CHAPTER 1: INTRODUCTION
The reported incidence of sport concussions has grown at an accelerated pace over
the last couple of years making it a widely researched area in the sports medicine field.
To have a better understanding of the definition of concussions, numerous organizations
have attempted to solidify a single definition of concussion, also referred to as mild
traumatic brain injury (mTBI). A concussion is defined as a complex pathophysiological
process affecting the brain, induced by traumatic biomechanical forces (McCrory,
Meeuwisse, Johnston, Dvorak, Aubry, Malloy, and Cantu, 2009). Several common
features that incorporate clinical, pathologic and biomechanical injury constructs that
may be utilized in defining the nature of a concussive head injury. According to
McCrory et al. (2009) these features include:
1.
Concussion may be caused either by a direct blow to the head, face, neck or
elsewhere on the body with an “impulsive” force transmitted to the head,
2.
Concussion typically results in the rapid onset of short-lived impairment of
neurologic function that resolves spontaneously.
3.
Concussion may result in neuropathological changes, but the acute clinical
symptoms largely reflect a functional disturbance rather than a structural injury.
4.
Concussion results in a graded set of clinical symptoms that may or may not
involve loss of consciousness. Resolution of the clinical and cognitive symptoms
typically follows a sequential course; however, it is important to note that, in a
small percentage of cases, post-concussive symptoms may be prolonged.
5.
No abnormality on standard structural neuroimaging studies is seen in
concussion.
The most recent definition however, was constructed during the International
Symposium on Concussion in Sport. McCrory et al. (2009) stated that, “Sports
concussion is defined as a complex pathophysiological process affecting the brain,
induced by traumatic biomechanical forces.” The pathophysiology of concussion was
investigated and was summarized as the pathway as a multi-layered neurometabolic
cascade (Giza and Hovda, 2001). The axonal injury that occurs during the movement of
the brain within the skull results in a disruption of ion gradients. This disruption leads to
numerous imbalances within the brain including ion concentrations, cerebral blood flow,
and metabolites (Collins et al., 2007). In most cased, the brain is able to return to its
normal state within 5-7 days (Collins et al, 2007; McCrea et al., 2003).
It is commonly reported that 300,000 sport-related concussions occur each year,
although it was estimated in a recent review that up to 3.8 million recreation and sportrelated concussions occur annually in the United States (Langlois et al., 2006). There is
such a great difference between the two because the estimated 300,000 concussions
included only TBIs for which the person reported a loss of consciousness while the
estimated 3.8 million concussions included those for which no medical care was sought
(2006). This estimate, however, still might be low as many of these injuries go
unrecognized and therefore uncounted.
According to McCrory et al. (2009) the diagnosis of acute concussion usually
involves the assessment of a range of domains including clinical symptoms, physical
signs, behavior, balance, sleep and cognition. The suspected diagnosis of concussion,
according to McCrory et al. (2009) can include one or more of the following clinical
domains:
1.
Symptoms: somatic symptoms could include a headache; cognitive symptoms
could include feeling like in a fog, and/or emotional symptoms which could
include lability.
2.
Physical signs: these signs include loss of consciousness and amnesia.
3.
Behavioral changes: these changes include irritability.
4.
Cognitive impairment: these can be seen as slowed reaction times.
5.
Sleep disturbances: this can be seen as drowsiness.
If any one or more of these components is present, a concussion should be suspected and
the appropriate management strategy instituted. The vast majority (80%-90%) of
concussions resolve in a short (7-10 day) period (2009), although the recovery time frame
may be longer in children and adolescents. Even though the vast majority of people who
sustain concussions recover in short period, concussions can be significant injuries that
result in distressing symptoms and clear declines in measure cognitive abilities (Iverson
et al., 2004). In sport, the risk for long-term problems is rarely, if ever, associated with a
single concussion. Rather, long-term problems are believed to be associated with
multiple concussions or repeated sub-concussive blows.
Traumatic brain injury (TBI) is an important public heath concern; the Centers for
Disease Control report that each year, more than 1.2 million Americans suffer head injury
(Guskiewicz et al, 2007). Over 50,000 head-related injuries result in fatalities each year,
and many others result in mild to severe physical, cognitive, and psychosocial disability
(Guskiewicz et al, 2007). The psychological sequelae are often debilitating and costly
and include short-term or acute, and sometimes lifelong, consequences. Recently, TBI
has been identified as a risk factor for chronic depression, as evidenced by a prospective
cohort of retired World War II veterans that were assessed for prevalence of depression
several decades after the initial injury (Guskiewicz et al, 2007). Depression is the most
cited psychological disturbance after TBI, with prevalence rates from 6% in cases of mild
traumatic brain injury to 77% in more severe TBI within the first year after injury
(Guskiewicz et al, 2007). TBI has also been identified as a potential risk factor for the
occurrence (or early expression) of neurodegenerative dementing disorders, including
mild cognitive impairment, Alzheimer disease, and Parkinson syndrome (Guskiewicz et
al, 2007). Although the formal diagnosis of major depression is not common among
patients with Alzheimer disease, a depressed mood is frequent and can precede the
development of Alzheimer disease (Guskiewicz et al, 2007 ). In 2007, Guskiewicz et al,
investigated the relationship between sport-related concussion and prevalence of lifetime
clinical depression. Out of the 2552 retired players, 1513 players reported having
sustained at least one concussion, 884 reported on or two previous concussions, and 595
reported three or more concussions. Of those retired players who had sustained
concussions, more than half reported experiencing loss of consciousness or memory loss
from at least one of their concussive episodes. Of the retirees who had sustained one or
two previous concussions, 102 reported that the injuries have had permanent effect on
their thinking and memory skills as they had gotten older. The number and prevalence
increased to 185 in those with three or more previous concussions, suggesting a positive
association between a higher number of concussions and the perception that those
concussion now negatively affect cognitive functioning (Guskiewicz et al, 2007).
Analysis of responses to questions regarding clinical depression revealed that 269 of the
2434 respondents with complete data reported having been diagnosed previously with
clinical depression. The group of retirees diagnosed with depression had lower (worse)
mental component scores and physical component scores on the SF-36 compared with
retirees not diagnosed with clinical depression. There was an association between
recurrent concussion and diagnosis of depression suggesting that the prevalence increases
in a linear fashion with increasing concussion history. Thus, retired players reporting a
history of three or more previous concussion were three times more likely to be
diagnosed with depression, and those with a history of one or two previous concussions
were 1.5 times more likely to have been diagnosed with depression, relative to retirees
with no concussion history (Guskiewicz et al, 2007). In this study there was also a
concern that the observed associated between depression and concussion could be
confounded by MCI. Thus, for the subset of subjects who completed the MCI follow-up
questionnaire, they conducted additional analyses, controlling for diagnosis of MCI. The
prevalence ratios for a history of three or more previous concussions and for one or two
previous concussion were essentially unchanged relative to the larger group. Thus,
prevalence of MCI did not confound the association between concussion history and
diagnosed clinical depression (Guskiewicz et al, 2007).
Guskiewicz et al. (2007) observed threefold prevalence ratio for retired players with
three or more concussions is daunting, given that depression is typically characterized by
sadness, loss of interest in activities, decreased energy, and loss of confidence and selfesteem. These finding call into question how effectively retired professional football
players with a history of three or more concussions are able to meet the mental and
physical demands of life after playing professional football. These studies suggest that
football players with three or more concussions are at a threefold risk for sustaining
future concussions, with a subsequent threefold risk of being diagnosed with clinical
depression compared with those with limited or no prior history (Guskiewicz et al, 2007).
Depression is common after TBI of all severities especially in those involving more
severe TBI (Guskiewicz et al, 2007). This sample included a unique group, retired
professional football players, who, for the most part, experienced mild TBI combined
with a number of subconcussive impacts, which also may have contributed to an
increased likelihood for neurologic decline. Because of this small, unique group we are
interested in investigating the quality of life in individuals that have sustained
concussions in a number of sporting settings.
People are becoming more aware of concussions and the effects on quality of life
as research is showing the dangers that may be sustained to a person that has had a
concussion earlier in their life. Therefore, the purpose of this investigation is to
investigate the long-term effects concussion has on one’s quality of life. Based on the
current status of literature, we hypothesize that those with a history of concussions will
have a decreased quality of life then compared to someone who has not had a concussion.
We further hypothesis that those with repetitive concussions or head trauma will have a
greater decrease in quality of life than someone who has only suffered from one
concussion.
CHAPTER 2: A REVIEW OF LITERATURE
Definition
The reported incidence of sport concussions has grown at an accelerated pace over
the last couple of years making it a widely researched area in the sports medicine field.
To have a better understanding of the definition of concussions, numerous organizations
have attempted to solidify a single definition of concussion, also referred to as mild
traumatic brain injury (mTBI). Historically, minor head injury, concussion, postconcussive syndrome, post-traumatic syndrome, and traumatic head syndrome were used
interchangeably. This created difficulty in diagnosing mTBI. Thomas Kay (1986)
explained that “minor head injury refers to an injury to the head, face, and neck area with
symptoms caused by damage to the skull, scalp, soft tissues, or peripheral nerves but
where there is not necessarily injury to the brain. MTBI refers to a minor head injury in
which there is also damage to the brain, or at least disruption of brain function, as
evidenced by alterations of consciousness at the time of injury.” There were many other
definitions including the Committee on Head Injury Nomenclature of Neurological
Surgeons which described it as “A clinical syndrome characterized by the immediate and
transient post-traumatic impairment of neural function such as alteration of
consciousness, disturbance of vision or equilibrium, etc., due to brain stem dysfunction”
(Congress 1966). The American Academy of Neurology describes concussions as “any
trauma induced alteration in mental status that may or may not include a loss of
consciousness” (American 1997). The difference in these two definitions is that the AAN
found that a concussion can happen with or without the loss of consciousness.
A clear definition of concussion requires consensus among many researchers,
clinicians, and patients. Some advocate using the term concussion while others advocate
using the term “mild traumatic brain injury” (mTBI). A recent study highlighted a
general misinterpretation that an injury described as a concussion is less severe than one
described as mild traumatic brain injury (McCrory, et al., 2009). More recently the
International Symposium on Concussion in sport defined concussion as “a complex
pathophysiological process affecting the brain, induced by traumatic bio-mechanical
forces” (McCrory, et al., 2009). These forces stated by McCrory, et al. (2009) includes 5
major features:
1.
Concussion may be caused either by a direct blow to the head, face, neck or
elsewhere on the body with an “impulsive” force transmitted to the head,
2.
Concussion typically results in the rapid onset of short-lived impairment of
neurologic function that resolves spontaneously.
3.
Concussion may result in neuropathological changes, but the acute clinical
symptoms largely reflect a functional disturbance rather than a structural injury.
4.
Concussion results in a graded set of clinical symptoms that may or may not
involve loss of consciousness. Resolution of the clinical and cognitive symptoms
typically follows a sequential course; however, it is important to note that, in a
small percentage of cases, post-concussive symptoms may be prolonged.
5.
No abnormality on standard structural neuroimaging studies is seen in
concussion.
Epidemiology
Traumatic brain injury occurs when an external force is directly or indirectly
applied to the cranium and brain. Inconsistency in the definition and classification of
traumatic brain injury, along with discrepancies in data collection, has made the
epidemiology of TBI difficult to describe accurately (Segun TD., 2009). Problems with
TBI data collection include a number of definitions over the previous decades and the
fact that many patients with mTBI present with differing clinical signs and symptoms at
the hospital or doctor. Severe TBI associated death at the scene of the accident or during
transport to a hospital also may not be accounted for completely in data collection.
Differences in diagnostic tools and admission criteria also may affect the classification
(Lee B., Newberg A., 2005).
Rimel, Giordani, & Barth (1981) first noted the importance of mTBIs in the
scientific literature by stating that minor brain injuries can have a large impact on the
patient’s psychological, social, and physiological status. Recent data from the Centers
for Disease Control and Prevention (2003) show that, on average, approximately 1.4
million people sustain a TBI each year in the United States. Males are about twice as
likely as females to sustain a TBI (Langlois et al., 2006). About 75% of those accidents
are concussions or other forms of mTBI (Control, 2003) with the leading causes of TBI to
be injuries from falls (28%), motor vehicle accidents (20%), collisions (20%), and
assaults (11%). Sports and recreation activities are also a major cause of mTBI,
including concussions, and an accurate approximation may be that 1.6 million to 3.8
million sports-related mTBIs occur each year, including those for which no medical care
is sought (Langlois et al., 2006). Recent epidemiological and prospective clinical studies
estimate that approximately 3% to 8% of high school and collegiate football players
sustain a concussion each season (Guskiewicz KM., Weaver NL., Padua DA., Garrett
WE., 2000). According to Guskiewicz, Weaver, Padua, and Garrett (2000), of the 17,549
football players evaluated, 5.1% (888) sustained at least one concussion, and 14.7% (131
of the 888) sustained a second injury during the same. Players who sustained one
concussion in a season were three times more likely to sustain a second concussion in the
same season compared with uninjured players (Guskiewicz KM., Weaver NL., Padua
DA., Garrett WE., 2000).
Within Emergency Departments across the United States, traumatic brain injury is
associated with the death of 51,000 people each year, accounting for about one third of
all injury deaths (Thurman DJ., Alverson C., Dunn KA., et al.). Traumatic brain injury is
a cause of long-term disability that annually affects an estimated 70,000 to 90,000 people
(Thurman DJ., Alverson C., Dunn KA., et al.). Because of these serious consequences,
public heath efforts to prevent the occurrence and mitigate the consequences of TBI have
increased attention in recent years (Kraus JF., McArthur DL., 1996). Some success in the
TBI prevention and treatment efforts is suggested by an analysis of national mortality
trends, which indicates a 22% decline in rates of death associated with TBI from 1979 to
1992 (Sosin DM., Schiezek JE., Waxweiler RJ., 1995). The Centers for Disease Control
and Prevention (2003) noted that this difference may demonstrate the fact that mTBIs are
increasingly handled by Emergency Departments and outpatient settings.
Rates of Concussions
It is commonly reported that 300,000 sport-related concussions occur each year
(Langlois et al., 2006), although it was estimated in a recent review that up to 3.8 million
recreation and sport-related concussions occur annually in the United States (2006).
Earlier studies have reported concussion incidence rates in high school football to be as
high as 20% (250,000 players annually) (Gerberich SG, Priest JD., Boen JR., et al. 1983)
and 15% (200,000 players annually) (Wilberger JE., 1993), while annual incidence
estimates of 10% were consistently reported in collegiate football during the late 1980s
(Barth JT., Alves W., Ryan T., et al. 1989). These figures exceed those reported by the
National Athletic Trainer’s Association high school studies of 1986 to 1988 and 1995 to
1997, which reported incidence rates of only 2.8% and 3.6%, respectively (Powell JW.,
1998).
These researchers concluded that the national figure for concussion in high
school football is an estimated 40,000 cases annually (Powell JW., 1998). The large
variance could be attributable to original estimates including concussions that only
involved loss of consciousness (Thurman DJ., Branche CM., Sniezek JE., 1998). This
highlights the difficulty with concussion epidemiology because of underreporting and the
lack of widespread use of an injury surveillance system in youth sports (McCrea M.,
Hammeke T., Olsen G., et. al., 2004). With the increasing access to recreational and club
sports, the number of diagnosed concussions will likely increase (McCrory, et al., 2005).
Concussions represent an estimated 8.9% of all high school athletic injuries (Gessel
LM., Fields SK., Collins CL., Dick RW., Comstick RD., 2007).
The Centers for
Disease Control and Prevention (2003) reported a high incidence of reported head injury
in several sports and warns that the likelihood of serious sequelae increases with repeated
head injury. Although American football is generally recognized as the sport most often
associated with concussions, published research reports moderate-to-high incidences of
concussions in basketball, softball, soccer, baseball, boxing, rugby, and ice hockey
(Leininger BE, Gramling S, Farrell AD, et al., 1990). Although concussions can be
caused by many sports, the highest risk of concussion in high school is from football
(Gessel LM., Fields SK., Collins CL., Dick RW., Comstick RD., 2007). In girls’ sports,
the rate of concussion is highest in girls’ soccer and girls’ basketball (McCrory, et al.,
2005). Rugby, ice hockey, and lacrosse also account for higher rates of concussions but
are often club sports, which limits their data inclusion in the larger high school sports
epidemiological studies (Goodman D., Gaetz M., Meichenbaum D., 2001).
Girls are reported to have a higher rate of concussion than boys in similar sports
(Gessel LM., Fields SK., Collins CL., Dick RW., Comstick RD., 2007). The exact
reason for this difference is unknown, although some have theorized that female athletes
have weaker neck muscles and a smaller head mass than their male counterparts (Barnes
BC., et. al., 1998). It is also theorized that females have their concussions documented
more than males as male athletes may be more reluctant to report their injuries for fear of
removal from competition (McCrea M., Hammeke T., Olsen G., et. al., 2004). It was
also mentioned that men are approximately twice as likely as women to sustain a TBI
(Kraus JF., Black MA., Hessol N., et al., 1985). Men are more likely to engage in riskier
behaviors during their teenage years, like driving too fast or not wearing helmets when
playing activities or driving a motorcycle type vehicle, causing the rate of men to be
higher than women. However when it comes to sports-related concussion women tend to
have a higher rates than men. The difference in information could also be from the age
group of the data that was collected. The risk of TBI peaks when individuals are between
the ages of 15-30 years old. The risk is highest for individuals aged 15-24 years (Kraus
JF., Black MA., Hessol N., et al., 1985). Twenty percent of TBIs occur in the pediatric
age group (birth to 17) (Segun TD., 2009).
Sports are not the only cause of concussions or traumatic brain injury. Motor
vehicle accidents are the leading cause of TBI in the general population, especially
among whites in the United States. Motor vehicle accidents account for approximately
50% of all TBIs (Segun TD., 2009). Falls are the second leading cause of TBI
accounting for 20-30% of all TBIs (Segun TD., 2009). Another cause of traumatic brain
injury are blast injuries resulting from combat. Wilk JW., et al. (2010) did a study to
determine blast mechanisms of concussions. Out of 3,952 United States Army soldiers
who were administered anonymous surveys 3 to 6 months after returning from a yearlong
deployment in Iraq, 587 of them had suffered a concussion (14.9% of the total surveyed).
Pathophysiology
To date, the pathophysiology of concussions in human models has not been
possible, however there are numerous theories based on animal models that have been
presented. It was initially felt that deformational strains produced by concussive forces
will result in only a temporary disturbance of brain function related to neuronal,
neurochemical, or metabolic function without associated structural brain injury
(Wilberger, Ortega, and Slobounov, 2006). In recent years, however it has been
recognized that structural derangements may indeed occur and that there may be a period
of selective vulnerability to additional insults, like the second impact syndrome, or
prolonged vulnerability to cumulative concussions and their long-term effects, like
dementia pugilistica (Wilberger, J., Ortega j., & Slobounov). During the minutes to few
days after a concussion blow, brain cells that are not irreversibly damaged remain alive
but exist in a vulnerable state (Wojtys et al. 1999). This vulnerability is caused by the
initial deformational strains produced by concussive forces on the brain causing a
disturbance in brain function related to neuronal, neurochemical, or metabolic function
without associated structural brain injury (1999). Some athletes suffering from
concussion may be extremely susceptible to the consequences of even minor changes in
cerebral blood blow, as well as slight increases in intracranial pressure and apnea (Hovda,
1995). Metabolic dysfunctions during acute post-concussive events may be responsible
for maintaining a state of brain vulnerability, characterized by increase in the demand for
glucose and an inexplicable reduction in cerebral blood flow.
Collins, Iverson, Gaetz, and Lovell (2007) noted that the pathophysiology of
concussions was the result of axonal stretching. They stated that this axonal stretching
that occurs during a concussion causes a disruption in ion gradients in the brain. An
over-excitation of the cerebral neurons stated by Herring et al. (2005) is possibly
contributed by neurotransmitters that are released in excess. These neurotransmitters
cause a greater ion imbalance within the brain causing the brain to activate ion pumps.
The activation of ion pumps cause a greater cellular demand for glucose that will be
converted to the ATP needed to power the ion pump. Simultaneously, the axonal
stretching that results in hyper-metabolism is counteracted by a decrease in cerebral
blood flow creating an imbalance between glucose availability and glucose demand.
Magnesium levels decrease causing ATP production to slow which can be observed for
several days post-injury. Axonal stretching can also cause an increase in calcium
concentration in mitochondria. This increase in calcium could eventually result in
metabolic dysfunction and decrease the affinity of tublin dimers leading to an irreversible
destruction of microtubules (Collins et al., 2007).
Quality of Life
Children and adolescents frequently experience a concussion in sports or other
physical activities. Fortunately, the vast majority of people who sustain a single
concussion show restoration of cognitive and motor performance relatively quickly and
fully. Although the vast majority of people who sustain concussions recover,
concussions can be significant injuries that result in distressing symptoms and clear
declines in measure cognitive abilities (Iverson et al., 2004). In sport, the risk for long-
term problems is rarely, if ever, associated with a single concussion. Rather, long-term
problems are believed to be associated with multiple concussions and potentially multiple
sub-concussive blows. Awareness of the detrimental effects of repetitive concussions has
excited in modern-era sports medicine for decades both anecdotally and in the clinical
literature. Early examples from boxing include Martland’s work on dementia pugilistic
(punch-drunk syndrome) and later chronic and traumatic boxer’s encephalopathy. More
recently, concussion in sport and the aftermath of multiple concussions has been
witnessed by the masses as numerous professional athletes have had their careers
prematurely ended due to these injuries.
In a large study involving American college football players, athletes with a history
of two or more concussions reported more preseason symptoms and performed worse on
two tests designed to measure information processing speed than athletes with no
previous concussions (Collins et al., 1999). Gronwall and Wrightson (1975) reported that
trauma patients with multiple concussions scored significantly lower on an auditory
processing task than patients with only one concussion. In addition, a recent study
demonstrated statistical differences in post-concussion symptoms and cognitive eventrelated potentials at baseline for young amateur hockey players with zero versus three or
more concussions (Gaetz, Goodman, & Weinberg 2000).
Depression is the most cited psychological disturbance after TBI, with prevalence
rates from 6% in cases of mild traumatic brain injury to 77% in more severe TBI within
the first year after injury (Guskiewicz et al, 2007). TBI has also been identified as a
potential risk factor for the occurrence (or early expression) of neurodegenerative
dementing disorders, including mild cognitive impairment, Alzheimer disease, and
Parkinson syndrome (2007). In 2007, Guskiewicz et al, investigated the relationship
between sport-related concussion and prevalence of lifetime clinical depression. They
studied a diverse group of retired professional football players, including recent retirees
and those who had played professional football before World World II. 11.1% of all the
respondents reported having prior or current diagnosis of clinical depression. There was
an associated between recurrent concussion and diagnosis of lifetime depression,
suggesting that the prevalence increases with increasing concussion history. Compared
with retired players with no history of concussion, retired players reporting three or more
previous concussions (24.4%) were three times more likely to be diagnoses with
depression; those with a history of one or two previous concussions (36.3%) were 1.5
times more likely to be diagnosed with depression (Guskiewicz et al, 2007). Other
studies by Guskiewicz found that athletes with a history of three or more concussions are
three times more likely to sustain an additional concussion and are more likely to have a
prolonged recovery from additional concussions (Guskiewicz et al, 2003). He also found
that retired NFL players with three or more concussions are five times more likely to
report mild cognitive impairment and to have an earlier onset of Alzheimer disease than
peers without a concussion history (Guskiewicz, 2005). Another study of his found that
retired NFL players with a history of three or more concussions are more likely to be
diagnosed with clinical depression (Guskiewicz, 2007).
The consequences of sport related concussions may have serious effects on the
health-related quality of life of athletes. Kuehl et al. (2010) defines health-related quality
of life as the “physical, psychological, and social domaines of health that are influenced
by the individual patient beliefs, perceptions, values, and experiences.” A number of
studies have reported decreases in health-related quality of life in headache populations,
which have symptomology similar to that of sport related concussion and for this reason
Kuehl et al. (2010) investigated health-related quality of life in concusses populations to
determine if similar reductions in health-related quality of life exist in athletes with a
history of sport related concussions. They studies a cross-sectional sample of collegiate
athletes from a variety of sports (football, lacrosse, women’s soccer, softball, baseball,
volleyball, wrestling, water polo, swimming, and tennis) and collegiate divisions
(Division I, Division II, and junior college) were used. These athletes were grouped
according to the number of previous self-reported concussions. A demographic form
including concussion history, the SF-36, and the HIT-6 were the main outcome measures
of this study. Collegiate athletes who self-reported three or more sport related
concussions scored significantly lower on the social functioning, bodily pain, and vitality
subclass of the SF-36, which measure health-related quality of life, and on the HIT-6 total
score, which measures the impact of headache on health-related quality of life, compared
to athletes with 1-2 sport related concussions or no history of one. Therefore, results
suggest that when athletes self-report more sport related concussions in the past, their
perception of their social functioning, bodily pain, vitality, and headache may be affected
(Kuehl et al, 2010). The present study found significant correlations that suggest a doseresponse relationship where the groups with higher numbers of previous sport related
concussions are associated with lower social functioning and higher HIT-6 scores (Kuehl
et al, 2010). These findings align with other work done identifying possible cumulative
effects of concussion.
People are becoming more aware of concussions and the effects from it on quality
of life as research is showing the dangers that may be sustained to a person that has had a
concussion earlier in their life. In 2011 Dave Duerson, a retired Chicago Bears football
player, fatally shot himself. Before shooting himself he had sent out text messages
requesting that his brain tissue be examined for chronic traumatic encephalopathy (CTE),
a degenerative brain disease that is linked to depression, dementia, and suicide. Duerson
believed that he had this condition as he knew of other football players with the same
disease. CTE first made headlines in January 2007 when it was found in the brain tissue
of Andre Waters, a former Philadelphia Eagles player, after he had committed suicide.
The increased awareness around the long-term impact of head trauma on football players
had become a major concern among the players. Thirteen of the fourteen deceased NFL
players who have been examined for the disease by the Boston University researchers
have been found to have CTE. Many of them died in part through acts linked to the
disease itself, like suicide, drug abuse or mental breakdown. In February 2008, John
Grimsley, a Houston Oilers NFL line backer, showed evidence of CTE (Talan, 2008).
Investigators at Boston University linked the condition to his past history of concussions.
Concussion on the heels of other athletic injuries could pave the way for Alzheimer
disease (AD) and other cognitive problems, according to growing evidence of chronic
traumatic encephalopathy (CTE) in athletes who had sustained multiple injuries to the
brain and died prematurely. At autopsy, their brains were riddled with TAU-filled
tangles that are also seen in AD. These athletes were in their thirties and forties and had
complained of memory loss and behavioral changes that made sense only in death when
their brains showed pathological signs of disease and cell death (Talan, 2008).
Chronic Traumatic Encephalopathy
Since 1920s it has been known that the repetitive brain trauma associated with
boxing may produce a progressive neurological deterioration, originally termed
“dementia pugilistic” and more recently, chronic traumatic encephalopathy (CTE)
(McKee et all. 2009). Besides boxing, this repetitive closed head injury occurs in a wide
variety of contact sports including football, wrestling, rugby, hockey, lacrosse, soccer,
and skiing. The concept of CTE was first introduced by Martland in 1928. He introduced
the term ‘punch-drunk’ to a symptom complex that appeared to be the result of repeated
sub-lethal blows to the head (Martland, 1928). The symptoms of CTE are insidious, first
manifest by deteriorations in attention, concentration, and memory, as well as
disorientation and confusion, and occasionally accompanied by dizziness and headaches
(McKee et. all. 2009). With progressive deterioration, additional symptoms such as lack
of insight, poor judgement, and overt dementia become manifest. In 1973, Corsellis,
Bruton, and Freeman-Browne described three stages of clinical deterioration as follows:
1.
Characterized by affective disturbances and psychotic symptoms
2.
Characterized by social instability, erratic behavior, memory loss, and initial
symptoms of Parkinson disease
3.
Consists of general cognitive dysfunction progressing to dementia and is often
accompanied by full-blown Parkinsonism, as well as speech and gait
abnormalities
Chronic traumatic encephalopathy is a progressive condition marked by neurofibrillary
tangles and neuritic threads starting in the neocortex and progressing to the hippocampus
(Cajigal 2007).
Prior to the development of the clinical features of CTW, many authors anecdotally
report a ‘pre-clinical’ stage of impairment, whereby some boxers begin to ‘soften up’
(McCrory, Zazryn, Cameron, 2007). This is reported to occur after several years or a
large amount of bouts. Common features of this state include boxers becoming
increasingly vulnerable to blows, being readily knocked down and taking longer to
recover from bouts (2007). Fighting skills and movement around the rind are also
impaired, and as a result the boxer may develop characteristic physiognomy of the
flattened nose and cauliflower ears during this time (2007).
In the mildest of CTE cases, the most common presenting symptoms are slurring
dysarthria (90% of cases) and this symptoms is often accompanied by a gat ataxia or
disequilibrium (2007). In most bases, boxers reported persistent and disabling headaches
(2007). Neurobehavioral changes may occur at any time during the development of CTE.
In the mildest stage, the affective changes are typically characterized by emotional
lability, euphoria and hypomaia (2007). Late neurobehavioral features include
psychomotor retardation, exacerbation of premorbid personality traits, aggression,
suspicious, childishness, loquacity and restlessness (2007). As CTE progresses, there is
difficulty with impulse control, disinhibition, irritability, inappropriateness and explosive
outbursts of aggression (2007).
Scientists at Boston University reported that Grimsley’s brain had all the
pathological signs of (CTE). Grimsley was 45 when he died and in the last two years of
his life he had noticeable problems with short-term memory. This finding adds to the
mounting evidence that repeated blows to the brain may seem benign but can have a
cumulative and devastating effect on the brain, setting in motion a dementia that is
generally seen in aging populations (Talan, 2008). There are two-dozen symptoms of
CTE, including memory disturbance, confusion gait disturbances or falls, speech
abnormalities and mood problems. Even though Grimsley has only one documented
concussion doctors estimated that he may have had eight others. Robert C. Cantu MD
stated that “the repeated trauma sets something in motion with the TAU protein.” Ann
McKee, MD, director of neuropathology at the Boston University Alzheimer’s Disease
Center, did the pathological assessment of Grimsley’s brain, including
immunohitochemistry to look for TAU deposition; and there it was, spread out over the
frontal cortex, amygdala, and just about everywhere they looked. Dr. McKee said that
the deposition of TAU observed in the brains of this handful of athletes provides
evidence that acquired injuries can lead to a progressive neurodegenerative disease. She
has also found similar taupathies in the brains of four professional boxers. Dr Mckee
stated, “There is a tremendous amount of deposition, that is not just in the cortex but in
white matter as well. Deposition is also seen around the blood vessels. The repeated
brain trauma triggers a breach in the blood-brain-barrier and is allowing toxins to leak
into the brain”.
Tau Protein
TAU proteins are proteins that stabilize microtubules. They are abundant in
neurons in the central nervous system and are less common elsewhere. When TAU
proteins are defective and no longer stabilize microtubules properly, they can result in
dementias, such as Alzheimer’s disease (Goedert and Spillantini, 2000). The TAUimmunoreactive neurofibrillary pathology is characteristically irregular in distribution
with multifocal patches of dense NFTs in the superficial cortical layers, often in a
perivascular arrangement. This superficial distribution of neocortical NFTs was
originally described by Hof and colleagues who noted that the NFTs in CTE were
preferentially distributed in layer II and the upper third of layer III in neocortical areas
and generally more dense than in AD (47).
Hyperphophorylation of the TAU protein can result in the self-assembly of tangles
of paired helical filaments and straight filaments, which are involved in the pathogenesis
of Alzheimer’s disease and other taupathies. All of the six TAU isoforms are present in
an often hyperphoporylated state in paired helical filaments from Alzheimer’s disease
brain. In other neurodegenerative diseases, the deposition of aggregates enriched in
certain TAU isoforms has been reported. When misfolded, this otherwise very soluble
protein can form extremely insoluble aggregates that contribute to a number of
neurodegenerative diseases.
In 2007 Christopher Benoit, a professional wrestler, was the fifth former athlete
with extensive brain damage believed to be caused by multiple concussions. Robert
Cantu MD had told reporters that of the former athletes they have studied, the former
World Wrestling Entrainment wrestler had by far and away the greatest amount of TAU
protein in his brain, a marker of brain trauma. Dr. Cantu and other concussion experts
reported this type of brain damage as chronic traumatic encephalopathy (CTE).
Neurosurgeons used immunostains to examine TAU protein in slices of Benoit’s brain.
They found neurofibrillary tangles, neuritic threads, and dead neurons throughout the
neocortex, basal ganglia, substantia nigra, and brainstem. According to the researchers,
TAU become phosphorylated and visible after prior traumatic brain injury. These areas
of TAU protein deposits are dead neurons, dead brain cells, and ghosts of old neurons.
CHAPTER 3: METHODS
Participants
A total of 1140 participants ranging from the ages of 18-81 (542 males/598
females) completed the investigation. The participants consisted of both concussed and
un-concussed persons. The participants needed access to a computer and internet to
participate in this experiment.
Procedure
The experiment consisted of a 20 minute survey consisting of 153 questions which
the participants completed on their own time. In this survey participants answered
questions from 7 different surveys. The survey consisted of the a Health History
Questionnaire, the Multidimensional Fatigue Inventory, the Hospital Anxiety and
Depression Scale, the Godin LTEQ survey, a Short Term Health Survey, the Satisfaction
with Life Scale, and Pittsburgh Sleep
Quality Index.
The Health History Questionnaire asks questions about a person’s personal health
history, health habits and personal safety, family health history, health maintenance, and
a review of systems to get a better knowledge about the patient.
The Multidimensional Fatigue Inventory was developed in 1995 and is widely used
especially in cancer researches. It is a 20-item self-report instrument designed to measure
fatigue. It covers the following dimensions: General Fatigue, Physical Fatigue, Mental
Fatigue, Reduced Motivation and Reduced Activity.
The Hospital Anxiety and Depression Scale is a self-assessment scale that was
developed to detect states of depression and anxiety. It is a series of questions based off
of a 4 point scale with a value of 3 meaning they are considered to possibly need a
clinical psychiatric treatment and a 0 meaning they are clinically stable. The anxiety and
depressive subscales are also valid measures of severity of the emotional disorder.
The Godin Leisure Time Exercise Questionnaire is a simple questionnaire to
measure a person’s leisure time exercise. This questionnaire can be used to monitor the
impact of health and physical fitness. The Short Term Health Survey is an eight question
survey relying on a single item to measure each of the eight domains of health.
The Satisfaction with Life Scale consists of 5-items to measure a persons
satisfaction with their life. Life satisfaction can be assessed specific to a particular
domain of life or globally and the SWLS is a global measure of life satisfaction.
The Pittsburgh Sleep Quality Index is a self-related questionnaire which assesses sleep
quality and disturbances over a one month time interval. Nineteen individual items
generate seven component scores: subjective sleep quality, sleep latency, sleep duration,
habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime
dysfunction. The sum of the scores for these seven components yields one global score.
Data Analysis
Based on a survey given the affects of concussions were compared to those without
a concussion through the questions answered.