1

INTRODUCTION

In the past, athletes who suffered a hit to the head during an athletic event were told to

“shake it off” and get back out there. Today, this would not be the case. Thousands of athletes

around the world, participating in various athletic events all suffer from a common injury. Unlike

a broken bone that can fully heal within months, the side effects of a concussion, both short and

long-term, can have a serious impact on an athlete’s future, and have high potential to

permanently end one’s career. Concussions are a constant, high-risk threat to athletes across the

sporting world, especially athletes in high contact sports such as football and hockey, where the

risk of head injury is increased due to the nature of the game. Although the concern for

concussions in today’s world of sports is much greater than it was 25 years ago, Cusimano’s

(2009) research suggests that still, a significant number of players and adults do not know what a

concussion is or how it occurs. She states that approximately one-quarter of adults, and ¼ to ½ of

young athletes who were surveyed could only recall one symptom of a concussion (Cusimano,

2009). Additionally, Cusimano (2009) found that ¼ of these athletes did not know if a player

experiencing symptoms of a concussion should forego participation. Without the most basic

understanding of concussions, one cannot possibly begin to fathom the serious impacts this

injury can have on one’s life.

To begin understanding the neuroanatomy and physiology of a concussion, one must first

grasp a basic understanding of the injury itself. According to the American Association of

Neurological Surgeons (2005) a concussion is “a clinical syndrome characterized by immediate

and transient alteration in brain function, including alteration of mental status and level of

consciousness, resulting from mechanical force or trauma.” In a more general sense, one may

describe a concussion as the brain hitting rigid areas of the skull violently, thus impairing normal

2

brain function. King (2003) states that post-concussion symptoms include, but are not limited to,

headache, dizziness, fatigue, poor memory and/or concentration, irritability, depression, sleep

disturbance, nausea, and potentially loss of consciousness. Research completed over the past two

decades has provided illustrations of the physical damage concussions have on the brain that can

lead to the risk of developing neurodegenerative disorders later in life.

REVIEW OF LITERATURE

Post-Concussive Pathophysiology

A cerebral concussion is not as simple as being described as a blow to the head that

causes the brain to hit off the projections of the skull, causing “bruising” to the brain that

requires time to heal. Although the previous statement has some validity, it does not accurately

describe the neurometabolic cascade of a concussion. In 2001 Giza determined that immediately

following the impact to the head, an abrupt, involuntary release of neurotransmitters and ion

influxes occur. Glutamate, the main excitatory

neurotransmitter of the brain, is released in

large quantities, which essentially causes the

brain to overwork. The excessive increase in

glutamate concentration drives the Sodium-

Potassium Pump (Na+/K+ pump) to activate,

thus releasing potassium, and bringing more

sodium into the cell; a process that leads to increased neuronal depolarization (Giza, 2001).

Increased neuronal depolarization will offset the normal ranges of ionic concentrations,

membrane potential of cells, and permeability of ions in which the brain typically functions. The

Na+/K+ pump is a primary example of a pump that uses active transport; meaning this pump

Figure1.TheDisruptionofIonConcentration,andNeurotransmitterReleaseintheBrainImmediatelyFollowingaConcussion.

3

requires adenosine triphosphate (ATP) in order to function. Due to the sudden increase of

glutamate in the brain, there is a high demand on this pump, which results in the immediate

demand for a large supply of energy. How does the brain attain this much ATP with such short

notice? By reducing glutamate into glutamine and ATP (using glutamine synthase), the Na+/K+

pump is able to function. However, this does not occur without harm to the brain.

Giza’s research shows that after this initial period of hyperactivity and excess

neurotransmitter release comes a period of “depressed metabolism” (Giza, 2003). He found that

this cascade of events creates a severe energy crisis in the brain, which can lead to cell death and

impairment of neuronal connectivity (Giza, 2003). It is this impairment of neuronal function that

can lead to the loss of consciousness, blurred vision, and imbalance associated with traumatic

brain injury (Powell, 2001). Although these neuronal changes occur at the time of impact to the

head, they are unfortunately commonly accompanied by the later onset of additional life-

threatening changes in the brain. After the impact of the brain on the skull, the brain becomes

susceptible to bruising, torn blood vessels and nerve fibers damage (Frost, 2011). If any of these

sequelae occur, the individual suffering from a concussion may also be at a high risk for

developing a cerebral hemorrhage and/or elevated intracranial pressure as a result of cerebral

edema; very commonly characterized by prolonged suffering of concussion symptoms. As the

brain swells after impact with the skull, blood flow becomes more limited due to the brain and

blood vessels becoming compressed (Frost, 2011).

During this phase of the metabolic cascade of a concussion, the injured individual must

be extremely cautious that they do not suffer another blow to the head. If this were to occur,

cerebral edema could further increase, preventing oxygen and glucose reaching the brain, thus

having potential to prevent adequate blood supply to reach the brain, resulting in a stroke (Frost,

4

2011). If the concussed individual were to go back into competition before adequate healing time

was given the athlete could be at elevated risk to develop second impact syndrome. Second

impact syndrome is a rare condition in which a second concussion occurs before the first

concussion has properly healed. This results in rapid and severe cerebral edema, typically

resulting in sudden death. While it is true that many concussion symptoms fade within a few

days, it is extremely important to understand that if a second concussion occurs within the first

days or weeks after the initial concussion, the risk of developing second impact syndrome is very

high. Thus, caution needs to be taken post-injury in order to ensure the best possible healing of

the brain.

Physiological Damage

One of the hardest components of concussions to understand in the past was determining

the specific areas of the brain that are damaged when one suffers a traumatic brain injury (TBI).

The discussion and interest in sports related concussions received minimal attention until the

1990s, and since then it has been an ever-growing area of

concern in the world of sports and science. Perhaps the

reasoning behind this prior ignorance is that the actual damage

of a concussion cannot be seen like a broken arm; it is much

harder to determine the extent of a brain injury than it is a

broken bone or torn muscle. Although it was once thought that

a concussion was simply a temporary disturbance of

function without long-term consequences, it is now fully

understood that irreversible structural changes in the brain do occur (Jantzen, 2004). More

specifically, research completed by Kelly Jantzen (2004) had a strong focus on the functional

Figure2.BrainActivationinConcussedSubject(left)andControlSubject(right).

5

Magnetic Resonance Imaging (fMRI) differences between healthy and previously concussed

participants. Referring to Figure 1, Jantzen (2004) found that athletes who had suffered a

concussion during their season showed an increase in activation while being asked to perform a

bimanual sequencing task. While comparing those fMRI images of concussed individuals to the

control, it was determined that although non-concussed participants showed an increase in

activation of brain sites, the increase in concussed participants was significantly greater (Jantzen,

2004). The increases in brain activation in concussed participants were in regions that are

associated with executive functioning, including working memory and motor planning;

suggesting that it took concussed individuals more effort to properly execute the sequencing task

than it did the non-concussed participants (Jantzen, 2004). Jantzen’s reasoning for this increase

in activation in post-concussive participants is the axonal damage caused by concussions. Axonal

damage is thought to reduce the efficiency of processing in the brain once it suffers from a

concussion, meaning more neuronal resources are required to carry out the same function as a

healthy brain (Jantzen, 2004). The functional Magnetic Resonance Images produced showed

significant increase in activity in the medial frontal gyrus, inferior parietal lobe, and the bilateral

cerebellum (Jantzen, 2004). The functions of the parietal lobe include, but are not limited to:

working memory, storage and manipulation of numerical information. Additionally, the

cerebellum is significantly involved in preparing for, and carrying out complex motor

movements, as well as the timing of these tasks. As seen in the fMRI concussive forces damaged

these two areas of the brain, and thus the somatosensory cortex (in the parietal lobe) and the

cerebellum must create new pathways in order to carry out normal function.

The concern surrounding delayed, interrupted and/or excess brain activation and

sequencing has increased in recent years as evidenced by recent studies that show

6

neurophysiological changes in the brain after suffering from (a) concussion(s). In 2015, Coughlin

et al conducted a study on several National Football League players who had suffered several

concussions, specifically looking at the pathologic changes that produce chronic traumatic

encephalopathy (CTE). CTE, a

progressive degenerative disease of the

brain commonly found in athletes, raises

concern as researchers have found a

significant link between CTE and

neuropsychiatric consequences including

cognitive decline, mood and anxiety

orders (Coughlin et al, 2015). Similar to

the study completed by Jantzen in 2004, Coughlin et al (2015) also found changes in the medial

temporal, and parietal lobe structures, as well as cognitive deficits such as verbal learning and

memory. While analyzing functional Magnetic Resonance Images of the NFL players in

comparison to those of healthy controls, researcher’s observed a very significant difference, that

would later impact the development of neuropsychiatric problems (Coughlin et al, 2015). Images

showed that the translocator protein (TPSO), a marker of brain injury and repair, had an

increased amount of [11C] DPA-713 binding (Figure 2.) in the brain, which lead Coughlin and

her team (2015) to infer that the brain never truly heals after suffering from a concussion. Rather

than healing as a typical bone or muscle injury would, research shows that the neuroanatomical

damage caused by a concussion seldom reverses itself and heals back to 100% function (Iverson,

2012). This lack of healing can be seen in both short and long term examples of patients

suffering from mild head traumas. For example, Nigel King (2003) found diffuse microscopic

Figure3.Comparison of [11C]DPA-713 Binding in the Brains of Healthy Elderly Controls and Former NFL Players.

7

axonal injury in post mortem exams in patients who had suffered only one mild head injury.

Additionally, King (2003) states that within the first few weeks of injury, an MRI scan can show

cellular damage and metabolic abnormalities in various areas of the brain. The studies of King

and Iverson both suggest that more than just physical damage to the brain occurs during a

concussion, and that a great amount of evidence supports the idea that organic features, such as

diffuse microscopic axonal injury and abnormal cerebral blood flow, play a large role in the

neurophysical impairment of the brain post-concussion.

Short-Term Effects

Although medical professionals better understand many of the common short-term

symptoms of concussions, the importance of ensuring that adequate recovery time is given is of

utmost importance today in sports. As King (2003) stated, these post concussion symptoms

include headache, fatigue, poor memory and/or concentration, irritability, depression, sleep

disturbance, nausea and potentially loss of consciousness. Although it is most common that

many of these symptoms are present immediately after the time of impact, other symptoms may

take longer for the individual to fully notice (King, 2003). Each year, approximately 1.2 million

Americans report suffering from a head injury, and although the majority of these are classified

as mild traumatic brain injuries (MTBI), many people resume activity much too quickly and

jeopardize their own long-term health. Being that glucose is the main excitatory neurotransmitter

in the brain, this results in a lack of activation in many cortical pathways that develop our motor

movements and cognitive thinking abilities. More specifically, Giza et al (2001) found that

cerebral glucose is completely diminished by 24 hours after injury, and remains significantly low

for 5 to 10 days (in experimental animals).

8

The timeline of recovery for concussions must be assessed in regards to individual cases,

as recovery time strongly depends on several factors: the force of impact to the head, the prior

health of the individual, and history of previous concussions. For the majority, concussion

symptoms will subside within 7-10 days, however others are not so lucky. If the symptoms of a

concussion have not subsided within 10 days after the injury, the patient may be diagnosed with

Post Concussion Syndrome (PCS) (White, 2012). Patients with PCS may not continue to

experience all symptoms after 10 days, but generally experience severe headaches, dizziness and

irritability for weeks or months post-injury (White, 2012). The next level of damage is described

as having serious neurological deficits; severe brain swelling, bleeding in the brain, repeated

seizures and/or coma are common symptoms (White, 2012). Again, dependent on several factors,

these symptoms may be experienced up until one year post-injury for the patient to still be

classified as suffering from serious neurological deficits. Lastly, Chronic Traumatic

Encephalopathy (CTE) is a neurological disorder that is prevalent in individuals who have

suffered from multiple concussions. This neurological disorder may develop years to decades

after one’s last concussion, but can potentially have a serious impact on one’s quality of life.

Repeated concussions are the biggest worry for researchers today, as many individuals continue

to return to sport after suffering from one or more head injuries; a decision that may seem

acceptable at the time, but that one may regret in their later years of life.

Long-Term Effects- Neurological Disorders

Although more difficult to imagine, the real consequences of repeated concussions are

not usually experienced until ten to twenty years after the impact. The damage occurring to the

brain has a permanent impact on one’s neurological function, and with decreased function comes

the risk of developing several early-onset neurological disorders. Recent studies have shown a

9

correlation between TBI and chronic depression, with prevalence rates from 6% (mild TBI) to

77% (more severe TBI) (Guskiewicz, 2006). Although the studies of Guskiewicz et al (2006)

focused on World War II veterans, the concept of injury to the brain is still very relevant to the

world of sports. After accounting for several other possible causes for depression, Guskiewicz et

al (2006) discovered that there was an 18.5% lifetime prevalence of depression in individuals

who had suffered a head injury, versus the observed 13.4% lifetime prevalence for those with no

history of head injury. Applying these statistics to the world of sports, it can be simply stated that

repeated concussions permanently alter one’s brain function over time, and have the potential to

be a key risk factor in developing chronic depression later in one’s life.

Suffering from a Traumatic Brain Injury (TBI) opens up a new spectrum of possible

pathologic injuries if one continues to put

themselves in situations that make them

susceptible to repeated concussions. TBI,

causing diffuse axonal injury, mechanical tissue

damage, and neuronal dysfunction can quickly

become Mild Repetitive TBI or Severe TBI if

patients continue to re-injure the same areas of

their cortex (DeKosky et al, 2010). Figure 3

illustrates the progression of Traumatic Brain

Injury into later-onset, chronic

neurodegenerative disorders of the brain caused

by repeated concussions. As illustrated in this

diagram, Mild Repetitive TBI and Severe TBI both have a positive correlation for resulting in

Figure4.Spectrum of Pathologic Features and Outcomes of Traumatic Brain Injury

10

Dementia Pugilistica, CTE, Parkinson’s disease, and Alzheimer’s Disease- all of which are

classified as neurological disorders. Through research completed on human subjects, DeKosky et

al (2010) discovered that 20 to 30% of patients with Alzheimer’s or Parkinson’s disease have

suffered a single-incident traumatic brain injury, a statistic that is true in only 8 to 10% of the

control subjects. In an additional study completed by Hazrati et al (2013), researchers studied

post-mortem brains of six retired Canadian Football League players who all had history of

multiple concussions and significant neurological decline. Results showed all six subjects having

progressive cognitive decline prior to death, but the neuropathological findings varied (Hazrati et

al, 2013). Within the group of 6 participants Hazrati et al found three individual cases of

Alzheimer’s disease, a single case of Amyotrophic Lateral Sclerosis (ALS), and one case of

Parkinson’s disease. In addition to these findings, Hazrati et al also found that 50% of patients

showed post-mortem findings consistent with CTE. Since CTE can only definitively be

diagnosed in post-mortem autopsies, it is very important for researchers to document the cases in

which CTE correlates with multiple concussions. Symptoms of this neuropathological disorder

include memory loss, confusion, impaired judgment, impulse control problems, depression, and

eventually dementia (Hazrati et al, 2013). Hazrati’s research suggests that CTE is a disorder that

correlates to the onset of Alzheimer’s as each patient in this study that had CTE, also reported to

have many symptoms of this disease as well.

Alzheimer’s disease, a neurological disorder linked to severe traumatic brain injuries, is

another example of the long-term effects concussions may have on one’s life. Rudelli’s research

completed in 1982 was of the earliest to speculate that trauma to the head could potentially play

a provocative role in the alteration of neuroanatomy. These studies suggested that dementia may

be attributed to brain contusions formed following head injury as a result of a cerebral edema or

11

swelling (Rudelli, 1982). More recent studies, such as that of Lehman et al (2012), have

analyzed the prevalence of neurodegenerative disorders such as Alzheimer’s, Parkinson’s and

ALS. These studies found that the prevalence of death caused by neurodegenerative disorders is

3 times greater in a concussed population than that of the general US population, and that for

Alzheimer’s and ALS it is 4 times higher (Lehman et al, 2012). These results are consistent with

the physical damages that were previously discussed, in that the degeneration of cortical neurons

and disruption of neuronal pathways are what lead to these neurodegenerative disorders. With

more concussions one suffers the loss of more cortical neurons, decreasing the efficiency of the

brain and thus contributing to the generation of these neurodegenerative disorders. In 2009, de

Beaumont and his team of researchers assessed the cognitive abilities and electrophysiological

functions of former athletes with no history of sports concussion, and of former athletes who

sustained their last sports concussion over 30 years ago. In their research, it was found that those

who had sustained a concussion showed similar cognitive and motor system deficits as

asymptomatic individuals who were tested at three years post-concussion (de Beaumont et al,

2009). This aspect of the study agrees with previous statements arguing that the physical

alterations of the brain caused by concussions never fully regenerate and recover, and that

multiple concussions only worsen these problems. In addition to this, de Beaumont et al (2009),

found the previously concussed subjects showed significant reductions on both

neuropsychological and electrophysiological measures of episodic memory, and functions of the

frontal lobe; both of which are known as factors contributing to early-onset Alzheimer’s disease.

From the time an individual suffers a strong enough impact to the head, the

neurometabolic cascade of a concussion begins. Once the brain comes into contact with the skull,

the involuntary release of sodium, potassium and calcium ions, as well as glutamate begins. This

12

sudden influx results in increased neuronal depolarization, which is what kick-starts the period of

depressed metabolism. During the initial days of a concussion, this depressed period is when

symptoms are at highest prevalence, and brain function is at its worst. As the brain heals itself, it

is important for patients to refrain from physical activity, bright light, and other stimuli that

cause a change in the chemical makeup of the brain. Finally, the brain will never be able to fully

recover from the damage it suffered, and therefore new pathways must be formed that require

more energy than before. Although the brain is a very strong, resilient and powerful organ, the

neuroanatomical damage suffered during a concussion is impossible to fully heal, which can lead

to the development of several very serious neurological disorders.

Summary

The previous research was combined and presented in order to give a detailed outline of

the neurometabolic cascade of a concussion, and how that cascade may still affect individuals far

into the future. The resources used to compile this literature review were organized in a fashion

that allowed the timeline of events in a concussion to be followed chronologically, ending with

arguably one of the largest areas of focus for researchers today. Research included was used to

provide various perspectives on concussions in sport, ranging from history of the injury through

the neurological disorders associated with TBI. This approach was used to highlight the

important neurometabolic features of a concussion that are relevant to the development of these

neurological disorders.

DISCUSSION

Only 30 years ago, athletes who suffered a blow to the head in a contact sport were

expected to shake it off and be back in the lineup for the next game, if not the next shift. For

years concussions went undiagnosed, untreated and individuals did not take the time off to allow

13

for proper healing. Spectators at the highest level of sports events watched as athletes

continuously beat up their bodies, but rarely wondered about what effect these injuries had on

athletes’ cognitive abilities; because to them, these people were solely athletes. Today, that

mentality has changed for the better. There are more rules in high contact sports that attempt to

reduce the number of head injuries in sport, due in large part to the fact that today we understand

that concussions are not just a temporary injury, rather they are and injury that will one will

never be able to fully recover from.

According to ESPN, there are over 21.5 million kids between the ages of 6 and 17

playing a team sport in America alone. With contact sports being some of the most popular for

young children to participate in, the focus on concussion prevention a young age is of the utmost

importance. Although research completed by McCrory in 2004 proves that children are more

resilient to traumatic brain injuries than adults are, the most common cognitive sequencing of

concussive injuries is the same. Additionally, concussions also have the potential to affect a

child’s social, and educational success- processes critical throughout both childhood and

adolescence (McCrory, 2004). A child being more resilient to concussions than an adult means

that it takes a larger impact to a child’s head to produce the same neurological effects as an adult

who suffered a less forceful blow to the head. More specifically, McCrory (2004) found that “it

takes a two to three fold greater impact force to produce clinical symptoms in children compared

to adults.” This means that when a child shows symptoms of a concussion, it is reasonable to

assume that they sustained a far greater impact force in comparison to an adult showing the same

post-concussive symptoms (McCrory, 2004). Although the resilience of a child’s brain is

beneficial, it is still important that society takes control of these risks to help reduce the number

of brain injuries in the future of sport.

14

Though many of the results in literature cannot confidently conclude that there is a

definitive correlation between multiple concussions and early on-set neurological disorders, a

definite trend towards significance can be inferred. Results from these studies provide a

provocative body of material that suggests the protocol for concussion assessment and

management still may not be as developed as it should be in sports. If a history of repeated

concussions has been shown in patients with Alzheimer’s disease, Parkinson’s disease, as well as

other neurological disorders, then why are athletes allowed to choose to return to play after their

3rd and 4th concussions?

Practical Application

As previously stated, the fact that athletes who have suffered from multiple concussions

in their careers are still allowed to participate in high contact sports is astonishing, and creates a

greater risk for life threatening diseases with advancing age. A large issue with this is that the

research is not made available, and/or understandable to the right people. There is only so much

that scientists can do to make this information available and understandable to the affected

groups that include athletes, coaches, and parents. That being said, doctors, physical therapists,

and athletic trainers are trained to their best ability to detect, prevent and help concussion

recovery. However, it is up to the athletes themselves to decide their own future. Perhaps with

the appropriate guidance from qualified medical professionals, the important conclusions of

these studies could be presented to athletes who participate in high contact sports. By giving

athletes, coaches and parents this reliable information one can only hope that people would

become more aware of the risk they are taking when going back to their sport after already

having suffered from multiple concussions. Additionally, athletes educated on the long-term

effects of concussions would be more aware of how an illegal head check to another player could

15

have potential to severely change his/her life in the future. The neurometabolic cascade of a

concussion is initiated at the time of impact, and although the human brain is arguably the most

powerful mechanism in the world, it is impossible to use to it’s full potential when circuitry is

being disrupted and cerebral edemas are being formed. Many scientists have proven the

provocative role that concussions have on long-term neuroanatomical alteration, but it is not until

society understands this that the world of sports will then be forced to rethink the need for high

contact in athletics. At the end of the day, society needs to decide if seeing replays of big hits is

more important than an athletes mental health and quality of life 20 years later; and if one does

not choose the later option, this is an issue that will never be resolved.

16

BIBLIOGRAPHY

Coughlin,J.M.etal(2015).NeuroinflammationandBrainAtrophyinFormerNFL Players:AninvivoMultimodalImagingPilotStudy.NeurobiologyofDisease,74,58- 65.http://ac.els-cdn.com/S0969996114003325/1-s2.0- S0969996114003325-main.pdf?_tid=f576a062-75f7-11e5-a34a- 00000aab0f27&acdnat=1445214534_9773418293812cafeb298bf6820edc4 7Cusimano,M.D.,ChipmanM.L.Volpe,R.,Donnelly,P(2009).CanadianMinorHockey Participants’KnowledgeaboutConcussion.TheCanadianJournalof NeurologicalSciences,36(03),315-320. http://journals.cambridge.org/download.php?file=%2FCJN%2FCJN36_03%2 FS0317167100007046a.pdf&code=085ea5e64672c161d36eebf438633b36 DeBeaumont,L.,etal(2009).BrainFunctionDeclineinHealthyRetiredAthleteswho SustainedtheirLastSportsConcussioninEarlyAdultgood.Brain:AJournalof Neurology.132.695-708. http://brain.oxfordjournals.org/content/132/3/695.shortDeKosky,S.T.,etal(2010).TraumaticBraininjury-Football,WarefareandLong- TermEffects.TheNewEnglandJournalofMedicine,363,1293-1296. http://www.nejm.org/doi/full/10.1056/NEJMp1007051Frost,C(2011).AnatomyoftheConcussion:MoreSeriousthanMeetstheEye? https://honors.usf.edu/documents/Thesis/U78133303.pdf

Giza,C.C.,etal(2001).TheNeurometabolicCascadeofConcussions.Journalof AthleticTraining,36(3),228-235. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155411/pdf/attr_36_03_0228.pdf

Guskiewicz,K.M.,etal(2007).RecurrentConcussionandRiskofDepressionin RetiredProfessionalFootballPlayers.JournalofMedicine&ScienceinSports &Exercise. http://indianasportsconcussionnetwork.com/recurrentriskofdepressionnfl.pdf

Hazrati,L.N.,etal(2013).AbsenceofChronicTraumaticEncephalopathinRetired FootballPlayerswithMultipleConcussionsandNeurological Symptomatology.JournalofHumanNeuroscience,7,222. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662898/

Iverson,G.L.,etal(2012).PossibleLingeringEffectsofMultiplePastConcussions. JournalofRehabilitationResearchandPractice. http://www.hindawi.com/journals/rerp/2012/316575/

17

Jantzen,K.J.,etal(2004).AProspectiveFunctionalMRImagingStudyofMildTraumatic BrainInjuryinCollegeFootballPlayers.AmericanJournalofNeuroradiology,25, 738-745.http://www.ajnr.org/content/25/5/738.full.pdf+html

King,N.S(2003).Post-ConcussionSyndrome:ClarityAmidtheControversy?British JournalofPsychiatry,183,276-278. http://bjp.rcpsych.org/content/bjprcpsych/183/4/276.full.pdf

Lehman,E.J.,etal(2012).NeurodegenerativeCausesofDeathAmongNational FootballLeaguePlayers.TheOfficialJournaloftheAmericanAcademyofNeurology, 79(19),1970-1974.http://www.neurology.org/content/79/19/1970.short

McCroy,P.,etal(2015).SportPsychologyandConcussion:NewImpactstoExplore.British JournalofMedicine.http://bjsm.bmj.com/content/38/5/519.full.pdf+html

Powell,J.W(2001).CerebralConcussion:Causes,Effects,andRisksinSports.Journalof AthleticTraining,36(3),307-311. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155423/pdf/attr_36_03_03 07.pdf

Rudelli,R.,etal(1982).PosttraumaticPrematureAlzheimer’sDisease.Journalofthe AmericanMedicalAssociation,39(9),570-575. http://archneur.jamanetwork.com/article.aspx?articleid=5811

White,J.(2012).CONCUSSION:ShortandLong-TermImpact.RetrievedNovember14, 2015,fromhttp://mnepilepsy.org/patient-information/concussion-short-and-long- term-impact/