite 110, Menlo Park, CA 94025