Foundations of Sport-Related Brain Injuries - S. Slobounov, W. Sebastianelli (Springer, 2006) WW.pdf - książki - Bio Med 11 - bibiariel

INTRODUCTORY CHAPTER

CONCUSSION IN ATHLETICS: ONGOING

CONTROVERSY

Semyon Slobounov^; Wayne Sebastianelli^

^ The Department of Kinesiology, The Pennsylvania State University, 19 Recreation Hall,

University Park, PA, 16802; smsl8@psu.edu

^ Department of Orthopaedics and Medical Rehabilitation, Milton Hershey Medical College,

Sport Medicine Center, The Pennsylvania State University, University Drive, University Park,

PA, J6802; wsebastianelli@psu.edu

Abstract:

Multiple traumas to the brain are the most common type of catastrophic

injury and a leading cause of death in athletes. Multiple brain injuries

may occur as the long-term disabilities resulting from a single mild

traumatic brain injury (MTBI, generally known as concussion) are often

overlooked and the most obvious clinical symptoms appear to resolve

rapidly. One of the reasons of controversy about concussion is that most

previous research has: a) failed to provide the pre-injury status of MBTI

subjects which may lead to misdiagnosis following a single brain injury

of the persistent or new neurological and behavioral deficits; b) focused

primarily on transient deficits after single MTBI, and failed to examine

for long-term deficits and multiple MTBI; c) focused primarily on

cognitive or behavioral sequelae of MTBI in isolation; and d) failed to

predict athletes at risk for traumatic brain injury. It is necessary to

examine for both transient and long-term behavioral, sensory-motor,

cognitive, and underlying neural mechanisms that are interactively

affected by MTBI. A multidisciplinary approach using advanced

technologies and assessment tools may dramatically enhance our

understanding of this most puzzling neurological disorder facing the sport

medicine world today. This is a major objective of this chapter and the

whole book at least in part to resolve existing controversies about

concussion.

Keywords:

Injury; Concussion; Collegiate coaches; EEG and Postural stability.

INTRODUCTION

Over the past decade, the scientific information on traumatic brain injury

has increased considerably. A number of models, theories and hypotheses of

traumatic brain injury have been elaborated (see Shaw, 2002 for review). For

example, using the search engine PubMed (National Library of Medicine) for

the term "brain injury" there were 1990 articles available between the years

of 1994-2003, compared to 930 for the years 1966-1993. Despite dramatic

advances in this field of medicine, traumatic brain injury, including the mild

Slobounov and Sebastianelli

traumatic brain injury (MTBI), commonly known as a concussion, is still one

of the most puzzling neurological disorders and least understood injuries

facing the sport medicine world today (Walker, 1994; Cantu, 2003).

Definitions of concussion are almost always qualified by the statement that

loss of consciousness can occur in the absence of any gross damage or injury

visible by light microscopy to the brain (Shaw, 2002). According to a recent

NIH Consensus Statement, mild traumatic brain injury is an evolving

dynamic process that involves multiple interrelated components exerting

primary and secondary effects at the level of individual nerve cells (neuron),

the level of connected networks of such neurons (neural networks), and the

level of human thoughts or cognition (NIH, 1998).

The need for multidisciplinary research on mild brain injury arises from

recent evidence identifying long-lasting residual disabilities that are often

overlooked using current research methods. The notion of transient and rapid

symptoms resolution is misleading since symptoms resolution is not

indicative of injury resolution. There are no two traumatic brain injuries alike

in mechanism, symptomology, or symptoms resolution. Most grading scales

are based on loss of consciousness (LOC), and post-traumatic amnesia, both

of which occur infrequently in MTBI (Guskiewick et al. 2001, Guskiewick,

2001). There is still no agreement upon diagnosis (Christopher & Amann,

2000) and there is no known treatment for this injury besides the passage of

time. LOC for instance, occurs in only 8% of concussion cases (Oliaro et al.,

2001). Overall, recent research has shown the many shortcomings of current

MTBI assessments rating scales (Maddocks & Saling, 1996; Wojtys et al.,

1999; Guskiewicz et al., 2001), neuropsychological assessments (Hoffman et

al., 1995; Randolph, 2001; Shaw, 2002; Warden et al., 2001) and brain

imaging techniques (CT, conventional MRI and EEG, Thatcher et al., 1989,

1998, 2001; Barth et al., 2001; Guskiewicz, 2001; Kushner, 1998; Shaw,

2002).

The clinical significance for further research on mild traumatic brain

injury stems from the fact that injuries to the brain are the most common

cause of death in athletes (Mueller & Cantu, 1990). It has been estimated

that in high school football alone, there are more than 250,000 incidents of

mild traumatic brain injury each season, which translates into approximately

20% of all boys who participate in this sport (LeBlanc, 1994, 1999). It is

conventional wisdom that athletes with uncomplicated and single mild

traumatic brain injuries experience rapid resolution of symptoms within 1-6

weeks after the incident with minimal prolonged sequelae (Echemendia et

al., 2001; Lowell et al., 2003; Macciocchi et al., 1996; Maddocks & Saling,

1996). However, there is a growing body of knowledge indicating long-term

disabilities that may persist up to 10 years post injury. Recent brain imaging

studies (MRS, magnetic resonance spectroscopy) have clearly demonstrated

the signs of cellular damage and diffuse axonal injury in subjects suffering

from MTBI, not previously recognized by conventional imaging (Gamett et

Concussion Controversy

al., 2000). It is important to stress that progressive neuronal loss in these

subjects, as evidenced by abnormal brain metabolites, may persist up to 35

days post-injury. Therefore, athletes who prematurely return to play are

highly susceptible to future and often more severe brain injuries. In fact,

concussed athletes often experience a second TBI within one year post

injury. Every athlete with a history of a single MTBI who returns to

competition upon symptoms resolution still has a risk of developing a post-

concussive syndrome (Cantu & Roy, 1995; Cantu, 2003; Kushner, 1998;

Randolph, 2001), a syndrome with potentially fatal consequences (Earth et

al.,2001).

Post-concussive syndrome (PCS) is described as the emergence and

variable persistence of a cluster of symptoms following an episode of

concussion, including, but not limited to, impaired cognitive functions such

as attention, concentration, memory and information processing, irritability,

depression, headache, disturbance of sleep (Hugenholtz et al., 1988;

Thatcher et al., 1989; Macciocchi et al., 1996; Wojtys et al, 1999; Earth et

al., 2001; Powell, 2001), nausea and emotional problems (Wright, 1998).

Other signs of PCS are disorientation in space, impaired balance and

postural control (Guskiewicz, 2001), altered sensation, photophobia, lack of

motor coordination (Slobounov et al., 2002d) and slowed motor responses

(Goldberg, 1988). It is not known, however, how these symptoms relate to

damage in specific brain structures or brain pathways (Macciocchi et al.,

1996), thus making accurate diagnosis based on these criteria almost

impossible. Symptoms may resolve due to the brain's amazing plasticity

(Hallett,2001).

Humans are able to compensate for mild neuronal loss because of

redundancies in the brain structures that allow reallocation of resources such

that undamaged pathways and neurons are used to perform cognitive and

motor tasks. This fiinctional reserve gives the appearance that the subject

has returned to pre-injury health while in actuality the injury is still present

(Randolph, 2001). In this context, Thatcher (1997, 2001) was able to detect

EEG residual abnormalities in MTEI patients up to eight years post injury.

This may also increase the risk of second impact syndrome and multiple

concussions in athletes who return to play based solely on symptom

resolution criteria (Earth et al., 2001; Kushner, 2001; Randolph, 2001).

NEURAL BASIS OF COGNITIVE DISABILITIES

IN MTBI

There is a considerable debate in the literature regarding the extent to

which mild traumatic brain injury results in permanent neurological damage

(Levin et al., 1987; Johnston et al, 2001), psychological distress (Lishman,

1988) or a combination of both (McClelland et al., 1994; Eryant & Harvey,

Slobounov and Sebastianelli

1999). Lishman's (1988) review of the literature suggested that

physiological factors contributed mainly to the onset of the MTBI while

psychological factors contributed to the duration of its symptoms. As a

result, causation of MTBI remains unclear because objective anatomic

pathology is rare and the interaction among cognitive, behavioral and

emotional factors can produce enormous subjective symptoms in an

unspecified manner (Goldberg, 1988).

To-date, a growing body of neuroimaging studies in normal subjects has

documented involvement of the fronto-parietal network in spatial attentional

modulations during object recognition or discrimination of cognitive tasks

(Buchel & Friston, 2001; Cabeza et al., 2003). This is consistent with

previous fMRI research suggesting a supra-modal role of the prefrontal

cortex in attention selection within both the sensori-motor and mnemonic

domains (Friston et al., 1996, 1999). Taken together, these neuroimaging

studies suggest the distributed interaction between modality-specific

posterior visual and frontal-parietal areas service visual attention and object

discrimination cognitive tasks (Rees & Lavie, 2001). Research on the

cognitive aspects in MTBI patients indicates a classic pattern of

abnormalities in information processing and executive functioning that

correspond to the frontal lobe damage (Stuss & Knight, 2002).

The frontal areas of the brain, including prefrontal cortex, are highly

vulnerable to damage after traumatic brain injury leading to commonly

observed long-term cognitive impairments (Levin et al., 2002; Echemendia

et al., 2001; Lowell et al., 2003). A significant percentage of the mild

traumatic brain injuries will result in structural lesions (Johnston et al.,

2001), mainly due to diffuse axonal injury (DAI), which are not always

detected by MRI (Gentry et al., 1988; Liu et al., 1999). Recent dynamic

imaging studies have finally revealed that persistent post-concussive brain

dysfunction exists even in patients who sustained a relatively mild brain

injury (Hofman et al, 2002; Umile et al, 2002).

Striking evidence for DAI most commonly involving the white matter of

the frontal lobe (Gentry et al., 1998) and cellular damage and after mild TBI

was revealed by magnetic resonance spectroscopy (MRS). Specifically,

MRS studies have demonstrated impaired neuronal integrity and associated

cognitive impairment in patients suffering from mild TBI. For example, a

number of MRS studies showed reduced NAA/creatine ratio and increased

choline/creatine ratio in the white matter, which can be observed from 3-39

days post-injury (Mittl et al., 1994; Gamett et al., 2000; Ross & Bluml,

2001). The ratios are highly correlated with head injury severity. More

importantly, abnormal MR spectra were acquired from frontal white matter

that appeared to be normal on conventional MRI. Predictive values of MRS

in assessment of a second concussion are high, because of frequent

occurrence of DAI with second impact syndrome (Ross & Bluml, 2001).

The language, memory and perceptual tasks sensitive to frontal lobe

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