Athletic Injuries and Their Differential Diagnosis

20 Athletic Injuries and Their Differential Diagnosis

Vincent J. Miele and Julian E. Bailes

Participation in sports carries an inherent risk of injury to the athlete. This population presents a unique and complex array of issues relating to on-field management, diagnosis, and treatment.1–4 In the spectrum of sports-related injuries, those to the nervous system have the most potential for significant morbidity and mortality. In fact, head and neck injuries account for up to 70% of traumatic deaths and 20% of permanent disability in athletes^5,6 and have been described in virtually every sport from boxing to golf. This association often necessitates involvement of the neurosurgical community in the field of sports medicine. Differentiation between minor and serious injuries is the foundation of management of the athlete. A seemingly minor blow to the head may result in a slowly developing subdural hematoma (SDH), whereas, paradoxically, a more severe impact may cause a loss of consciousness but only a concussion. This chapter serves as a guide in this differentiation and outlines management strategies for neurological injuries in the athlete.

Head Injuries

One of the greatest threats to the athlete are high-speed encounters with other objects providing sufficient kinetic energy to result in major brain trauma. The possibility of major injury or death, despite their relative rarity, remains a constant in nearly every sport.^7–20 During the last century, our level of understanding of the types of cerebral insults, their causes, and their treatment has advanced significantly. Recent research has better defined the epidemiological issues related to sports injuries involving the central nervous system and has also led to classification and management paradigms that help guide decisions regarding athletes’ return to play. Severe sports-related head injuries include epidural hematomas (EDHs), SDHs, brain contusions/parenchymal hemorrhages, diffuse axonal injury (DAI), traumatic subarachnoid hemorrhage (SAH), and cerebral edema. Mild traumatic brain injury (MTBI) is a common injury that poses difficulty with patient management, particularly when consideration for return to competition is necessary. Because neurosurgical intervention is ultimately necessary in 3% of MTBI patients,²¹ it is also discussed here.

Incidence of Head Injury in Sports

It is estimated that 750,000 Americans suffer injuries annually in recreational activities, with 82,000 (10.9%) sustaining some form of head injury. The frequency of all sports-related concussions has been estimated to be up to 300,000 annually in the United States.²² Head injuries are more common in sports than spinal injuries.

The incidence and severity of head injury and its impact on the player’s role in the contest vary greatly with the sport involved. It is beneficial to consider athletic endeavors in a category that allows the nature of the play and the participants to be defined in terms of types of sporting events and motivations of the players involved. The most useful classification is that of recreational and nonorganized sports versus organized, sanctioned sports. The former have little formal structure, fewer rules, no refereed officials, less use of protective equipment, and participation by a wide variety of people under a variable set of conditions. In contrast, organized sporting events have structure regarding training, rules and their enforcement, specialized equipment, and physicians and athletic trainers dedicated to the care of those who are injured.

American football, ice hockey, and boxing are commonly referred to when discussing sports-related head injury because of the frequent and obvious violent contact. However, head injuries are commonly observed in sporting activities considered less violent. The United States Consumer Product Safety Commission (USCPSC) reported in 1990 that four of the top five sports that cause head injury requiring hospitalization are not the traditional “collision” games. These were basketball, bicycling, baseball, and playground activities (football was the only collision sport to break the top five).²³ Equestrian sports account for ~46,000 emergency room visits annually, with nearly 20% involving the head or neck and 70% of deaths related to head injuries.^24,25 Approximately seven fatalities occur annually related to skateboard injuries, with 90% involving severe injury to the head.¹⁶ Recreational and commuter bicyclists have between 1000 and 1300 fatalities each year, and the majority are the result of brain injury.^26–28 Although sports such as gymnastics and cheerleading have traditionally been responsible for the highest number of head injuries in the female athlete,²⁹ women are now crossing into previously male-dominatedsports such as boxing, and increasing numbers of serious head injuries are being incurred in contact/collision sports.7

Head injuries occur at one of the highest rates in downhill skiing and often occur as a result of collisions with trees and boulders as well as with other skiers.^12,30,31 Other recreational sports that are considered to be a high risk for head injury include snowboarding, hang-gliding, skydiving, mountaineering, and race-car driving.³² The head often initiates the impact in football, and the involved activities are usually blocking or tackling. It is estimated that 250,000 MTBIs occur annually in high school football alone.^23,33 Twenty percent of all high school football players suffer a concussion annually and an average of eight fatalities occur secondary to head injuries during participation in the sport every year.^20,23

Epidural Hematoma

Epidural hematomas are a common traumatic brain injury in the athletic population, especially in sports in which the players do not wear helmets. They are classically associated with temporal skull fractures, which can tear the middle meningeal artery or vein. This has been described in baseball players and golfers struck on the head by a high-velocity ball.^34–37 This lesion is usually associated with a brief loss of consciousness (LOC) followed by a lucid interval and then rapid deterioration. A typical example of this would be a pole-vaulter whose head strikes the ground outside the landing pit. After being stunned for a brief period, the athlete may walk off the field fully alert. Within 15 to 30 minutes a sudden excruciating headache is accompanied by progressive neurological deterioration. Although this classic “lucid interval” presentation only occurs in one third of athletes with this condition, an understanding of this clinical picture is crucial for all caregivers, especially athletic trainers, coaches, and team physicians.³⁸ It requires that an adequate observation period be planned for those athletes who display potential for delayed hematoma formation and neurological deterioration. Early recognition and management are essential, and if treated early complete neurological recovery can be expected because EDHs are not usually associated with other brain injuries.

Subdural Hematoma

SDHs are the most common form of sports-related intracranial bleeding. They are more common than epidural hematomas and account for the majority of lethal brain injuries seen in both organized and recreational athletic activities.^10,32 It is important to understand that SDHs in athletes are not the same as those commonly seen in the elderly. The athlete usually does not have the large potential subdural space that an elderly patient possesses so mass effect and increases in intracranial pressure occur more rapidly. In addition to injury from the mass effect of blood under the dura, there is often significant associated damage to the underlying brain (contusion or edema). Therefore, even with prompt treatment, prognosis is less favorable than for an EDH, with mortality rates as high as 60%. SDHs can occur at any location in the brain, and presentation is usually within 72 hours of injury. Athletes that suffer an SDH may become immediately unconscious and/or have focal neurological deficits or may develop symptomatology insidiously over days or even weeks.

Brain Contusions/Parenchymal Hemorrhage

Brain contusions and parenchymal hemorrhages represent regions of primary neuronal and vascular injury. They contain edematous, punctate parenchymal hemorrhages that may extend into the white matter and the subdural and subarachnoid spaces and are most commonly the result of either direct trauma or acceleration/deceleration. The latter causes the brain to strike the skull, most commonly resulting in damage to the inferior frontal and temporal lobes. The areas of the brain adjacent to the floor of the anterior or posterior cranial fossa, the sphenoid wing, the petrous ridge, the convexity of the skull, and the falx or tentorium are also vulnerable. Contusions are also observed in the lateral midbrain, the inferior cerebellum and adjacent tonsil, and the midline superior cerebral cortex.

Importantly, these types of injuries often demonstrate progression over time with respect to the size and number of contusions and the amount of hemorrhage within the contusions. This progression most commonly occurs over the first 24 to 48 hours, with one fourth of cases demonstrating delayed hemorrhage in areas that were previously free of blood. Additionally, initial computed tomographic (CT) findings can be normal or minimally abnormal because the partial volumes between the dense microhemorrhages and the hypodense associated edema can render contusions isoattenuating relative to the surrounding brain.

Diffuse Axonal Injury

Diffuse axonal injury plays a significant role in sports-related head injury. It occurs in nearly half of athletes that have suffered a severe head injury and is partially responsible for one third of all head injury-related fatalities.³⁹ Radiographically, DAI typically consists of several focal white matter lesions in a characteristic distribution.

The pathophysiology of DAI was first described in 1943. It is the result of the shearing of multiple axons secondary to rotational forces on the brain commonly from lateral rotation of the head. These forces exert more effect on areas of the brain where tissue density is greatest, such as at the gray-white junction. DAI was classically believed to represent a primary injury (occurring at the instant of the trauma). However, it is apparent that the axoplasmic membrane alteration, transport impairment, and retraction ball formation may represent secondary (or delayed) components to the disease process. Although the initial trauma may not completely tear the axon, it can still produce focal alteration of the axoplasmic membrane, resulting in subsequent impairment of axoplasmic transport. This results in axoplasmic swelling and rupture. A retraction ball forms, which is a pathological hallmark of shearing injury, followed by wallerian degeneration.

Although areas of the brain with different tissue densities have a predilection for DAI, the exact location depends on the plane of rotation and is independent of the distance from the center of rotation. The magnitude of injury depends on the distance from the center of rotation, the arc of rotation, and the duration and intensity of the force.

Traumatic Subarachnoid Hemorrhage

Sports-related head trauma can result in SAH. Some degree of SAH is usually present in any serious head injury. Although this usually results in meningeal irritation from blood between the pia and arachnoid, the condition is usually not life threatening, and immediate treatment is not required for a good outcome.40 In large amounts subarachnoid blood may lead to vasospasm. SAH may also result in the development of a communicating hydrocephalus, which can present clinically with a slower-than-expected recovery or late clinical deterioration.

Second-Impact Syndrome

In 1984, the death of a college football player was reported that seemed to have resulted from a second, seemingly minor, blow to the head. At the time it was hypothesized that this fatality was the result of “a repeat blow to an already compliance-compromised brain which precipitated a catastrophic increase in intracranial pressure, perhaps through a loss of vasomotor tone.”¹⁷ The term vascular congestion syndrome was coined in 1991 following the death of a 17-year-old high school football player from an uncontrollable increase in intracranial pressure.⁴¹ Both of these deaths are thought to have been the result of what is now known as second-impact syndrome (SIS). SIS is defined as a fatal uncontrollable increase in intracranial pressure secondary to diffuse brain swelling, which occurs after a blow to the head incurred before recovery from a previous blow to the head.⁴² Significant controversy exists over the validity of this condition due to problems with documentation of the initial event, persistent symptoms, and severity of the second impact.⁴³

The pathophysiology of SIS is thought to involve a loss of autoregulation of the brain’s blood supply, edema, and uncontrolled intracranial hypertension. This loss of autoregulation leads to vascular engorgement within the cranium, which in turn markedly increases intracranial pressure and leads to a syndrome of uncal herniation, cerebellar herniation, or both. Animal research has shown that vascular engorgement in the brain after a mild head injury may be difficult, if not impossible, to control in this “double impact” setting. The usual time from second impact to uncontrollable edema is rapid, taking 2 to 5 minutes.³² There have been 21 reported cases of this condition,⁹ which is most often seen in boxing, football, and ice hockey and in most cases involves adolescent males or young adults.

Typically, the athlete experiences some degree of post-concussion symptoms after the first head injury. These may include visual, motor, or sensory changes and difficulty with cognitive and memory processes. Before these symptoms resolve, which may take days or weeks, the athlete returns to competition and receives a second blow to the head. The second blow may be minor, perhaps only involving a blow to the chest that jerks the athlete’s head and indirectly imparts accelerative forces to the brain. Affected athletes may seem stunned but usually do not lose consciousness and often complete the play. They usually remain on their feet for 15 seconds to a minute or so but seem dazed, similar to a grade I concussion without LOC. Often, affected athletes remain on the playing field or walk off under their own power. What happens in the next few moments to several minutes sets this syndrome apart from a concussion or SDH. Usually, within seconds to minutes of the second impact, the athlete, who is conscious yet stunned, precipitously collapses to the ground and becomes comatose, with rapidly dilating pupils, loss of eye movement, and evidence of respiratory failure

The condition is associated with a 50% mortality and nearly 100% morbidity rate.³² It is important to understand this condition when making return-to-play decisions following a head injury in an athlete. Any athlete still symptomatic from a previous head injury should not be allowed to return to full practice or participation in a contact or collision sport.

Concussion/Mild Traumatic Brain Injury

Concussions are by far the most common type of sports-related head injury. They account for approximately three fourths of all head injuries in this population. The recognition in the early 1980s that MTBI exists as an important clinical entity began to pave the way for an increased appreciation of concussion in sports. In the 1990s, there was an increased focus on defining and categorizing the athlete with MTBI. More evidence suggested that concussion may be more common and serious than previously believed,^42,44–46 and the long-term sequelae of repetitive head trauma may be far from benign. In contrast to the attitudes in earlier times, when being concussed was considered an acceptable occurrence for a contact athlete, new evidence provided proof that ongoing cerebral dysfunction often persists.45,47–49 The concept of MTBI or concussion has evolved in recent years, aided in great part by the application of formal neuropsychological and cognitive studies and by studies of patients involved in vehicular and other significant trauma.

There are many characteristics and nuances of the sports-related MTBI population that make diagnosis and treatment difficult. One such difficulty is that athletes are the only group of patients who routinely and often fervently ask to be returned to play, thus invariably subjecting themselves to multiple future instances of head impact.³² Many of these impacts will result in at least subclinical head injury. Although a single episode of MTBI seems to be well tolerated overall in the majority of athletes, long-term mental status morbidity has been thought to be associated with two or more episodes of concussion.^50,51 Advances in the fields of diagnostic neuroradiology, neurobiology, neuropsychology, and sports medicine now provide the neurosurgeon with more accurate and objective methods of analyzing this population of patients.³²

There has been no universal agreement on the definition and grading of concussion, and attempts at classification have tended to focus on the presence or absence of a period of LOC and amnesia. However, concussion may present with any combination of the following signs and symptoms: a feeling of being stunned or seeing bright lights, a very brief LOC (seconds), lightheadedness, vertigo, loss of balance, headaches, cognitive and memory dysfunction, tinnitus, blurred vision, difficulty concentrating, lethargy, fatigue, personality changes, inability to perform daily activities, sleep disturbance, and motor or sensory symptoms. Numerous classification systems exist for grading the severity of concussion. Although there is little evidence-based support for any of the systems because most have been developed through clinical experience, three are in widespread use. These are the Cantu,¹ Colorado Medical Society,⁵² and American Society of Neurology systems,⁵³ which also have associated return-to-play guidelines.

On-the-Field Management

Athletes that suffer catastrophic injuries to the head or spinal cord are usually easy to identify, as are those that develop an immediate neurological deficit. More challenging is the diagnosis of an injury with minimal initial symptomatology. The Inter-Association Task Force for Appropriate Care of the Spine-Injured Athlete was formed in 1998 and developed guidelines for the management of the catastrophically injured athlete.⁵⁴ There are five categories of on-field management: (1) preparation for any neurological injury, (2) suspicion and recognition, (3) stabilization and safety, (4) immediate treatment and possible secondary treatment, and (5) evaluation for return to play. It is mandatory that a spine board, cervical collar, and cardiopulmonary resuscitation equipment be on site and easily accessible during a contest. Specific equipment for protective gear removal (e.g., football face mask) should also be readily available. If a head or neck injury is suspected, an athlete should immediately be assessed for level of consciousness while still on the field. Following the initial evaluation, as in any head trauma patient, an athlete with a head injury should be assumed to have an associated cervical injury, and spinal stabilization is essential to limit any further injury. If an athlete is wearing protective gear with a face mask, the face mask should be removed. The helmet itself or shoulder pads do not usually require removal on the field.⁵⁵ Several situations have been identified that would require removal of the helmet and chinstrap. These include a loose-fitting helmet that would not hold the head securely so that if the helmet is immobilized the head will still be mobile, if the airway cannot be controlled or ventilation provided even after removal of the face mask, if the face mask cannot be removed after a reasonable period of time, and if the helmet prevents immobilization for transportation in an appropriate position.⁵⁴ If necessary, helmet removal should be performed with concomitant occipital support or simultaneous removal of shoulder pads. If left in place following helmet removal, the shoulder pads may cause cervical hyperextension. Obviously, if the helmet is removed cervical immobilization must be maintained during the procedure.

In a neurologically intact athlete with a normal mental status, once cervical spine involvement has been excluded the athlete may be assisted to a sitting position and if stable in this position to a standing position. If able to stand the athlete can then be walked off the field for further evaluation. Unconscious athletes need to be stabilized before any neurological appraisal. Initial evaluation should begin with the airway, breathing, and circulation assessment of basic cardiopulmonary life support. Cardiopulmonary support can most often be accomplished by face mask removal for airway access. The front of the shoulder pads can also be opened to allow compression or defibrillation.⁵⁴ When sudden unconsciousness without preceding craniospinal trauma occurs, cardiac etiology should be considered. Immediate transfer to a facility with neurosurgical capabilities should be performed for an athlete with prolonged alteration of consciousness, worsening symptoms, or focal neurological deficit. Transport should be performed under the assumption of a concomitant spinal cord injury (SCI), and spinal stabilization is mandatory.

Imaging

Specific guidelines on when to perform brain imaging on a head-injured athlete do not exist. Because of this the physician needs to individualize when to perform imaging on a patient-to-patient basis. Those who exhibit focal neurological deficits, persistent alterations in mental status, Glasgow Coma Scale score of 13 or less, and the concern for a skull fracture are common examples of when an athlete would require at least a CT scan.56 In cases that are not as clear-cut, the duration of LOC or amnesia has been used to aid in this decision.⁴⁰ If there is any doubt, CT imaging is a rapid and efficacious diagnostic modality.

Nontraumatic Sports-Related Brain Injury

Brain injuries to athletes can occur by mechanisms other than trauma. The two main causes of nontraumatic sports-related brain injury are cerebral air embolism and high-altitude cerebral edema (HACE). These conditions result from participation in underwater diving and mountaineering. Due to the increased number of people participating in these activities as well as an increase in access, it is imperative that the signs and symptoms of these conditions as well as management strategies be understood.

Recreational scuba diving has become a popular sport in the United States, with almost 9 million certified divers.⁵⁷ One of the most severe injuries that participants are at risk for is the development of cerebral air embolisms. Cerebral air embolisms are the most serious and rapidly fatal of all diving injuries and are second only to drowning as the leading cause of death associated with the sport.⁵⁸ Approximately 60% of divers with decompression sickness will have symptoms and signs of central nervous system involvement. The condition is most often the result of a rapid ascent from depths greater than 10 m when air-filled body spaces fail to equalize their pressure to changing ambient pressures. This results in air released from an overpressurized alveolus entering the pulmonary capillaries and traveling through the arterial circulation, causing occlusion of cerebral blood flow. In more than 80% of patients, symptoms develop within 5 minutes of reaching the surface, but they can also occur during ascent or after a longer surface interval. The athlete may complain of diplopia, tunnel vision, or vertigo, or may display seizure activity, loss of memory and changes in affect, hemiplegia, or dysarthria. Importantly, this diagnosis should be high on the differential if a diver surfaces with an alteration in mental status-almost two thirds of patients have changes of consciousness (i.e., coma or obtundation).⁵⁹ Treatment consists of basic or advanced cardiac life support, 100% oxygen, rehydration, and transport to a recompression facility.^59–61 Oxygen reduces ischemia in affected tissues and accelerates the dissolution of air emboli. Supportive care for seizures, shock, hyperglycemia, and pulmonary dysfunction should be anticipated. Recompression therapy should be initiated immediately, using the United States Navy (USN) algorithm.^{58,59,61–63} Recompression therapy reduces the size of air emboli by increasing ambient pressure. This expedites the passage of emboli through the vasculature and reestablishes blood flow to ischemic tissues.

HACE can result in significant increases in intracranial pressure and is responsible for up to 5% of deaths in climbers above 4000 m. Originally thought to be separate disorders, HACE is now largely considered to be the end-stage of severe acute mountain sickness (AMS).⁶⁴ AMS and HACE are likely on a continuum based on a common underlying pathophysiological process in an unacclimatized individual at high altitude. Affected athletes develop symptomatology most commonly within 72 hours that includes ataxia, vertigo, confusion, and hallucinations. The main contributor to high altitude illness is hypoxia with resultant cerebral edema. Treatment consists of the immediate return to a lower elevation with the goal of reaching the lowest possible altitude,⁶⁵ oxygenation, and supportive care. Pharmacological agents such as acetazolamide and dexamethasone have also been used to treat this condition with varying success. Acetazolamide, a sulfonamide carbonic anhydrase inhibitor, enhances the renal excretion of bicarbonate, producing a mild acidosis. Ventilation increases in response to this acidosis, which is thought to mimic the process of acclimatization. Acetazolamide also lowers the cerebral spinal fluid volume and pressure by lowering production, increasing the minute ventilation oxygen saturation, and decreasing periodic breathing at night.⁶⁶ Dexamethasone, a synthetic glucocorticoid, has been traditionally used in the treatment of altitude sickness. It is thought to be valuable in the treatment of HACE because of its ability to stabilize cerebral vascular integrity, thereby reducing vasogenic edema and lowering intracranial pressure.^67,68

Spinal Injuries

Each year, there are ~10,000 cases of SCI in the United States.² Sporting events are the fourth most common cause of these injuries (behind motor vehicle accidents, violence, and falls) and account for ~7.5% of the total injuries since 1990.⁶⁹ Sports-related SCIs also occur at a younger mean age of 24 and are the second most common cause of SCI in the first 3 decades of life.^70,71 A spectrum of soft-tissue, bony, and nervous system injury can occur to the spine of athletes that often result in significant disability and time lost from competition and can become the source of chronic pain with functional limitation. Injury to the spinal cord, however, is perhaps the most feared consequence of athletic activities, and no other sports injury is potentially more catastrophic.

A structural distortion of the cervical spinal column associated with actual or potential damage to the spinal cord is classified as a catastrophic cervical spine injury. Because this condition is fortunately rare, few physicians have extensive experience in the emergency care of these injuries. Improper handling of the patient on the field or during transport can worsen or precipitate spinal cord dysfunction. Failure to appropriately manage a catastrophic neck injury can result in compromise of the athlete’s cardiac, respiratory, and neurological status. Improved understanding of these injuries can facilitate early diagnosis and effective on-field management.

Incidence

Spinal injuries are more common in nonorganized sports such as diving and surfing.2,72 The challenge in this population, which accounts for the majority of sports-related spinal injury, is that rules, supervision, and training are limited. This makes it difficult to improve injury patterns by enforcing safety guidelines and manufacturer standards.

Although less frequent, spinal injury in organized sports has a much higher public profile. Several organized sports have been identified as placing the participant at high risk for SCI. These include football, ice hockey, rugby, skiing, snowboarding, and equestrian sports.^73–76 In the United States, annual participation in football is estimated to be 1.3 million athletes per year. The majority participate at the junior/senior high school level, 75,000 in college, and ~2000 at the professional level.¹¹ Although American football has a lower per participant rate of catastrophic cervical spine injuries than ice hockey or gymnastics, the huge number of participants translates into the largest overall number with catastrophic cervical spine injuries.¹¹

A significant increase of catastrophic cervical trauma coincided with the development of the modern football helmet. Rule changes in 1976 prohibiting playing techniques that used the top of the helmet as the initial point of contact for blocking and tackling (spearing) have significantly reduced this trend. From 1976 to 1987, the rate of cervical injuries decreased 70% from 7.72 per 100,000 to 2.31 per 100,000 at the high school level.⁷⁷ Traumatic quadriplegia decreased ~82% over the same time period.²⁰ The sport of ice hockey has experienced a marked increase in the occurrence of cervical spine injuries through its history.⁷⁸ Major vertebral column injury occurred at an increased rate between 1982 and 1993, with a mean of 16.8 fractures/ dislocations per year during that time period. Checking an opponent from behind, which typically produces a headfirst collision of the checked player with the boards, has been identified as an important causative factor of cervical spine trauma in hockey. Changes in the rules that prohibit checking from behind and checking of an opponent who is no longer controlling the puck seem to be decreasing the incidence of these injuries, and data suggest that fewer cases of complete quadriplegia have been caused by these playing techniques since the rule changes have been instituted.⁷⁸

Etiology

Cervical spine injury can be divided into several categories; unstable fractures and dislocations, transient quadriplegia, and acute central disk herniation.⁷⁹ These produce neurologic symptoms and signs that involve the extremities in a bilateral distribution. Sports-related cervical spine injuries have been previously divided into three groups, which provide useful information when making return-to-play decisions.^2,72,80

Type I injuries are those in which the athlete sustains permanent SCI. This includes both immediate, complete paralysis and incomplete SCI syndromes. The incomplete injuries are of basically four types: Brown-Séquard syndrome, anterior spinal syndrome, central cord syndrome, and mixed types. Mixed types include the finding of crossed motor and sensory deficits with upper extremities more prominently involved, which is considered to be a central cord/Brown-Séquard variant. There are, in addition, a few individuals in whom the neurologic injury may be relatively minor, but is associated with demonstrable spinal cord pathology on imaging studies. For example, a high-intensity lesion within the spinal cord seen on MR imaging documents a spinal cord contusion. Type 2 injuries occur in individuals with normal radiographic studies. These deficits completely resolve within minutes to hours, and eventually the athlete has a normal neurologic examination. An example of the type 2 injury is the “burning hands syndrome,” a variant of central cord syndrome characterized by burning dysesthesias of the hands and associated weakness in the hands and arms.⁸¹ Most of these patients have normal radiographic studies, and their symptoms completely resolve within ~24 hours. Type 3 injuries comprise players with radiographic abnormality without neurologic deficit. This category includes fractures, fracture-dislocations, ligamentous and soft-tissue injuries, and herniated intervertebral discs.

SCI can also be divided into upper (occiput, atlas, and axis) and lower (C3-T1) cervical spine. A thorough understanding of the normal anatomy and unique motion of the spine at various segments is mandatory when treating these injuries.

Unstable fracture and/or dislocation are the most common causes of catastrophic cervical spine trauma. The most common primary injury vector is axial loading with flexion in football and hockey.^82,83 Eighty percent of injuries to the cervical spine result from the accelerating head and body striking a stationary object or another player.^84,85

The cervical spine is compressed between the instantly decelerated head and the mass of the continuing body when an axial force is applied to the vertex of the helmet. In neutral alignment, the cervical spinal column is slightly extended as a result of its normal lordotic posture and it is believed that compressive forces can be effectively dissipated by the paravertebral musculature and vertebral ligaments. This buffering cervical lordosis is eliminated when the cervical spinal column is straightened and large amounts of energy are transferred directly along the spine’s longitudinal axis.83 Under high enough loads, the cervical spine can respond to this compressive force by buckling.

Two major patterns of spinal column injury result from the compression injury vector. Compressive-flexion injury is the most common variant that results from the combination of axial loading and flexion. It results in shortening of the anterior column because of compressive failure of the vertebral body and lengthening of the posterior column because of tensile failure of the spinal ligaments.⁸⁶ If the cervical vertebra is subjected to a relatively pure compression force both the anterior and posterior columns shorten, resulting in a vertical compression (burst) fracture. The vertebral body essentially explodes, during which it is possible that disk material extrudes through the fractured endplate and retropulsion of osseous material into the spinal canal results in cord damage.⁸⁷ Alternately, there may be significant SCI without major disruption of the spinal column’s integrity. This type of injury is the result of transient spinal column distortion with energy transfer to the spinal cord.

Catastrophic cervical trauma caused by the primary disruptive vector flexion generally results from either a direct blow to the occipital region or rapid deceleration of the torso. Flexion-distraction injury most likely to result in spinal cord dysfunction is a bilateral facet dislocation.^88,89 Unilateral facet dislocation that is associated with cord injury in up to 25% of cases can occur with the addition of axial rotation to the distractive force.⁹⁰ It should be recognized that unstable cervical fractures/dislocations do not always result in upper motor neuron dysfunction. A unilateral facet dislocation can cause a monoradiculopathy due to foraminal compression of a nerve root on the side of the dislocated articular process. In other cases, major osseous or ligamentous damage will produce no neurological impairment. SCI in these scenarios is potential rather than actual based on the amount of loss of structural integrity of the vertebral column.⁷⁹

Upper Cervical Spine Injury

For the purposes of sports-related injuries, the upper cervical spine is considered to be the occiput, atlas (C1), and axis (C2). The major function of the atlanto-occipital joint is motion in the sagittal plane, which accounts for 40% of normal flexion and extension of the spine and 5 to 10 degrees of lateral bending. The midline atlantodens articulation is stabilized by the transverse atlantal ligament, which prevents forward translation of the atlas. This specialized osseoligamentous anatomy allows the atlas to rotate in a highly unconstrained manner. The atlantoaxial complex is responsible for 40% to 60% of all cervical rotation.⁹¹ This rotation is limited by the alar ligaments extending from the odontoid process to the inner borders of the occipital condyles. The apical ligaments attach the odontoid centrally to the anterior foramen magnum. Atlantoaxial joint strength is provided by the transverse ligament and the lateral joint capsules.³⁹

Spinal cord damage due to fractures or dislocations involving the upper cervical spine is rare because there is proportionately greater space available within the spinal canal compared with the lower cervical segments. Injuries that destabilize the atlantoaxial complex (fracture of the odontoid or rupture of the transverse atlantal ligament) are most likely to result in spinal cord dysfunction. Flexion is the most common cause of injury at the atlantoaxial joint. Odontoid fractures can also result from extension injuries. Unilateral rotary dislocations are usually the result of rotational forces. Cord compression is unusual with a burst fracture of the atlas or traumatic spondylolisthesis of the axis because these osseous injuries further expand the dimensions of the spinal canal. If anteroposterior radiographs are performed and there is spreading of the lateral masses of greater than 7 mm, the transverse ligament is likely torn. Bilateral pedicle fractures of the axis may occur from extension of the occiput on the cervical spine. Importantly, although these injuries can result in instability, they usually do not cause neurological deficits secondary to the anatomically wide spinal canal, which is also present at this level.³⁹ If an upper cervical cord injury does occur, diaphragmatic paralysis with acute respiratory insufficiency can occur along with quadriplegia because the phrenic nerve arises from three cervical nerve roots (C3 to C5).

Lower Cervical Spine Injury

The lower cervical spine is composed of the C3 through C7 vertebrae. This area accounts for the remaining arcs of neck flexion, extension, lateral bending, and rotation and has several important anatomical differences with respect to the upper cervical spine. The spinal canal is not as wide at this level, and the facet joints are oriented at a 45-degree angle. Because of this angulation, axial rotation is somewhat limited. The facet articulations also restrain forward vertebral translation.

Each motion segment can be separated into an anterior and a posterior column. Stability of a cervical segment is derived mainly from the anterior spinal elements. Compression of the spinal column is primarily resisted by the vertebral bodies and intervertebral disk, whereas shearing forces are opposed primarily by paraspinal musculature and ligamentous support. Instability of the lower cervical spine has been defined radiographically as translatory displacement of two adjacent vertebrae greater than 3.5 mm or angulation of greater than 11 degrees between adjacent vertebrae.⁹²

The majority of fractures and dislocations occur in the lower cervical region. Lower cervical spine injuries are defined by the forces acting on the area (i.e., flexion, extension, lateral rotation, axial loading). Dislocated joints are usually the result of a flexion mechanism with either distraction or rotation. The ligamentous structures are the primary restraints to distraction of the spine.91 Compression of the posterior structures as well as damage to the anterior structures is usually the result of extension or whiplash injuries. This mechanism of injury commonly results in tearing of the anterior longitudinal ligament and fractures of the posterior elements.³⁹ Compressive forces usually result in vertebral body fractures. These are commonly seen in spear-tackler’s spine, which consists of four characteristics: reversal of cervical lordosis, radiographic evidence of previous healed minor vertebral body fractures, canal stenosis, and the habitual use of spear-tackling techniques.⁹³ This population commonly has a flexed posture to the head and a loss of the protective cervical lordosis.³⁹ Large axial loads can result in protrusion of disk material or fractured bone into the spinal canal. This is the most common mechanism for sports-related quadriplegia 94,95 The C3-C4 level is most commonly involved in cases of quadriplegia secondary to cervical dislocations.^96,97

Central Cord Syndrome/Burning Hands Syndrome

Injury to the lower cervical cord can result in a spectrum of neurological dysfunction. Incomplete SCI can occur with partial preservation of sensory or motor function. Central cord syndrome is the most common manifestation of this, followed in frequency by the anterior cord syndrome.

Burning hand syndrome is considered to be a variant of central cord syndrome. It is characterized by burning dysesthesia in both upper extremities and is likely the result of vascular insufficiency affecting the medial aspect of the somatotopically arranged spinothalamic tracts.^81,98 The lower extremities may occasionally be involved, and weakness may occasionally be evident. Cervical spine fracture or soft-tissue injury is seen radiographically in 50% of the patients with this syndrome. Any athlete that exhibits this condition should be initially managed as an SCI.⁹⁹

Cervical Cord Neurapraxia/Transient Quadriplegia

Neurapraxia of the cervical spinal cord resulting in transient quadriplegia has been estimated to occur in seven per 10,000 football players.¹⁰⁰ This alarming injury is characterized by a temporary loss of motor or sensory function and is thought to be the result of a physiological conduction block without true anatomical disruption of neuronal tissue. The affected athlete may complain of pain, tingling, or loss of sensation bilaterally in the upper and/or lower extremities. A spectrum of muscle weakness is possible, varying from mild quadriparesis to complete quadriplegia. The athlete has a full, pain-free range of cervical motion and does not complain of neck pain. Hemiparesis or hemisensory loss is also possible.

This condition is thought to result from a pincer-type mechanism of compression of the cord between the posteroinferior portion of one vertebral body and the lamina of the vertebra below.¹⁰¹ The condition can also occur during hyperflexion, but usually with extension movements with infolding of the ligamentum flavum, which can result in a 30% or more reduction of the anteroposterior diameter of the spinal canal.¹⁰² The spinal cord axons become unresponsive to stimulation for a variable period of time, essentially creating a “postconcussive” effect.¹⁰³

This condition is described by the neurological deficit, the duration of symptoms, and the anatomical distribution. A continuum of neurological deficits that range from sensory only, sensory disturbance with motor weakness, or episodes of complete paralysis may occur. These may be described as paresthesia, paresis, and plegia. An injury is defined as grade I if the cervical cord neurapraxia (CCN) symptoms do not persist for over 15 minutes. Grade II injuries are defined as lasting from 15 minutes to 24 hours. Grade III injuries persist for 24 to 48 hours. All four extremities may be involved; this is considered a “quad” pattern. Upper and lower extremity patterns may also be observed.¹⁰⁴

By definition, this condition is transient, and complete resolution generally occurs within 15 minutes but may take up to 48 hours. Steroid administration in accordance with the Bracken protocol¹⁰⁵ in this population is controversial. There have been no controlled studies reporting that the administration of steroids has altered the natural history of athletes that have suffered CCN.¹⁰⁶

In players who return to football, the rate of recurrence has been reported to be as high as 56%.¹⁰⁴ A considerable amount of controversy exists regarding whether the presence of cervical stenosis makes an athlete more prone to sustaining permanent neurological injury or transient quadriparesis. 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) determined from lateral cervical spine radiographs is considered normal if more than 15 mm between C3 and C7. Cervical stenosis is considered to be present if the canal diameter is less than 13 mm. However, this measurement has significant variability secondary to variations in landmarks used for measurement, changes in target distances for making the radiographs, patient positioning, differences in the triangular cross-sectional shape of the canal, and magnification of the canal because of a patient’s large body habitus. In an effort to eliminate this variability, Torg and Pavlov designed a ratio method for determining the presence of cervical stenosis, comparing the sagittal diameter of the spinal canal to the sagittal midbody diameter of the vertebral body at the same level.107 A ratio of 1:1 was considered normal and less than 0.8 was indicative of significant cervical stenosis. This ratio was found to mislabel many athletes with adequately sized canals but large vertebral bodies as being stenotic. This observation, as well as an unprecedented ability to image the vertebral column, intervertebral disks, spinal canal, cerebrospinal fluid (CSF), and spinal cord directly, has made magnetic resonance imaging (MRI), and not bone landmarks, currently the preferred method of choice for assessing “functional spinal stenosis.” MRI assessment of CSF signal around the spinal cord, termed the functional reserve, can be determined and the visualization of the CSF signal, its attenuation in areas of stenosis, and changes on dynamic sagittal flexion-extension MRI studies are paramount in the diagnosis of this condition. In cases involving an absent CSF pattern on axial and, particularly, sagittal MR images, functional stenosis is diagnosed.

Developmental or acquired cervical stenosis seems to be a predisposition to CCN.^108,109 Torg had previously argued that young patients who suffered an episode of CCN were not predisposed to permanent neurological injury.^109,110 This assumption has recently been called into question now that a player who had experienced a CCN subsequently sustained a quadriplegic injury.¹¹¹

Traumatic Intervertebral Disk Herniation

Acute herniation of an intervertebral disk can occur during participation in sports and in the athletic population. Extrusion of disk material into the central spinal canal can result in acute cord compression and a transient or permanent cord injury. Clinically, the athlete may present with acute paralysis of all four extremities and a loss of pain and temperature sensation. A traumatic central disk herniation is also typically accompanied by the sudden onset of posterior neck pain/paraspinal muscle spasm, as well as true radicular arm pain or referred pain to the periscapular area.⁷⁹

Stingers/Burners/Transient Brachial Plexopathy/Nerve Root Neurapraxia

This condition is one of the most common occurrences in collision sports and is not the result of an SCI. It was first described in 1965 by Chrisman et al.¹¹² Because the mechanism was thought to be direct force applied to the shoulder with the neck flexed laterally away from the point of contact, the condition has also been referred to as cervical pinch syndrome.¹¹³ This is a transient neurological event characterized by pain and paresthesia in a single upper extremity following a blow to the head or shoulder. The symptoms most commonly involve the C5 and C6 spinal roots. The affected athlete can experience burning, tingling, or numbness in a circumferential or dermatomal distribution.¹¹³ The symptoms may radiate to the hand or remain localized in the neck. These athletes often maintain a slightly flexed cervical spine posture to reduce pressure on the affected nerve root at the neural foramen, or hold/ elevate the affected limb in an attempt to decrease tension on the upper cervical nerve roots.

Weakness in shoulder abduction, external rotation, and arm flexion is a reliable indicator of the injury.¹¹⁴ If weakness is a component, it usually involves the C5-C6 neurotome. The radiating arm pain tends to resolve first (within minutes) followed by a return of motor function (within 24 to 48 hours). Although the condition is usually self-limiting, and permanent sensorimotor deficits are rare, a variable degree of muscle weakness can last up to 6 weeks in a small percentage of cases.

This injury is usually the result of downward displacement of the shoulder with concomitant lateral flexion of the neck toward the contralateral shoulder. This is thought to result in a traction injury to the brachial plexus. The condition may also result from ipsilateral head rotation with axial loading resulting in neural foramen narrowing and compression/impaction of the exiting nerve root within the foramen.^115,116 Direct blunt trauma at Erb’s point, located superficially in the supraclavicular region, has also been reported to be an etiology for stingers.¹¹⁷ This can occur when an opponent’s shoulder or helmet is driven into the affected athlete’s shoulder pad and directly into this area.

This injury has been graded using Seddon’s criteria. A grade I injury is essentially a neurapraxia defined as the transient motor or sensory deficit without structural axonal disruption. This type of injury usually completely resolves and full recovery can be expected within 2 weeks. Grade II injuries are equivalent to axonotmesis. This involves axonal disruption with an intact outer supporting epineurium. This results in a neurological deficit for at least 2 weeks, and axonal injury may be demonstrated on electromyographic studies 2 to 3 weeks following the injury. Grade III injuries are considered neurotmesis or total destruction of the axon and all supporting tissue. These injuries persist for at least 1 year with little clinical improvement.

Cervical canal stenosis has been implicated as a risk factor for stingers.¹¹⁸ The dimensions of the spinal cord remain relatively constant in the subaxial cervical spine,¹¹⁹ with an average midsagittal cord diameter in the range of 8 to 9 mm. In contrast, the size of the vertebral canal in the lower cervical region shows significant individual variation. Determining the “functional reserve” (amount of CSF surrounding the spinal cord) can be accomplished using MRI and is currently the preferred method for assessing “functional spinal stenosis.”

Stingers with prolonged neurological symptoms are the most common reason for high school and college athlete cervical spine evaluations in an emergency room.106,120,121 The athlete commonly demonstrates a full, pain-free arc of neck motion with no midline palpation tenderness on examination. If tenderness is present or unilateral neurological symptoms persist, a paracentral disk herniation with associated nerve root compression should be considered. This is usually accompanied by the sudden onset of posterior neck pain and spasm. Monoradiculopathy characterized by radiating pain, paresthesias, or weakness in the upper extremity also occurs secondary to compression and inflammation of the cervical root.

On-the-Field Management

The immediate treatment of the player that has suffered an SCI should follow standard trauma protocols that address airway, breathing, and circulation. The initial objective in this primary survey is to assess the athlete for immediately life-threatening conditions and to prevent further injury. During this primary survey, appropriate resuscitation procedures are instituted and the emergency medical system is activated immediately on recognizing a life-threatening problem or serious spinal injury.¹²²

Following the primary survey, one of three clinical scenarios will become apparent: actual or impending cardiopulmonary collapse, altered mental status but no compromise of the cardiovascular or respiratory system, or normal level of consciousness and normal cardiopulmonary function.

If the athlete is experiencing cardiopulmonary collapse, the use of advanced cardiac life support principles is essential. An athlete lying prone must be carefully logrolled into a supine position on a rigid backboard if available. Any face mask should be rapidly removed to provide adequate airway access. As mentioned earlier in this chapter, removal of the helmet and shoulder pads is not routinely indicated unless they interfere with resuscitation of the patient. If still in place, the mouthpiece should be taken out while manual stabilization of the neck in a neutral position is maintained. Airway evaluation should be performed with the understanding that obstruction can be secondary to a foreign body, facial fractures, or direct injury to the trachea or larynx. A depressed level of consciousness can also contribute to the inability to maintain an airway.

If breathing is of insufficient depth or rate assisted ventilation is required. On the field, this is usually performed by using a bag-valve device and face mask. Hypoxia should be rapidly corrected by providing adequate ventilation with protection of the vertebral column at all times. In a patent airway, respiratory collapse could be the result of an upper cervical SCI due to paralysis of the diaphragm and accessory breathing muscles. Indications for definitive airway control by endotracheal intubation include apnea, inability to maintain oxygenation with face mask supplementation, and protection from aspiration. Circulation must also be addressed during the primary survey. Neurogenic shock secondary to SCI could result in diminished amplitude of the peripheral pulses in combination with bradycardia. If the femoral or carotid pulses are not palpable, cardiopulmonary resuscitation is required. If this is the case, the front of the shoulder pads can be opened to allow for chest compressions and defibrillation.

If the athlete is found to have an altered mental status without cardiopulmonary compromise, a brief neurological examination can be performed. The prevention of further injury to the cord is of primary importance, and once initial resuscitation and evaluation are performed, focus should be placed on immobilization. The helmet and shoulder pads should remain in place unless removal is required to access the airway. Neutral axial alignment and occipital support must be maintained. An unconscious player should be logrolled into a supine position and the mouthpiece removed.

If, after completion of the primary survey, the athlete is found to have a normal mental status without cardiopulmonary compromise, a neurological assessment should be performed. If the athlete exhibits symptoms or signs referable to cord damage, a catastrophic cervical cord trauma should be assumed. If the neurological assessment is normal but the athlete exhibits cervicothoracic pain, focal spinal tenderness, or restricted neck motion, an unstable spinal column injury with potential cord compromise is assumed.

Removal from the field should be performed, with strict attention to immobilization of the spine. A rigid backboard with cervical collar or bolsters on the sides of the head should be used. It is important to remember that the athlete’s helmet may cause unintended cervical flexion on a rigid spine board. Once the athlete arrives at the hospital, if still in place the helmet and shoulder pads should be removed before radiographic examination.

Athletes that suffer a burner should be immediately removed from competition until symptoms have fully resolved. Management of the participant that receives this injury is often dependent on the presence of residual symptoms. They are usually considered an isolated benign injury. On-field evaluation should include palpation of the cervical spine to determine any points of tenderness or deformity. Evaluation of sensation and muscle strength should be performed using the unaffected limb as a point of reference if necessary. Weakness in the muscles innervated by the upper trunk of the brachial plexus is often observed. These include the deltoid (C5), biceps (C56), supraspinatus (C56), and infraspinatus (C56).^123,124 The shoulder of the affected limb should also be evaluated, with particular attention to the clavicle, acromioclavicular joint, and supraclavicular and glenohumeral regions. Percussion of Erb’s point can be performed in an attempt to elicit radiating symptoms. Obviously, the athlete should be evaluated for other serious injuries such as cervical spine fractures and dislocations. It is unusual to find lower brachial trunk injury patterns involving the C7 or C8 nerve roots. It is also not common to see persistent sensory deficits involving either the lower or upper extremities. This condition is always unilateral and has never been reported to involve the lower extremities. If bilateral upper extremity deficits are present, SCI should be at the top of the differential diagnosis. Localized neck stiffness or tenderness with apprehension toward active cervical movement should alert the examiner to a potentially serious injury and the subsequent initiation of full spinal precautions, including spine board immobilization and transport for advanced imaging.

If there are no complaints of neck pain, decreased range of motion, or residual symptoms, the player can usually return to competition. If symptoms do not resolve or there is persistent pain prompt imaging of the brachial plexus via MRI is recommended. If the symptoms persist for over 2 weeks electromyography can be performed to establish the distribution and degree of injury.39 Residual muscle weakness, cervical anomalies, or abnormal electromyographic studies are exclusion criteria for return to play.¹⁰⁶

By definition stingers and burners are transient phenomena. They usually do not require formal treatment. The athlete should be followed closely with repeat neurological examinations because, although the condition usually resolves in minutes, motor weakness may develop hours to days following the injury.^114,121 Repeated stingers may result in long-term muscle weakness with persistent paresthesias.¹²⁵ Other options for participants to decrease the risk of future occurrences are to change their field position or modify their playing technique.

Conclusion

Improvements in safety equipment and rule changes have led to a substantial drop in the number of catastrophic neurological injuries suffered during athletic competition. When these injuries do occur, they must be treated promptly and correctly to optimize outcome. It is hoped that this chapter will serve as a guide for the rapid diagnosis and treatment of neurological emergencies in this population.