Volume 5, Issue 1
Andrew Reisner, M.D., F.A.C.S., F.A.A.P.; Natalie Tillman, R.N., B.S.N.; Linda Cole,
R.N.; Elizabeth Atkins, R.N.; Greg Pereira, R.N., B.S.N., M.B.A., Mary Thacher, R.N.,
Concussion is currently a high-profile topic that is receiving intense
media attention. Numerous recent front page articles in major lay
publications, and other news outlets are devoted to this subject.23 This
attention is deserved.
The known statistics are frightening. Approximately 3.8 million
concussions are sustained in the U.S. per year.23 The fact that there
are millions more unreported or unrecognized concussions makes this
issue even more concerning. Although the true statistics of this problem
are not known, it is a health problem of unquestionably epidemic
Concussions are an emotional issue, as they often involve a youth in
his or her prime, be they athletes or not. Concussions probably occur
more commonly now than in the past given the increasingly competitive
nature of sports at all levels. Recent evidence suggests that
concussions may be associated with permanent neurologic
consequences, which only adds to the concern of this disturbing trend.
Head injuries have been part of human existence since the dawn of man. Fossilized craniums of
prehistoric skulls were found with evidence of traumatic brain injuries (TBI).
Hippocrates (460 BCE to 377 BCE), the father of medicine, offered great insight into a variety of diseases
and complicated pathophysiological processes, including TBI.3 He wrote a treatise on Wounds in the
Head. He described different types of cranial trauma and placed special emphasis on the value of "taking
the medical history," from either the patient or a witness. Hippocrates used the accompanying symptoms
to assess major or minor cranial injuries, direct to treatment and to prognosticate. For example, he found
that a history of falling to the ground, losing consciousness, blurred vision or vertigo suggested a poor
prognosis. In his treatise, he describes first aid, bandaging the head and the importance of palpating the
skull wound, even exploring it with a "probe" or "sound." It is noteworthy that trephination, a small burr
hole craniectomy, was described in that manuscript and is still one of the most popular procedures
performed in contemporary neurosurgery.
Hippocrates’s admonitions of the importance of getting an adequate history, thorough analysis of the facts
and instituting appropriate treatments are as applicable now as when first described.
Definitions and grading of coma and concussion
Coma is difficult to define. Consciousness is not simply an on-or-off issue as there are many intermediate
degrees of wakefulness between extremes. According to respected researchers in the field, Plum and
Posner, “Consciousness is the state of awareness of the self and the environment and coma is it’s
opposite.”4 Descriptive terms used to describe comatose patients, such as stuporous, dazed or confused,
are subjective and associated with significant interobserver variability, and they are unreliable and
In 1974, Teasdale and Jennet introduced a coma scoring system that has found widespread acceptance,
the Glasgow Coma Score (GCS).5 It has excellent predictive value and has minimal interobserver
variability. The score is obtained from the sum of three parts: motor response, verbal and eye-opening
(Table 1).
Table 1.
Glasgow Coma Scale (GCS)—adapted from Wikipedia
Makes no
Extension to painful
stimuli (decerebrate
Abnormal flexion
to painful stimuli
Flexion /
Withdrawal to
painful stimuli
Makes no
Does not
open eyes
Opens eyes in
Opens eyes in
Opens eyes
response to painful
response to voice spontaneously
Best motor response (M)
There are six grades starting with the most severe:
Obeys commands—Patient does simple things as asked.
5. Localizes to pain—Purposeful movements toward painful stimuli e.g., hand crosses midline and
gets above clavicle when supra-orbital pressure is applied.
4. Flexion/withdrawal to pain—Flexion of elbow, supination of forearm, flexion of wrist when
supra-orbital pressure is applied. Patient pulls part of body away when nail bed is pinched.
3. Abnormal flexion to pain—Adduction of arm, internal rotation of shoulder, pronation of forearm
and flexion of wrist, and the patient has a decorticate response.
2. Extension to pain—abduction of arm, internal rotation of shoulder, pronation of forearm and
extension of wrist, and the patient has a decerebrate response
1. Patient has no motor response.
Best verbal response (V)
There are five grades starting with the most severe:
5. Oriented—Patient responds coherently and appropriately to questions, such as the patient’s
name and age, where they are and why, the year and month.
4. Confused—Patient coherently responds to questions, but there is some disorientation and
3. Inappropriate words—Patient makes random or exclamatory articulated speech but no
conversational exchange.
2. Incomprehensible sounds—Patient moans but no words.
1. Patient has no verbal response.
Best eye response (E)
There are four grades starting with the most severe:
4. Patient’s eyes open spontaneously.
3. Eye-opening to speech—Not to be confused with an waking a sleeping person, these patients
receive a score of 4, not 3.
2. Eye-opening in response to pain—Patient responds to pressure on the patient’s fingernail bed.
If this does not elicit a response, supraorbital and sternal pressure or rub may be used.
1. Patient does not open his eyes.
The GCS range is from 3 (deeply comatose) to 15 (fully awake). The degree (severity) and categorization
of the TBI is based on degree of the coma.
Table 2.
Definition of TBI severity (mild, moderate or severe)
Grade of TBI
Severe TBI
Moderate TBI
9 to 12
≥ 13
The term concussion is derived from the Latin word concutere, to strike together. Although all involved in
this field generally know what concussion means, to date, there is no single definition that is universally
accepted. As with the definition of coma, the definition and grading of concussion is seemingly
straightforward, but it has been debated among many. The 1993 American Congress of Rehabilitation
Medicine (ACRM) Mild Traumatic Brain Injury Committee was the first organized interdisciplinary group to
advocate for specific criteria for the diagnosis of concussion and mild TBI. This ACRM definition of
concussion is widely used and states .
Concussion is a traumatically induced physiological disruption of brain function, as manifested by at least
one of the following:
Any loss of consciousness
Any loss of memory for events immediately before or after the accident
Any alteration in mental status at the time of the accident e.g., feeling dazed, disoriented or
Focal neurological deficits that may or may not be transient
The severity of the injury does not exceed the following:
Loss of consciousness for approximately 30 minutes or less
After 30 minutes, an initial GCS of 13 to 15 and posttraumatic amnesia not greater than 24 hours
It is important that other causes of alterations in level of consciousness be excluded. These include drug
and alcohol toxicity, medication over-dosages or any non-neurological physical injuries or co-existing
medical diseases.
Grading a concussion
There is some controversy whether grading a concussion is beneficial or clinically useful. For those that
do, the concussion grading system forwarded by the American Academy of Neurology is widely used.
Table 3.
Concussion Grading Scale
Grade 1
No loss of consciousness, transient confusion and symptoms resolve in less than 15 minutes.
Symptoms include headache, dizziness and mental status changes e.g., inability to focus
attention or post-traumatic amnesia.
Grade 2
No loss of consciousness, transient confusion and symptoms of mental changes that last
more than 15 minutes.
Grade 3
Loss of consciousness, either seconds or minutes.
Postconcussion syndrome
Although the symptoms associated with concussion have been recognized for centuries, the term
postconcussion syndrome was first used in 1934. It refers to a constellation of symptoms that may
persist 24 hours following a TBI. These symptoms may include some or all of the following; headache,
irritability, inability to concentrate, memory impairment, generalized fatigue, dizziness or generalized loss
of well-being. Commonly, the course is self-limiting and resolves within months of the incident. While
present, the postconcussion syndrome may affect daily activities.
Subconcussion refers to a trauma induced injury to the brain with negligible, if any symptomatology.
These injuries are frequently unrecognized.
Repetitive TBIs and the “second impact syndrome”
Second impact syndrome (SIS) is rare and potentially fatal. SIS occurs when a patient who has sustained
an initial head injury, most often a concussion, sustains a "second head injury before symptoms
associated with the first are fully cleared." The pathophysiology in severe forms of SIS includes
increased cerebral vascular congestion and swelling, which can result in herniation or death, if severe.
It is not known how many concussions are too much. However, there does appear to be a dose curve,
when after a certain number of TBIs, permanent damage may occur. There may be a genetic
predisposition that exaggerates the effects of TBIs. Current genetic research is focusing on a gene that
codes ApoE, a protein involved in Alzheimer’s disease.
The developing brain may be especially vulnerable to a TBI. Not only can trauma affect the structure of a
child’s brain, but it also negatively influences further development and maturation.
Chronic traumatic encephalopathy and dementia pugilistica
Chronic traumatic encephalopathy (CTE) is a progressive degenerative disease found in individuals who
had multiple TBIs. A variant is dementia pugilista found in boxers. The clinical syndrome is characterized
by early senility and Parkinson-like movement disorder. It may lead to chronic disability.
The brains of patients with CTE contain an abnormally large amount of tau proteins. Tau proteins
maintain the structure of microtubles within nerve cells. They are implicated in the pathogenesis of
degenerative diseases such as Alzheimer’s disease. In cases of TBI, tau proteins are released from
injured nerves and accumulate within the brain substance.
The pathophysiology of concussion is the subject of intense investigation. Numerous theories have
been forwarded to explain the neurologic dysfunction, especially the immediate loss of consciousness. To
date, none have found universal acceptance. These theories include the following:
Vascular Hypothesis – suggests that concussion is due to cerebral hypo-perfusion. It is now
discredited as more recent animal studies have demonstrated concussive states with normal
blood flow.
Convulsive hypothesis—attributes concussion to generalized neuronal firing. This theory is
supported by the fact that concussion is characterized by a period of cerebral hyperexcitability
followed by a longer period of EEG depression acutely after head injury.
Centripetal hypothesis—suggests that in cases of MTBI, there is actual neuronal disruption
caused by shear forces.
Pontine cholinergic theory—supports the notion that activation of cholinergic neurons in the
brainstem causes concussive symptoms.
Reticular theory—suggests that the angular acceleration/deceleration process involved in TBI
disrupts the physiology of the brainstem reticular formation activity. The brainstem reticular
activating system is responsible for wakefulness.
Whatever the pathophysiologic mechanism, it appears a chain of events is initiated following mechanical
injury to the brain. On a chemical level, N-methyl-D-aspartate (NMDA) receptors are activated after
trauma, which impairs oxidative metabolism, leading to energy failure. There are other neurochemical
changes, including a decrease in Gabba Amino Butyric Acid (GABA) and other inhibitory
neurotransmitters. On a cellular level, this may include a number of pericellular and intracellular changes,
including dysfunction of the neuronal membrane and axons. This may lead to an increase in extracellular
potassium and release of excitatory neurotransmitters. This has been termed neurotransmitter storm. In
more severe cases, there is a physical disruption of the nerve cells and axons.
Alterations in cerebral blood flow regulation appear to be involved in the pathophysiology of TBI,
especially in cases where there is cerebral edema.
It is hoped that an understanding of these events will lead to newer and more efficacious treatments.
Clinical manifestations
The symptoms of concussion are often more elusive than moderate or severe TBIs. This makes the
diagnosis of concussion difficult, especially if the symptoms resolve quickly, and there are no visible
objective signs or abnormal radiographic features. It is worth mentioning that only one-tenth of patients
who sustain a concussion lose consciousness.
The symptoms of concussion fall into three categories; somatic, cognitive and emotional.
• Somatic symptoms—include headache, nausea, vomiting, balance problems, dizziness, visual
problems, fatigue, sensitivity to light, sensitivity to noise, numbness or tingling and sleeping more
or less than usual.
• Cognitive symptoms—include feeling mentally foggy, feeling slowed down, difficulty
concentrating, difficulty remembering, confusion or disorientation.
• Emotional manifestations—include irritability, sadness, being/feeling more emotional than usual
and nervousness. Most symptoms increase with both physical and mental exertion.
Risk factors for protracted recovery include prior concussion, history of headaches, such as migraine, as
well as developmental history issues, such as learning disabilities, attention deficit hyperactivity disorder
and other developmental disorders. In addition, a protracted recovery can occur with anxiety and a prior
psychiatric history.
Each patient recovers from a concussion in a unique and differing manner. This may reflect differing
degrees of mechanical force applied to the brain, differing vectors and angulations and differing
susceptibility. The latter has been the subject of research. Some individuals may have an exaggerated
response following a concussion compared to others, suggesting a genetic influence. Females tend to
have more protracted postconcussive symptoms than males, suggesting a hormonal influence on the
speed of recovery. It appears that, for as of yet unknown reasons, females are more at risk for SIS than
Most commonly, concussion is diagnosed clinically based on the analysis of symptoms and signs as
taught to us by Hippocrates. The clinical assessment of children with concussion is currently being
standardized at Children’s Healthcare of Atlanta. It is based on the Acute Concussion Evaluation (ACE)
from the Centers for Disease Control and Prevention. Usually, no further testing is needed. However, if
the patient is not making the expected rapid recovery, or if in the case of athletes, “return to play” is an
issue, further testing may be warranted. Further tests may be radiologic, neuropsychological or
A. Radiologic
In the setting of TBI, computed tomography (CT) is the initial radiographic study of choice. Any lesions
which may require prompt surgical evaluation, such as an epidural hematoma, can be diagnosed on a
head CT. Currently, evidence-based guidelines for the use of CT in children who have sustained a
concussion are being introduced at Children's Healthcare of Atlanta. The guide for obtaining a head CT
scan for these children include a GCS of less than 15, altered mental status, evidence of a skull fracture
or seizure. Additional indications for obtaining a head CT are the clinical red flags listed in Table 3.
Magnetic resonance imaging (MRI) is rarely indicated immediately following a concussion. However, it
has proved to be useful in evaluating those with postconcussive syndrome and as a research tool. MRI is
a more sensitive imaging modality than CT. Specific MRI sequences have been found to be particularly
useful in the diagnosis of TBI. These include T2-weighted images, fluid attenuation inversion recovery
(FLAIR MRIs), and gradient echo MRI, which is sensitive at detecting hemorrhage. Diffusion weighted
imaging (DWI) has been shown to be even more sensitive at identifying shear injuries not evident on T2
or FLAIR or gradient echo sequences.
Despite the sophistication of the MRI, to date, studies have not shown a good correlation between
abnormal MRI findings and postconcussive symptoms or long-term outcomes.
MRI is a useful tool in TBI research. For example, diffusion tense imaging (DTI) may identify critically
injured neuronal pathways. Functional MRI (fMRI) is another MRI technique that has promise. The fMRI
demonstrates physiology, which is correlated to function as well as anatomy. The fMRI can be tailored to
collect data on the physiological substates involved with other neurologic functions, such as executive
skill, motor or vision areas, that may be affected in TBI. Association, or relay integrative areas can be
studied as well. It has been shown that after concussion, patients had less activation in the prefrontal
cortex than comparison subjects.
Positron emission tomography (PET) and single photon emission computed tomography (SPECT) have
demonstrated metabolic disturbances following concussion at rest and during memory tests. Their role
in TBI research remains undetermined.
B. Neuropsychological testing
Neuropsychological testing plays an integral role in the evaluation of patients who have sustained a
concussion and are used both immediately and in a follow-up setting.
Methods of testing range from sideline clinical assessments to computer-based inventories. There are a
variety of clinical neuropsychological tests that can be done in an outpatient setting. Typically, these tests
measure cognitive skills, including immediate and delayed recall, orientation, verbal memory, attention
span, word fluency, visual scanning and coordination. Computerized tests include the Immediate Post
Concussion Assessment and Cognitive test (ImPACT). The results of the postinjury test are compared
to a baseline neuropsychological test obtained for that individual or an age-matched control. These tests
allow more accurate guidance regarding degree of injury and allow informed decisions to be made
regarding resumption of activities.
C. Neurophysiologic testing
Standard electroencephalogram (EEG) techniques have not proved to be useful in concussion
management. This is disappointing as that there are EEG changes following a concussion that suggest a
potential EEG-related pathophysiologic mechanism.
However, evoked potentials (EP) and event-related potentials (ERP) are more promising as diagnostic
and research tools for concussions. Both are obtained by measuring and averaging EEG response to
certain stimuli.
Magnetoencephalography (MEG) measures the neuromagnetic fields of the dendrites organized parallel
to the skull surface—as compared to EEG that measures potential gradients perpendicular to the skull
surface. So far, results indicate that MSI (magnetic source imaging), a technique that integrates
anatomic data from MRI with electrophysiological data from MEG, is very sensitive in diagnosing
postconcussive deficits.
Patients who have sustained a concussion require evaluation, monitoring and education. The concussion
is diagnosed and graded according to criteria given above.
During the initial evaluation, red flags that a more thorough evaluation is indicated (evaluation by PMD or
emergency department visit) include the following: (Table 4)
Table 4:
Red flags following a concussion—(adapted from Gioia)
Cannot recognize people or places
Change in state of consciousness
Focal neurological signs
Headaches that worsen
Increased confusion or irritability
Looks very drowsy and cannot be awakened
Neck pain
Numbness or weakness in the arms or legs
Repeated vomiting
Slurred speech
Unusual behavioral changes
The mainstay of treatment of a patient who has sustained a concussion is rest, both physical and mental.
Given that no two patients or concussive events are alike, these recommendations need to be
individually tailored.
There are several return-to-play guidelines that have been developed. There are slight differences in the
definition of grades of concussion and recommendations. The commonly quoted guidelines include the
Roberts, Cantu, Colorado and American Academy of Neurology guidelines. There is simply no
evidence based data to support one rather than the other. More recently at Children’s Healthcare of
Atlanta, a stepwise return-to-play guideline is used, as advocated by many including the American
Academy of Pediatrics. (Table 5)
Regardless which guideline is used, all children are required to limit physical activity and scholastic
activities while symptomatic.
The advantage of the stepwise return to play guideline is that it individualizes the activity level to the
patient’s recovery rather than mandate a set time that may not be appropriate for that patient. Typically,
the patient progresses though each stage every 1 or 2 days. This may be extended at any stage if
symptoms return. On occasion, backtracking to a less strenuous preceding stage may be needed.
Table 5
Concussion Rehabilitation/Stepwise Return to Play
Rehabilitation stage
Functional exercise
1. No activity
2. Light aerobic activity
1. Complete physician and cognitive rest
2. Walking, swimming, stationary cycling at 70
percent maximum heart rate; no resistance
3. Specific sport-related drills but no head impact
4. More complex drills, may start light resistance
5. After medical clearance, participate in normal
6. Normal game play
3. Sport-specific exercise
4. Noncontact training drills
5. Full-contact practice
6. Return to play
While “return-to-play” guidelines are becoming more accepted and widely instituted, this is not the case
for return to scholastic activity. The brain uses approximately 25 percent of the body’s energy, 20 percent
of cardiac output and 25 percent of oxygenation. The cerebral energy demand is increased during
mental activity. Given that energy is required for the brain to self-repair following concussion, any
increased demand may hamper the reparative processes. Patients should be advised not to engage in
strenuous mental activities while symptomatic. Schooling should be deferred, and stimulating activities,
such as watching TV, playing video games and texting, avoided until asymptomatic, at least. It is not
clearly defined how long these patients should refrain from vigorous mental activity following a TBI. In a
paper presented by the Second International Conference on Concussion in Sport in 2004, it was
suggested that return to baseline profile on neuropsychological testing is the most sensitive indicator of
resolution of postconcussive symptoms. Thus, neuropsychological testing, rather than resolution of
symptomatology, may be the best guide of return to mentally challenging tasks.
The treatment of post concussive symptoms can be problematic. We typically treat minor headaches with
over the counter analgesics. If this fails, a short course of oral narcotics may be used. Patients with
chronic post traumatic headaches may also respond to anti-depressive and/or anti-convulsive
medications. DHA omega-3 fatty acid is being investigated as a drug to prevent and treat concussions,
but does not as yet have widespread usage. Aspirin should be avoided. Although the indications for
steroids has not been established, a short course may be useful in the early stages following a
concussion. If the post-traumatic headache has a migrainous component, anti-migrainous treatment
including the Raskin protocol, has met with some success (unpublished data).
Early seizures immediately following a TBI are more common in children than adults. They are often a
major source of concern, but typically do not predispose the patient to a permanent seizure disorder. We
usually do not advocate anti-epileptic drugs for early posttraumatic seizures.
Education of the patient and family is the key to maximizing compliance with recommendations and
improving the outcome. Myths need to be dispelled. For example, it is important that the patient
understand that although the manifestations of concussion are usually brief, long-term consequences are
possible, especially in cases of multiple concussions. Other commonly heard misconceptions that should
be corrected include that trauma predisposes the development of brain tumors and seizures.
Potential complications of a TBI that may present in a delayed fashion include academic decline or
behavioral difficulties months or years after the event. Early detection of these disturbances and a
neuropsychological referral can positively influence the outcome. The patient and family must be made
aware of these late manifestations of a TBI and be encouraged to seek help if they develop.
It is critical to give individual counseling. While there is a large amount of printed literature and discharge
instructions, there is no substitute for personal counseling. It allows the patient and family to voice their
concerns and dispel any misconceptions. The importance of adhering to return to activities and sport
guidelines cannot be emphasized enough. The family needs to act as extenders, so that any red flags
(Table 3) can be detected and addressed in a timely fashion. It is important to prevent secondary injuries
and safety-oriented behavior should be prescribed, such as using automobile restraints and bicycle
Judgments regarding returning to play and activities cannot be left to the individual, who may have needs
and pressures that conflict with an adequate and appropriate post-TBI rest time. Physicians, parents,
coaches and schools need to be involved in the treatment plan.
Legislation at school, college, professional sports organizations, and states are being introduced to
enforce these guidelines and prevent unnecessary, potentially permanent brain injuries that can occur
from repetitive TBIs.
For some patients with a TBI, the term minor is a misnomer. This was clearly brought to our attention in a
landmark paper written by Rimel et al. in 1981. In this study, 538 adult patients who sustained a minor
head injury were examined at three months after the injury. The authors found a high rate of morbidity
and unemployment in patients 3 months after a seemingly insignificant head injury. Fifty-nine percent had
memory problems and 79 percent complained of persistent headaches. Of patients who had been
gainfully employed before the accident, 34 percent were unemployed. This, and similar papers alerted the
medical community that concussion and mTBI may be associated with significant consequences.
Although large, long-term prospective studies looking at the prognosis of children who have sustained a
concussion are unavailable, it is apparent that most make a full recovery. Although the incidence of
postconcussive syndrome is low, probably less than 10 percent of all those that have a mTBI, they
represent an important group to identify as remediation may be beneficial.
Future research
Greater public awareness of concussion has heightened the need to have basic questions answered.
These include clinical questions, such as the best practice regarding return to activity and play guidelines,
and identifying appropriate role for imaging and neuropsychological testing. Future studies will hopefully
identify those at risk for delayed consequences, such as postconcussive syndrome and SIS. There is a
body of literature that has shown that biochemical markers may be useful to grade the degree of head
injury. These include S100B that is a marker of astroglial tissue and neuron-specific enolase (NSE),
which is a marker of neuronal tissue. It is hoped that research will identify a simple serologic test that
may be used for prognostication following a concussion.
Ultimately, an understanding of the pathophysiogical mechanisms involved in TBI will be needed. It is
hoped that an understanding of the molecular and cellular chain of events initiated by mechanical injury to
the brain, will allow for the development of new treatments.
1. The American Heritage Dictionary of the English Language, Fourth Edition, 2000.
2. Ruff, RM, Iverson, GL, Barth, JT, Bush, SS, Broshek, DK, and NAN Policy and Planning
Committee; Recommendations for Diagnosing a Mild Traumatic Brain Injury: National
Academy of Neuropsychology Education paper. Archives of Clinical Neuropsychology, 24:310, 2009.
3. Panourias TG, Skiadas, PK, Sakas, DE, Marketos, SG; Hippocrates: A Pioneer in the Treatment
of Head Injuries. Neurosurgery 57:181-189, 2005.
4. Plum, Fred and Posner, Jerome B, “Plum and Posner’s the Diagnosis of Stupor and Coma” Third
edition F.A. Davis Company 1987.
5. Teasdale G, Jennett B; . Assessment and prognosis of coma after head injury Acta Neurochir
(Wien). 1976;34(1-4): Pages 45-55.
6. Mendez, CV, Hurley, RA, Lowsonde, N, Zhang, L, Tabor, KH; Mild Traumatic Brain Injury:
Neuroimaging of Sports Related Concussion, Journal of Neuropsychiatry, Clin Neurosci 17:3,
page 297-303, 2005.
7. McCrory, P, Does Second Impact Syndrome Exist? Clin J Sports Med, 2001; 11:144-149, 2001
8. Cantu, RC, Voyr: Second Impact Syndrome: A Risk in any Contact Sport. Phys Sports Med
23:27-34, 1995.
9. Gioia, GN, Cowlin MP. Adapted from acute convulsion evaluation toolkit - available on CDC
website "Heads Up: Brain Injury in Your Practice"
10. Kuppermann, N, Holmes, JF, Dayan, PS, et al: Identification of children at very low risk of
clinically important brain injuries after head trauma, a prospective cohort study - Lancet
374:1160-1170, 2009.
11. Hughes, DJ, Jackson, A, Mason, DL, et al: Abnormalities on Magnetic Resonance Imaging Seen
Acutely Following Mild Traumatic Brain Injury: Correlation with Neuropsychological Tests and
Delayed Recovery. Neuroradiology 46:555-558, 2004.
12. Huisman, TAGM, Sorensen, AG, Hergan, K et al; Diffusion Weighted Imaging for the evaluation
of diffuse external injury in closed head injury, Journal Comput Assist Tomogr 27:5-11, 2003.
13. Arfanakis, K, Haughton, VM, Carew, JD, et al.: Diffusion Tensor MR imaging in diffuse axonal
injury, AJNR 23:794-802, 2002.
14. Iverson, GL, Lovell, MR, Collins, MW: Interpreting Changes on ImPACT Following Sports
Concussion. Clin Neuropsychol 17:460-467, 2005.
15. Pellman, EJ, Lovell, MR, Viano DC, et al: Concussion in Professional Football:
Neuropsychological Testing - Part 6. Neurosurgery 55:1290-1305, 2004.
16. Lewine, JD, Davis, JT, Sloan, JH et al: Neuromagnetic assessment of pathophysiologic brain
activity induced by minor head trauma. 20:857-866, 1999.
17. Patel, DR, Shivdasani, V, and Baker, RJ; Management of Sports-Related Concussion in Young
Athletes. Sports Med 35 (8-page, 671-684, 2005).
18. Rimel, RW, Giodani, B, Barth, JT, Bowl, TJ, and Jane, JA; Disability caused by minor head injury.
Neurosurgery, Vol. 9, #3, 1981, Pages 221-228.
19. Mehta, SS, Biochemical Serum Markers in Head Injury, An Emphasis on Clinical Utility - Clinical
Neurosurgery, Vol. 57, Pages 134-140, 2010.
20. Straume-Naesheim, T, Anderson, THE, Jochum, M, et al, Minor Head Trauma in Soccer and
Serum Levels of S100B, Neurosurgery 62:6, 2008, Pages 1297-1306.
21. Paul McCrory, Willem Meeuwisse, Karen Johnston, Jiri Dvorak, Mark Aubry, Mick Molloy and
Robert Cantu (2009) Consensus Statement on Concussion in Sport: The 3rd International
Conference on Concussion in Sport Held in Zurich, Nov. 2008. Journal of Athletic Training:
Jul/Aug 2009, Vol. 44, No. 4, Pages 434-448.
22. Harmon, KG: Assessment and management of concussion in sports. American family physician.
Sept 1999.
23. Kluger J; Headbanger nation. Concussions are clobbering US kids. Here’s why. Time magazine.
Pages 42-51 Jan. 31, 2011.
24. Mannix RC, Zhang J, Park J, Zhang X, Bilal K, Walker K, Tanzi RE, Tesco G, Whalen MJ. Agedependent effect of apolipoprotein E4 on functional outcome after controlled cortical impact in
25. Mills JD, Bailes JE, Sedney CL, Hutchins H, Sears B.; Omega-3 fatty acid supplementation and
reduction of traumatic axonal injury in a rodent head injury model. J Neurosurg. 2011
Jan;114(1):77-84. Epub 2010 Jul 16.
26. Broshek DK, Kaushik T, Freeman JR, Erlanger D, Webbe F, Barth JT. Sex differences in
outcome following sports-related concussion. J Neurosurg. 2005 May;102(5):856-63
27. Ganong WF: Review of Medical Physiology. Eighth edition Lange medical publications, Los Altos
CA 94022
28. Halstead, Mark E., Walter, Kevin D., and the Council on Sports Medicine and Fitness, “Sportrelated Concussion in Children and Adolescents,” Pediatrics 2010; VOL 126; 605; originally
published Aug 30, 2010; DO I: 10.1542/peds.2010-2005.
29. Miele VJ, Bailes J.E.; Mild Brain Injury. Chapter 9, page 175 – 207; In Neuro Trauma and Critical
Care of the Brain. Jallo J, Loftus, CM (EDS); Theme, 2009.
30. Gioia, Gerard A. PhD; Collins, Michael PhD; Isquith, Peter K. PhD; Improving Identification and
Diagnosis of Mild Traumatic Brain Injury with Evidence: Psychometric Support for the Acute
Concussion Evaluation. J Head Trauma Rehabilitation. 2008 Jul – August; pages 23 and
32. Logan, K; Cognitive Rest Means I Can’t Do What?!: Authentic Training and Sports Health Care.
VOL 1, No. 6, 2009. Page 251-252.
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