eMedicine Specialties > Sports Medicine > Neurological

Repetitive Head Injury Syndrome

David Cifu, MD, The Herman J Flax, MD Professor and Chairman, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University; Chief of PM&R Services, Virginia Commonwealth University Health System, Medical College of Virginia Hospital; Co-Principal Investigator of the NIDRR Traumatic Brain Injury Model Systems and NIH Traumatic Brain Injury Network Sistes Programs, Virginia Commonwealth University
Brian D Steinmetz, DO, Resident, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University; David F Drake, MD, Director of Musculoskeletal and Sports Medicine, Department of Physical Medicine and Rehabilitation, Assistant Professor, Medical College of Virginia

Updated: Mar 24, 2008

Introduction

Background

Primary head injury can be catastrophic, but the effects of repetitive head injuries must also be considered. Second-impact syndrome (SIS), a term coined in 1984, describes the situation in which an individual sustains a second head injury before the symptoms from the first head injury have resolved.

The second injury may occur from days to weeks following the first. Loss of consciousness is not a requirement of this condition, the impact may seem relatively mild, and the athlete may appear only dazed initially. However, this second impact causes cerebral edema and herniation, leading to collapse and death within minutes. Only 17 cases of confirmed SIS have been reported in the medical literature. Thus, the true risk and pathophysiology of SIS has not been clearly established.

Importantly, even if the effects of the initial brain injury have already resolved (6-18 mo post injury), the effect of multiple concussions over time remains significant and can result in long-term neurologic and functional deficits. These multiple brain insults can still be termed repetitive head injury syndrome, but they do not fit the classification of SIS. True SIS would most likely have a devastating outcome.

A study of American high school and college football players demonstrated 94 catastrophic head injuries (significant intracranial bleeding or edema) over a 13-year period.¹  Of these, only 2 occurred at the college level. Seventy-one percent of high school players suffering such injuries had a previous concussion in the same season, with 39% playing with residual symptoms. On the other hand, results from a study of concussion by the National Football League demonstrated no cases of SIS or catastrophic head injury in players returning to play in the same game after resolution of symptoms.²

The outcome of multiple minor head injuries over a prolonged period has not been well studied and is not well understood. The preponderance of data assessing the impact of repetitive head injuries on short- and long-term neurologic (cognitive) performance has been focused on the sports of boxing and American football.^{1,2,3,4,5,6,7,8,9,10,11,12,13,14,15}

Numerous studies of professional boxers have shown that repeated brain injury can lead to chronic encephalopathy, termed dementia pugilistica.^12,13,14,15 Likewise, the autopsies of 2 former professional football players with a history multiple concussions demonstrated changes that were consistent with chronic encephalopathy.^5,6
Another investigation of retired professional football players showed a 3-fold increase of depression in players with a history of 3 or more concussions.³ Older studies of American and Australian rules football showed no effect from repetitive mild head injuries.¹¹ However, more recent studies of collegiate football players showed an association between multiple concussions and reduced cognitive performance, prolonged recovery, and the increased likelihood of subsequent concussions.

Evidence has also been gleaned from other sports that involve head impact. Nonrandomized studies of soccer players who have had multiple minor concussions have demonstrated that these individuals performed worse on neuropsychologic tests compared with a control group.^16,17,18,19

Neuropsychologic testing is the standard for monitoring cognitive recovery after concussion. However, 2 studies suggest that abnormalities in visual motor and motor cortex function persist after neuropsychologic testing has normalized.^8,20  Slower recovery in patients with a second concussion was also seen.

Basic science research is also ongoing. Experiments in concussed rats demonstrated prolonged abnormalities in metabolic markers of brain activity when a second impact was administered at 3 days^21,22  This implies there may be a metabolic window of vulnerability to a second impact that leads to chronic or prolonged symptoms. Clinically useful biomarkers for brain injury are also being investigated.

Certainly, more research is needed to better understand the chronic and catastrophic effects of repetitive head injuries.

For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center and Dementia Center. Also, see eMedicine's patient education articles Concussion and Dementia in Head Injury.

Frequency

United States

The National Center for Catastrophic Sports Injury Research in Chapel Hill, NC, reported 35 cases of SIS among American football players from 1980-1993. Seventeen were confirmed by necropsy, surgery, or magnetic resonance imaging (MRI) findings. Eighteen were probable cases of SIS, despite inconclusive necropsy findings.

The number of reported SIS cases increased from 1992-1998, but this increase is thought to be due to more frequent recognition and reporting. Some clinicians believe that SIS is overreported. Boden et al reported an average of 7.08 catastrophic head injuries per year in high school football, compared with 0.15 for college football from 1989-2002.¹  The incidence was 0.67/100,000 for high school players and 0.21/100,000 for college players. Thirty-nine percent of the affected athletes reported playing with residual symptoms.¹  There were 8 fatalities, of which 1 individual had cerebral edema as the only radiographic finding. It was unclear as to whether a second impact occurred in this case.

With the advent and improvement of the helmet in American football and with the introduction of new rules that make spearing illegal, the incidence of head-injury fatalities has decreased from 2.64 cases per 100,000 persons in 1968 to 0.20 cases per 100,000 persons since 1977. The US Centers for Disease Control and Prevention estimates a 20% rate of concussion from football brain injuries (predominantly high-school and college level), which equates to an estimated 300,000 concussions per year.

Collins et al showed that 20% of the college football players they studied had 2 or more concussions during their career.⁷ Furthermore, a study by Daniel et al found that the symptoms of an estimated 60,000 football players who suffer concussion may persist for 4 or more months in up to 24% of these individuals.²⁰

Schulz et al reported on a prospective cohort study of North Carolina high-school athletes followed from 1996–1999.²³ Subjects were clustered by school and sport, and the sample included 15,802 athletes, with 1–8 seasons of follow-up per athlete. Concussion rates ranged from 9.36 concussions per 100,000 athlete-exposures in cheerleading to 33.09 concussions per 100,000 athlete-exposures in football, where "athlete-exposure" is 1 athlete participating in 1 practice or game. The overall rate of concussion was 17.15 concussions per 100,000 athlete-exposures.

Cheerleading was the only sport for which the practice rate of concussions was greater than the game rate.²³ Almost two thirds of cheerleading concussions involved 2-level pyramids. Concussion rates were elevated for athletes with a history of concussion, and they increased with the increasing level of body contact permitted in the sport.

Powell and Barber-Foss reported a 2-year review of 235 US certified athletic high-school training records. The authors estimated a total of 62,816 cases of mild traumatic brain injury (TBI) annually among high-school varsity athletes, with football accounting for approximately 63% of these cases and a varied incidence among 10 other popular sports.²⁴

Matser et al showed that 23% of the amateur soccer players they studied had 2-5 concussions during their career.¹⁶ Boden et al found that the overall prevalence of college soccer-related concussions was 0.6 cases per 1000 athlete-exposures for men and 0.4 cases per 1000 athlete-exposures for women.¹⁷ The authors reported that the vast majority (72%) of these concussions were grade 1, and none were grade 3.¹⁷

The actual number of athletes who may be affected by repeated minor head injuries is largely unknown.

Functional Anatomy

SIS is thought to occur because of a loss of autoregulation of the cerebral blood flow, which leads to vascular engorgement, increased intracranial pressure (ICP), and eventual herniation. This herniation may involve the medial temporal lobe and may occur medially across the falx cerebri or inferiorly through the tentorium. Herniation can also force the cerebellar tonsils to move inferiorly through the foramen magnum. The athlete's condition rapidly worsens, and brainstem failure occurs in 2-5 minutes.

Sport-Specific Biomechanics

The brain is protected by bone and is cushioned by tough meninges and cerebrospinal fluid. Despite these protective surroundings, blunt-force trauma to the head can cause injury to the site of impact (coup injury) and the site immediately opposite of the impact (contrecoup injury). Factors that dissipate the force (eg, equipment, neck muscle strength) can minimize this trauma.

Clinical

History

The history is a key element in evaluating an athlete with a suspected head injury. However, the athlete may not be able to provide a good history because of slowed mentation or confusion. In such cases, obtain the history from a teammate, coach, or observer. Symptoms of a head injury may include the following:

• Headache
• Memory impairment
• Confusion
• Diplopia
• Fatigue
• Photophobia, phonophobia, or both
• Blurred vision
• Dizziness
• Hemiplegia
• Nausea
• Sensory loss
• Impairment of hand-eye coordination
• Irritability
• Depression

Physical

The goals of the physical evaluation are to (1) recognize that a head injury may have occurred, (2) determine which athletes require immediate transport to a medical facility, and (3) decide when the athlete can return to competition. Emergency management includes the ABCs of first aid. That is, assess and manage the individual's airway, breathing, and circulation. Signs of head injury include the following:

• Altered levels of consciousness
• Posttraumatic or retrograde amnesia
• Gait abnormalities
• Weakness
• Visual abnormalities
• Sensory loss
• Pupillary concordance and/or accommodation
• Poor concentration
• Apprehension
• Increased symptoms with exertion
• Focal symptoms – Facial or extremity twitching, smelling of atypical odors, tasting of atypical tastes
• Generalized symptoms – Tonic-clonic movements of body, incontinence, altered level of arousal

The brief neurologic examination should be performed without moving the athlete until the patient's ABCs and spine are deemed stable. The following are assessed:

• Verbal quality and appropriateness
• Memory (eg, to event), orientation (eg, to date), cognitive (eg, ability to perform the serial 7 s test)
• Visual findings – Pupillary size and reaction, tracking, nystagmus, gross visual fields, diplopia
• Motor findings – Coordination (finger to nose), strength (focal findings), balance (eg, single-leg stance, heel to toe)
• Romberg test results
• Tone
• Reflexes
• Sensory abnormalities – Touch, pinch, and pain

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Causes

Factors that may increase the risk of a poor outcome with a repetitive head injury include the following:

• Previous head injury
• Persistence of symptoms from a previous head injury
  • Headache
  • Labyrinthine dysfunction (balance disorder)
  • Visual, motor, or sensory changes
  • Mental difficulties that affect thought and memory processes
• Alcohol or illicit drug use

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Differential Diagnoses

Concussion
Facial Fractures
Facial Soft Tissue Injuries

Other Problems to Be Considered

Brain mass (eg, tumor, abscess, infection, congenital abnormality)
Cerebral contusion
Dehydration/Hyperthermia
Diffuse axonal injury
Epidural hematoma
Intoxication (alcohol or illicit drug use)
Medication effect (pain, allergy)
Meningeal irritation/infection
Seizure disorder
Psychiatric disorder
Subarachnoid hemorrhage
Subdural hematoma or intracerebral hematoma

Workup

Laboratory Studies

No laboratory tests help in diagnosing repetitive head injury. Most cases are diagnosed on the basis of the clinical findings.

Imaging Studies

Imaging studies are reserved for athletes with more significant injuries, such as those that cause loss of consciousness, persistent symptoms, neurologic deficits, or neurologic deterioration. Imaging studies should be considered in all athletes who have had more than 1 concussion. In addition, imaging studies should be ordered if symptoms last longer than 12 hours. Consultation with a neurosurgeon is imperative if any imaging findings are abnormal.

• Plain skull radiography yields few findings in persons with mild brain trauma, and it should not be ordered unless facial fractures are suspected. Plain film radiography (cervical spine [C-spine] radiographs) can be ordered to rule out neck pathology, which can occur with head trauma.
• Head computed tomography (CT) scanning is sensitive for detecting intracranial pathology associated with blunt-force trauma, even in a mild head injury (eg, Glasgow Coma Scale score of 13-15).
  • Nonenhanced CT scanning is the imaging examination of choice because acute hemorrhage must be excluded before performing contrast-enhanced CT scanning.
  • The advantages of CT scanning compared with MRI include (1) more rapid image acquisition in an emergency situation; (2) better depiction of bone; (3) lower cost, although cost should not influence clinical decision making in a potentially life-threatening situation such as the setting of a head injury; (4) correlation of negative results with a successful outcome; and (5) better sensitivity in detecting skull fractures.
  • Compared with the initial (first 12-24 h) head CT scan, the follow-up CT scan may better reveal small hemorrhages, which coalesce to form a brain contusion.
  • CT scanning can depict acute hemorrhages, skull fractures, cerebral edema, and cerebral herniation. An acute subdural hematoma is approximately 3 times more common than an epidural hematoma in sports-related head injuries.
• MRI of the head is more sensitive than CT scanning for detecting subtle changes such as small hemorrhages, edema, and diffuse axonal injury (DAI).
  • MRI should not be ordered in emergency situations because CT scanning is faster than MRI and has the advantages listed above.
  • The advantages of MRI compared with CT scanning include the ability of MRI to better depict subtle edema, small hemorrhages, arteriovenous malformations, and DAI.
  • DAI is seen in severe head injuries and is thought to result from the shearing of multiple axons. DAI is represented on MRIs as diffuse, high-signal intensity specks in the white matter.
  • MRI should be ordered if the patient's symptoms persist and CT scanning results are normal or if the symptoms are atypical or worsen despite normal or stable CT scan findings.

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Brain, Contusion
Brain, Herniation
Facial Fractures

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Other Tests

• Neuropsychologic testing
  • This is an in-depth examination of the injured athlete's thought processes and is considered the criterion standard for the initial and follow-up assessment of concussion patients, especially those with SIS.
  • A neuropsychologist certified by the American Board of Professional Psychology is the best resource for these assessments, and a consultative approach is preferred, as opposed to merely a description of test data.
  • A range of cognitive and behavioral tests are used, based on the preferences of the neuropsychologist, the severity of the injury, the specific clinical issue at hand (eg, return to school, return to work, manage finances), the educational and cultural background of the examinee, and the time post injury.
  • The occurrence of multiple concussions is associated with reduced cognitive performance on neuropsychologic tests.
  • Hinton-Bayre et al showed that impaired performance on psychometric tests continued even after the athletes (professional rugby players) were symptom free.²⁵
• Electroencephalography (EEG)
  • EEG yields conflicting and typically nonspecific results. Most of the research with EEG has involved boxers.
  • Busse and Silverman showed that 37% of abnormal EEG findings occurred in boxers who have had a concussion.²⁶
  • Kaplan and Browder studied 1400 electroencephalograms in boxers and found that 34% of the athletes had normal EEG findings.²⁷ The authors concluded that fighters with a lower ring rating had a higher percentage of disorganized EEG findings.
  • Johnson used EEG to evaluate retired professional boxers and found chronic brain damage in 12 of 15 of these individuals 22 years after their careers had ended.¹⁵
  • Other studies show abnormal EEG findings in 20-30% of boxers.
  • However, early studies by Beaussart and Beaussart-Boulengé did not find any correlation between EEG changes and the severity of postconcussion syndrome in 3100 cases.¹⁴
• Dynamic imaging
  • Single-photon emission computed tomography (SPECT) scanning and positron emission tomography (PET) scanning have high sensitivity, but the specificity of these modalities is unclear and the clinical correlation is limited. At present, these tests are used primarily for research activities.
  • In addition, these examinations are expensive and not easily available to most clinicians.
  • Results from these tests may be overinterpreted or underinterpreted in medicolegal settings; the use for these types of activities should be discouraged until further definitive research is performed and has undergone peer review.

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Procedures

• ICP monitoring may help in severe TBI, but it has limited usefulness in patients with mild TBI.
• Patients with an ICP greater than 25 mm Hg generally have more unfavorable outcomes than those with lower ICP measurements.

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

The goal of all therapy is to maximize the patient's strength and functional independence.

Athletes who have had severe head injuries may require rehabilitation for a prolonged period. In most patients, mild brain injuries do not require extensive rehabilitation, but they do require focal medical and rehabilitation care based on the individual's clinical evaluation and diagnostic test results.

Physical therapy is helpful in patients with increased tone, motor deficits, or mobility problems after a brain injury. Range-of-motion exercises are helpful in managing spasticity and preventing contractures.

Occupational Therapy

Occupational therapy is helpful in patients with brain injuries who may have motor and/or cognitive processing deficits and who may need to improve their ability to perform activities of daily living. The use of assistive devices can also be addressed.

Speech Therapy

Speech therapy is often useful in detecting subtle changes in the patient's thought processes and speech patterns. A speech therapist can help a patient with brain injury overcome barriers related to these changes.

Recreational Therapy

Medical Issues/Complications

Medical issues in patients with brain injuries include the following:

• Homeostatic abnormalities: Loss of autonomic control of blood pressure or respiration and cardiac abnormalities may occur.
• Endocrine abnormalities: The syndrome of inappropriate antidiuretic hormone (SIADH) and diabetes insipidus are common problems.
• Behavioral issues: The patient may become uninhibited, impulsive, or agitated. Aggressive treatment with behavioral programs, counseling, and short-term medication usage is most effective. Medication usage (mood stabilizers, atypical antipsychotics) should be instituted carefully and with full knowledge of the indicators of clinical success, duration of treatment, and potential adverse effects.
• Deep venous thrombosis: Cifu et al showed that approximately 20% of patients admitted to a brain-injury rehabilitation unit had deep venous thrombosis.²⁸
• Pulmonary embolus: This is a rare condition, but if it is suspected, emergent treatment is indicated.
• Complications of severe brain injury: Brainstem herniation, rebleeding, and death may occur.

• Dizziness: Most commonly, this is due to limitations in neck movement (pain) and peripheral trauma to the vestibular/labyrinthine system. Rarely, it is due to injury to the brainstem (central) balance coordinating structures. Dizziness is treated with medications and therapy.
• Insomnia: This is commonly related to issues of pain, dizziness, behavioral problems, nightmares/flashbacks, altered physical activity levels, or idiopathic reasons. Insomnia is best treated with a rapid return to activity, treatment of secondary issues, and short-term nonaddictive sleep aides.
• Behavioral issues: Behavior may vary from excessive (see above) or depressed. Normalizing sleep-wake cycles, controlling pain, reactivating physical skills, and reassurance help most individuals. Individualized psychotherapy is also highly effective. 
• Photophobia/hyperacusis: These conditions are rarely significant long-term issues. They should be treated aggressively initially with dark glasses/white-noise generators and then a rapid weaning program. Sustained difficulties may suggest an undetected injury or secondary psychologic issues.

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Diabetes Insipidus
Syndrome of Inappropriate Antidiuretic Hormone Secretion

Surgical Intervention

Evacuation is required for epidural hematomas, significant subdural hematomas, and large intracerebral hematomas that cause mass effect. Ventriculostomy may be required for significant edema and/or possible herniation.

Recovery Phase

Rehabilitation Program

Physical Therapy

In the case of a severe head injury, many of the aforementioned therapies can be continued in an outpatient setting, but most of the rehabilitation process is focused on reintegrating patients with brain injuries into their home environment and community.

Maintenance Phase

Rehabilitation Program

Physical Therapy

Patients with TBI may require educational or neuropsychologic support for an extended period, depending on the severity of the head injury.

Occupational Therapy

See Acute Phase, Rehabilitation Program, Occupational Therapy.

Speech Therapy

See Acute Phase, Rehabilitation Program, Speech Therapy.

Recreational Therapy

See Acute Phase, Rehabilitation Program, Recreational Therapy.

Medication

Care should be used when instituting therapy with medications that potentially have sedating effects, because sedation may complicate the monitoring of a patient with a brain injury. Some medications that can have significant sedating effects on such patients include H2 blockers (eg, ranitidine, famotidine), diphenhydramine, narcotic pain relievers, nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, antipsychotics, and seizure medications.

Some medications may improve the patient's focus and alertness. A few of these medications are discussed below. In addition to the agents that may enhance thinking skills, aggressive management of specific symptoms is also warranted, including insomnia (trazodone), headaches (butalbital, aspirin, and caffeine [Fiorinal]; isometheptene mucate, dichloralphenazone, and acetaminophen [Midrin]; acetaminophen; NSAIDs; local agents), dizziness (meclizine, buspirone, vestibular programs, liberatory technique), and depression (cognitive behavioral therapy, selective serotonin reuptake inhibitors [SSRIs]).

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CNS Stimulants

Central nervous system (CNS) stimulants are used to treat the hypoarousal and poor initiative often seen in patients with brain injuries.

Methylphenidate (Ritalin, Ritalin SR)

Although most notably used in children with attention-deficit/hyperactivity disorder (ADHD), this agent often helps with hypoarousal. Frequently the first drug used in patients with brain injury.

Not used as often in children with brain injury; when used, administer as in children with ADHD.

Administered in morning and at noon before a therapy session to facilitate stimulant effect and increase attention to tasks. If no response is achieved, can be discontinued and another medication can be used.

Dosing

Adult

5 mg PO bid initially; can be increased 5 mg/d; not to exceed 20 mg PO bid

Pediatric

5 mg PO bid initially; can be increased 5 mg/d; not to exceed 10-15 mg PO bid

Interactions

Reduces the effects of guanethidine and bretylium; may increase the toxicity of concurrent phenytoin, TCAs, warfarin, primidone, and phenobarbital; MAOIs increase toxicity

Contraindications

Documented hypersensitivity; glaucoma; Tourette syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with dementia, seizures, and hypertension; monitor patient's BP and heart rate

Anti-Parkinson agents

Anti-Parkinson medications have been useful in patients with brain injuries because these drugs increase their arousal and attention to tasks.

Amantadine (Symmetrel)

Unknown mechanism of action; may release dopamine from remaining dopaminergic terminals in patients with Parkinson disease or from other central sites. Less effective than levodopa in treating Parkinson disease; slightly more effective than anticholinergic agents.

Dosing

Adult

100 mg PO bid initially; increase to 150 mg PO bid if no or minimal response

Pediatric

Not established

Interactions

Drugs with anticholinergic or CNS-stimulating activity increase toxicity; concurrent administration of hydrochlorothiazide plus triamterene may increase plasma concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with liver disease, uncontrolled psychosis, eczematoid dermatitis, seizures, and in those who have use of CNS stimulants; reduce dose in the presence of renal disease when treating Parkinson disease; do not discontinue abruptly

Carbidopa/levodopa (Sinemet)

May increase alertness and attention to task in patients with brain injury.

Dosing

Adult

1 tab (10 mg/100 mg) PO tid initially; increase to effect q3d; not to exceed 4 tabs (25/250) PO tid

Pediatric

Not established

Interactions

Hydantoins, pyridoxine, phenothiazine, and hypotensive agents may decrease effects; toxicity increases with antacids and MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; malignant melanoma; undiagnosed skin lesions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse CNS effects (eg, dyskinesias) may occur at lower doses and earlier in therapy with the SR form; caution in patients with a history of myocardial infarction, arrhythmias, asthma, and peptic ulcer disease; sudden discontinuation may cause worsening of Parkinson disease; high-protein foods should be distributed throughout the day to avoid fluctuations in levodopa absorption

Central Nervous System Stimulant, Nonamphetamine

Nonamphetamine CNS agents have actions that are similar to sympathomimetic agents.

Modafinil (Provigil)

May exert stimulant effects by decreasing GABA-mediated neurotransmission. Has wake-promoting actions similar to sympathomimetic agents. Improves wakefulness in patients with excessive daytime hypersomnolence. Has been used in narcolepsy and primary hypersomnia. Mechanism of action is unclear.

Dosing

Adult

200 mg/d PO in am; may increase to 400 mg/d

Pediatric

<16 years: Not established
>16 years: Administer as in adults

Interactions

May decrease the levels of cyclosporine or steroidal contraceptives, and to a lesser degree, theophylline; modafinil may increase the drug concentration levels of diazepam, propranolol, and phenytoin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor patients closely for signs of misuse or abuse, especially those with a history of drug or stimulant abuse, such as methylphenidate, amphetamine, and cocaine; leukopenia has been reported in pediatric patients; may cause serious life-threatening rash (ie, Stevens-Johnson Syndrome, toxic epidermal necrolysis, drug rash with eosinophilia and systemic symptoms), hypersensitivity reactions (eg, angioedema, multiorgan reactions), and psychiatric symptoms (eg, anxiety, mania, hallucinations, suicidal ideation)

Follow-up

Return to Play

No good parameters have been proposed for repetitive head injury. As a result, most physicians use the parameters for concussion. The following systems present 2 options for concussion management, although many options are available. Note that in the following descriptions, asymptomatic means that the patient is symptom free at rest and with exertion.

Concussion scales with return-to-play criteria

Cantu system^29,30,31

• Grade I – No loss of consciousness, or posttraumatic amnesia for less than 30 minutes
  • First concussion – Return to play if patient is asymptomatic for 1 week
  • Second concussion – Return to play if patient is asymptomatic for 2 weeks
  • Third concussion – Terminate season
• Grade II – Loss of consciousness for less than 5 minutes, or posttraumatic amnesia for 30 minutes to 24 hours
  • First concussion – Return to play if patient is asymptomatic for 1 week
  • Second concussion – Return to play if, after at least 1 month, patient asymptomatic for 1 week
  • Third concussion – Terminate season
• Grade III – Loss of consciousness for more than 5 minutes, or posttraumatic amnesia for longer than 24 hours
  • First concussion – Return to play if, after at least 1 month, patient asymptomatic for 1 week
  • Second concussion – Terminate season

Kelly system³²

• Grade I – No loss of consciousness, transient confusion for less than 15 minutes
  • First concussion – Return to play if patient is asymptomatic within 15 minutes
  • Second concussion in same contest – Remove from play
  • After fourth concussion in season – Terminate season
• Grade II – No loss of consciousness, transient confusion for longer than 15 minutes
  • First concussion – Return to play if patient is asymptomatic for 1 week
  • Second concussion – Return to play if patient  is asymptomatic for 2 weeks
  • Third concussion – Terminate season
• Grade III – Loss of consciousness, brief (seconds) or prolonged (minutes)
  • First concussion with brief loss of consciousness – Return to play if patient is asymptomatic for 1 week
  • First concussion with prolonged loss of consciousness – Return to play if patient is asymptomatic for 2 weeks
  • Second concussion – Return to play if patient is asymptomatic for 1 month

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Management and Staging of Traumatic Brain Injury

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Complications

The most common complication at follow-up is further head injury and/or cognitive decline. Matser et al found that concussion is specifically associated with impaired performance in memory and planning functions.¹⁶

Prevention

Equipment and rule changes have significantly reduced the number and severity of head injuries in American football over the last 25 years. The dramatic difference seen in football has sparked debate about equipment and rule changes in soccer because a significant number of concussions are now known to occur when players hit the ball with their head.

In preventing SIS, the recognition of a concussion is the key factor. Preventing an athlete from returning to play while he or she still has symptoms from a concussion and following the guidelines for concussion management may help avert a catastrophic outcome.

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Prognosis

The prognosis varies with the severity of the injury. By definition, repetitive head injury is worse than a single minor concussion; neuropsychologic test results are worse in patients with repetitive minor concussions. Regarding SIS, rapid transport to a medical facility with neurosurgical specialists may prevent or limit the rapid decline often seen with SIS.

Education

Educate athletes, coaches, and healthcare professionals about the potentially catastrophic effects of SIS. Coaches and healthcare professionals need to know how to prevent SIS by not allowing the athlete to return to play while he or she is still recovering from a previous head injury.

Miscellaneous

Medicolegal Pitfalls

Allowing a player to return to play while the symptoms from a previous head injury persist can lead to his or her death. This outcome can result in a significant malpractice action.

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Resource Center Patient Safety

References

1. Boden BP, Tacchetti RL, Cantu RC, Knowles SB, Mueller FO. Catastrophic head injuries in high school and college football players. Am J Sports Med. Jul 2007;35(7):1075-81. [Medline].

2. Pellman EJ, Viano DC, Casson IR, Arfken C, Feuer H. Concussion in professional football: players returning to the same game--part 7. Neurosurgery. 2005;56(1):79-90; discussion 90-2. [Medline].

3. Guskiewicz KM, Marshall SW, Bailes J, et al. Recurrent concussion and risk of depression in retired professional football players. Med Sci Sports Exerc. Jun 2007;39(6):903-9. [Medline].

4. Cantu RC. Chronic traumatic encephalopathy in the National Football League. Neurosurgery. Aug 2007;61(2):223-5. [Medline].

5. Omalu BI, DeKosky ST, Hamilton RL, et al. Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery. Nov 2006;59(5):1086-92; discussion 1092-3. [Medline].

6. Omalu BI, DeKosky ST, Minster RL, et al. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. Jul 2005;57(1):128-34; discussion 128-34. [Medline].

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Keywords

second impact syndrome, second-impact syndrome, SIS, primary head injury, secondary head injury, traumatic brain injury, TBI, concussions, chronic traumatic encephalopathy, CTE, dementia pugilistica

Contributor Information and Disclosures

Author

David Cifu, MD, The Herman J Flax, MD Professor and Chairman, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University; Chief of PM&R Services, Virginia Commonwealth University Health System, Medical College of Virginia Hospital; Co-Principal Investigator of the NIDRR Traumatic Brain Injury Model Systems and NIH Traumatic Brain Injury Network Sistes Programs, Virginia Commonwealth University
David Cifu, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Medical Association, Association of Academic Physiatrists, Brain Injury Association, and National Stroke Association
Disclosure: Nothing to disclose.

Coauthor(s)

Brian D Steinmetz, DO, Resident, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University
Brian D Steinmetz, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Osteopathic Association
Disclosure: Nothing to disclose.

David F Drake, MD, Director of Musculoskeletal and Sports Medicine, Department of Physical Medicine and Rehabilitation, Assistant Professor, Medical College of Virginia
David F Drake, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, International Society of Physical and Rehabilitation Medicine, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

Gerard A Malanga, MD, Founder and Director, New Jersey Sports Medicine Institute; Director of Pain Management, Overlook Hospital; Director of Sports Medicine, Sports Medicine Fellowship Director, Mountainside Hospital; Clinical Chief, Rehabilitation Medicine and Electrodiagnosis, St Michael's Medical Center; Medical Director, Consultant, Horizon Healthcare Worker's Compensation Services, Blue Cross and Blue Shield Worker's Compensation
Gerard A Malanga, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Invaluable assistance in the preparation of this manuscript was received from Ingrid A. Prosser, MD.

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