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Repetitive Head Injury Syndrome

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David Cifu, MD, eMedicine.com

Repetitive Head Injury Syndrome
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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 two 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 three-fold increase of depression in players with a history of three 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, two 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 three 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.

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 eight fatalities, of which one 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 two 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

The US Consumer Product Safety Commission tracks product-related injuries through its National Injury Information Clearinghouse. According to the Consumer Product Safety Commission, an estimated 311,766 sports-related head injuries were treated at US hospital emergency departments in 2004.

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 one athlete participating in one 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 two-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 two-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 7s 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

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

Differentials

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

Lab 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.

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-Boulenge 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.

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
Recreational therapy is helpful in achieving community reintegration of the patient. Neuropsychologic measures may be good indicators of residual injury, and repeated testing may reveal when the athlete reaches a plateau.

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.

Minor issues in patients with brain injuries include the following:

  • 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.

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]).

Drug Category: CNS Stimulants

Central nervous system (CNS) stimulants are used to treat the hypoarousal and poor initiative often seen in patients with brain injuries.
Drug Name: Methylphenidate (Ritalin, Ritalin SR)
Description: 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.

Adult Dose: 5 mg PO bid initially; can be increased 5 mg/d; not to exceed 20 mg PO bid
Pediatric Dose: 5 mg PO bid initially; can be increased 5 mg/d; not to exceed 10-15 mg PO bid
Contraindications: Documented hypersensitivity; glaucoma; Tourette syndrome
Interactions: Reduces the effects of guanethidine and bretylium; may increase the toxicity of concurrent phenytoin, TCAs, warfarin, primidone, and phenobarbital; MAOIs increase toxicity
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

Drug Category: Anti-Parkinson agents
Anti-Parkinson medications have been useful in patients with brain injuries because these drugs increase their arousal and attention to tasks.
Drug Name: Amantadine (Symmetrel)
Description: 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.
Adult Dose: 100 mg PO bid initially; increase to 150 mg PO bid if no or minimal response
Pediatric Dose: Not established
Contraindications: Documented hypersensitivity
Interactions: Drugs with anticholinergic or CNS-stimulating activity increase toxicity; concurrent administration of hydrochlorothiazide plus triamterene may increase plasma concentrations
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

Drug Name: Carbidopa/levodopa (Sinemet)
Description: May increase alertness and attention to task in patients with brain injury.
Adult Dose: 1 tab (10 mg/100 mg) PO tid initially; increase to effect q3d; not to exceed 4 tabs (25/250) PO tid
Pediatric Dose: Not established
Contraindications: Documented hypersensitivity; narrow-angle glaucoma; malignant melanoma; undiagnosed skin lesions
Interactions: Hydantoins, pyridoxine, phenothiazine, and hypotensive agents may decrease effects; toxicity increases with antacids and MAOIs
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

Drug Category: Central Nervous System Stimulant, Nonamphetamine
Nonamphetamine CNS agents have actions that are similar to sympathomimetic agents.
Drug Name: Modafinil (Provigil)
Description: 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.
Adult Dose: 200 mg/d PO in am; may increase to 400 mg/d
Pediatric Dose: <16 years: Not established >16 years: Administer as in adults
Contraindications: Documented hypersensitivity
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
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 two 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

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

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.

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

Medical/Legal 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.

Acknowledgements

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

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 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

Coauthor(s): 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

Editors: 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; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; 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; 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; Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago

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].

7. Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and neuropsychological performance in college football players. JAMA. Sep 8 1999;282(10):964-70. [Medline]. [Full Text].

8. McCrory P, Makdissi M, Davis G, Collie A. Value of neuropsychological testing after head injuries in football. Br J Sports Med. Aug 2005;39(suppl 1):i58-63. [Medline].

9. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA. Nov 19 2003;290(19):2549-55. [Medline].

10. Mueller FO. Fatalities from head and cervical spine injuries occurring in tackle football: 50 years' experience. Clin Sports Med. Jan 1998;17(1):169-82. [Medline].

11. Maddocks DL, Saling MM, Dicker GD. A note on the normative data for a test sensitive to concussion in Australian Rules footballers. Aust Psychol. 1995;30:125-7.

12. Ryan AJ. Intracranial injuries resulting from boxing. Clin Sports Med. Jan 1998;17(1):155-68. [Medline].

13. Kaste M, Kuurne T, Vilkki J,. Is chronic brain damage in boxing a hazard of the past?. Lancet. Nov 27 1982;2(8309):1186-8. [Medline].

14. Beaussart M, Beaussart-Boulengé L. "Experimental" study of cerebral concussion in 123 amateur boxers, by clinical examination and EEG before and immediately after fights. Electroencephalogr Clin Neurophysiol. Nov 1970;29(5):530. [Medline].

15. Johnson J. Organic psychosyndromes due to boxing. Br J Psychiatry. Jan 1969;115(518):45-53. [Medline].

16. Matser EJ, Kessels AG, Lezak MD, Jordan BD, Troost J. Neuropsychological impairment in amateur soccer players. JAMA. Sep 8 1999;282(10):971-3. [Medline].

17. Boden BP, Kirkendall DT, Garrett WE Jr. Concussion incidence in elite college soccer players. Am J Sports Med. Mar-Apr 1998;26(2):238-41. [Medline].

18. Jordan SE, Green GA, Galanty HL, Mandelbaum BR, Jabour BA. Acute and chronic brain injury in United States National Team soccer players. Am J Sports Med. Mar-Apr 1996;24(2):205-10. [Medline].

19. Tysvaer AT, Storli OV, Bachen NI. Soccer injuries to the brain. A neurologic and electroencephalographic study of former players. Acta Neurol Scand. Aug 1989;80(2):151-6. [Medline].

20. Daniel JC, Olesniewicz MH, Reeves DL, et al. Repeated measures of cognitive processing efficiency in adolescent athletes: implications for monitoring recovery from concussion. Neuropsychiatry Neuropsychol Behav Neurol. Jul 1999;12(3):167-9. [Medline].

21. Vagnozzi R, Tavazzi B, Signoretti S, et al. Temporal window of metabolic brain vulnerability to concussions: mitochondrial-related impairment--part I. Neurosurgery. Aug 2007;61(2):379-88; discussion 388-9. [Medline].

22. Tavazzi B, Vagnozzi R, Signoretti S, et al. Temporal window of metabolic brain vulnerability to concussions: oxidative and nitrosative stresses--part II. Neurosurgery. Aug 2007;61(2):390-5; discussion 395-6. [Medline].

23. Schulz MR, Marshall SW, Mueller FO, et al. Incidence and risk factors for concussion in high school athletes, North Carolina, 1996-1999. Am J Epidemiol. Nov 15 2004;160(10):937-44. [Medline].

24. Powell JW, Barber-Foss KD. Traumatic brain injury in high school athletes. JAMA. Sep 8 1999;282(10):958-63. [Medline]. [Full Text].

25. Hinton-Bayre AD, Geffen GM, et al. Concussion in contact sports: reliable change indices of impairment and recovery. J Clin Exp Neuropsychol. Feb 1999;21(1):70-86. [Medline].

26. Busse EW, Silverman AJ. Electroencephalographic changes in professional boxers. J Am Med Assoc. Aug 23 1952;149(17):1522-5. [Medline].

27. Kaplan HA, Browder J. Observations on the clinical and brain wave patterns of professional boxers. J Am Med Assoc. Nov 20 1954;156(12):1138-44. [Medline].

28. Cifu DX, Kaelin DL, Wall BE. Deep venous thrombosis: incidence on admission to a brain injury rehabilitation program. Arch Phys Med Rehabil. Nov 1996;77(11):1182-5. [Medline].

29. Cantu RC. Return to play guidelines after a head injury. Clin Sports Med. Jan 1998;17(1):45-60. [Medline].

30. Cantu RC. Second-impact syndrome. Clin Sports Med. Jan 1998;17(1):37-44. [Medline].

31. Cantu RC. Second impact syndrome: immediate management. Physician Sportsmed. 1992;20:55-60.

32. Kelly JP, Rosenberg JH. The development of guidelines for the management of concussion in sports. J Head Trauma Rehabil. Apr 1998;13(2):53-65. [Medline].

33. Clarke KS. Epidemiology of athletic head injury. Clin Sports Med. Jan 1998;17(1):1-12. [Medline].

34. De Beaumont L, Lassonde M, Leclerc S, Théoret H. Long-term and cumulative effects of sports concussion on motor cortex inhibition. Neurosurgery. Aug 2007;61(2):329-36; discussion 336-7. [Medline].

35. Delaney JS, Lacroix VJ, Leclerc S, Johnston KM. Concussions during the 1997 Canadian Football League season. Clin J Sport Med. Jan 2000;10(1):9-14. [Medline].

36. Harad FT, Kerstein MD. Inadequacy of bedside clinical indicators in identifying significant intracranial injury in trauma patients. J Trauma. Mar 1992;32(3):359-61; discussion 361-3. [Medline].

37. Macciocchi SN, Barth JT, Littlefield LM. Outcome after mild head injury. Clin Sports Med. Jan 1998;17(1):27-36. [Medline].

38. Masters SJ, McClean PM, Arcarese JS, et al. Skull x-ray examinations after head trauma. Recommendations by a multidisciplinary panel and validation study. N Engl J Med. Jan 8 1987;316(2):84-91. [Medline].

39. McCrory P. Does second impact syndrome exist?. Clin J Sport Med. Jul 2001;11(3):144-9. [Medline].

40. McCrory PR, Berkovic SF. Second impact syndrome. Neurology. Mar 1998;50(3):677-83. [Medline].

41. McQuillen JB, McQuillen EN, Morrow P. Trauma, sport, and malignant cerebral edema. Am J Forensic Med Pathol. Mar 1988;9(1):12-5. [Medline].

42. Slobounov S, Slobounov E, Sebastianelli W, Cao C, Newell K. Differential rate of recovery in athletes after first and second concussion episodes. Neurosurgery. Aug 2007;61(2):338-44; discussion 344. [Medline].

43. Stewart DG, Cifu DX. Neuroendocrinologic management after TBI. Phys Med Rehabil Clinics N Am. 1997;8(4):827-42.

44. Sturmi JE, Smith C, Lombardo JA. Mild brain trauma in sports. Diagnosis and treatment guidelines. Sports Med. Jun 1998;25(6):351-8. [Medline].

45. Vegso JJ, Lehman RC. Field evaluation and management of head and neck injuries. Clin Sports Med. Jan 1987;6(1):1-15. [Medline].

46. Warren WL Jr, Bailes JE. On the field evaluation of athletic head injuries. Clin Sports Med. Jan 1998;17(1):13-26. [Medline].

From eMedicine.com. Reprinted with permission. www.emedicine.com/sports/TOPIC113.HTM.

Comments [5]

Dear Sharon,

My friend went to a physical therapist recommended by her Neuro MD . the PT was able to get the crystals in her inner ear back in to the proper canals by using eye movement and gentle head manipulations..this helped her dizzy episodes.Apparently the concussion can cause the salt crystals to be dislodged and migrate in to the wrong canals which causes the nausea and dizziness. Best wishes with your healing.

Carol

Apr 7th, 2014 11:29am

I sustained many beatings as a child resulting in loss of consciousness and I know for a fact I also had many broken bones that never healed. I am in my 30's now and my life is a mess, i can't work, I have no friends, I have dysphagia, can't walk, am irritable, I light a cigarette and forget so I light another one, I can't do up buttons, I can't think properly I just wish I knew what was going on. Does anyone know the long term effects of repeated blows to the head in children?

Jun 27th, 2013 6:17am

Have you done any studies in children? My now four year-old hits his head frequently, probably a good blow once every-other-week. He is very prone to it. I have two other kids and they rarely do this. We are concerned about long-term effects. He has never lost consciousness. Any information would be helpful. We also plan on talking with our pediatrician.

Jul 24th, 2012 11:36am

I suffered from migraines for years due to perimenapausal symptoms. then in may of 2010 i sustained my first concussion. it was really terrible and i walked around not knowing a thing, what had happened, what i should do and so on. two days ago i sustained another blow to the head in the same place my first concussion/contusion was. i am very grateful for a website like brainline to help those who are left to find their own way through the dark. i can already tell this is going to be really bad. so i\'m praying

Oct 2nd, 2011 8:13pm

It has been a month, since I hit my head on the ice. I suffered the first concussion approx. 3 years ago. I still have dizziness,nausea,headaches,neck pain, loss of balance,focusing and sleep problems. When will these symptoms from the concussion go away. I had a CT scan and there was no bleeding, in which I'm grateful. The Dr. said I have a concussion. Should I go back to the Dr. or wait it out. I am not able to drive and I want my life to get back to NORMAL!!!!!!!!!!!!!!My family have been very helpful throughout this. If you have any ideas or information that might help me, I would appreciate it. Sharon

Mar 7th, 2010 2:41pm


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