external image AntrelRolle.png


Alexa Low, Ashleigh Philips, Felicity Rodriguez, Kelly Tiro

Media Item: http://www.onionsportsnetwork.com/articles/keep-safe-what-to-do-if-you-see-a-braindamaged-for,18787/

| Introduction | Neuroscientific Context | Analysis | Search Process | References


Introduction



‍The media item chosen is a satirical article published by the website Onion Sports Network that bases its content on satirizing real news and press release websites. It takes the abrupt way in which news is presented and applies it to current sports issues, providing an amusing view on the way media is received by regular audiences.
It is of interest because the particular media item selected, an article titled Keep Safe: What To Do If You See A Brain-Damaged Former NFL Players contains content that draws on the preconceived notions or myths behind head trauma and injury in football players. Although at first glance the article doesn’t seem to be informative, perhaps it is more revealing than the target audience may think. It may simply be satirical in that it paints the players as animalistic, base and simplistic in their ways of thinking, but might there be some scientific base to it?

Why would a player be confused by a hard snap count? Are they actually more prone to epileptic fits? Are linebackers actually more able to detect movement? Do flashing lights actually hurt the player? Do they have an increased predisposition for being violent? What kind of injuries can cause these effects? What actually causes injury in these players? What parts of the brain are affected? And what are the real results of these injuries?

All these questions can actually be answered with real neuroscientific information ‍

Neuroscientific Context



Affects of American Football on the Brain

The National Football League (NFL), formed in 1920, is the highest level of professional American football in the United States. NFL is a contact sport in which players frequently sustain blunt blows to the head. Despite protective helmets, blows are often significant enough to result in concussion. Amen et al. (2011) performed detailed imaging studies on the brains of current and retired professional footballers. It was shown that compared to a randomised comparison group the footballers had significant and widespread areas of decreased cerebral blood flow. Wendel (2011) also stated in the NFL footlock health care that not only are brain related injuries common but they increase as the season wears on .

Protective helmets are an important part of protecting the brain from sustaining injuries however as Rowson and Duma (2011) noted, no helmet will be 100% effective. Augmenting this is the varied standards in the ability of helmets to protect the brain from large changes in velocity which are cited as the cause of brain injury (Rowson and Duma, 2011).



Primary and Secondary Brain Related Injury

Brain injuries are often classified as primary or secondary to aid treating clinicians in their decision making. Primary injury results from initial trauma and occurs at the moment of trauma. This could be bone fractures, contusions (bruises), axonal injury, damage to blood vessels, lacerations and haematoma. Secondary injuries, usually result from primary injuries and are not caused by mechanical damage. These include ischemia, edema, cell death, inflammation, hypotension, meningitis and raised intracranial pressure among others. Mendelow (2011) mentions that secondary injuries play a large role in permanent brain damage and potential fatality. It is important for a clinician to recognise and promptly treat primary injuries to reduce the incidence and severity of secondary outcomes.



What is Concussion?
Mechanism_of_concussion.jpg
Figure 1: Mechanism of Concussion (Ropper and Gorson, 2007)


One of the most common head injuries in American football is concussion (or minor traumatic brain injury (MTBI)). A concussion is a period of altered mental status
following a blow to the head and may be characterised by confusion, retrograde or anterograde amnesia and in serious cases, loss of consciousness among a myriad of other symptoms. As many of the symptoms of concussion resolve spontaneously within a few minutes or hours many players do not seek medical treatment (Kelly et al. 1991).

Concussions are a result of the anatomy of the brain within the skull. The brain is floating within the cerebrospinal fluid and is not attached in any way to the skull (Drake, Vogl and Mitchell 2005). When the head experiences a severe jolt, although the skull stops moving, the brain is carried forward by momentum. This causes a rotational shearing force on the mid brain and thalamus (fig. 1). This can result in axonal stretching and damage which is responsible for the symptoms observed (Ropper and Gorson, 2007). The brain may also strike the interior of the cranium with a large force resulting in bleeding and neuronal cell death (Amen et al. 2011).

Casson, Pellman and Viano (2008) showed that although repeated concussions do not increase an individual's risk of potentially catastrophic outcomes from concussion, they do increase the incidence of concussion in these players. This is hypothesised as being due to concussions reducing the concussive threshold so that lighter blows result in concussion.

Concussions are of particular concern to players and medical staff as they can be potentially fatal if not treated appropriately. Concussions may result in potentially fatal cerebral swelling or hematomas (either subdural or epidural) (Randolph and Kirkwood, 2009). Randolph and Kirkwood (2009) also highlight the worrying connection between multiple concussions during a footballers career and early onset of neurodegenerative diseases such as dementia and Alzheimer's.



Epilepsy Induced by Brain Damage

Epilepsy is a common, chronic neurological disorder characterised by recurrent seizures. Seizures are periods of abnormal, excessive or hypersynchronous neuronal activity in the brain. Head trauma causes about 10-15% of epilepsy. The risk of developing epilepsy after head trauma is proportional to the severity of the blow. For example, a minor concussion most likely wouldn't trigger the onset of epilepsy. This is in contrast to a heavier blow leading to comas, haematoma or crushing of brain tissues which will often trigger epilepsy. Head trauma resulting in skull fractures tend to incite epilepsy in 80% of cases[1] .

The development of seizures can occur either directly after trauma or much later. Many different types of trauma can contribute to the development of seizures such as hypoxia in the brain resulting from decreased flow following pinching of arteries. Anoxia may also present due to an injury to the chest, restricting the lungs in their gas exchange capabilities. When the brain receives a high velocity impact, brain hemorrhage may occur with blood bleeding either into the spinal column or directly into the brain tissue. This irritates the nerve cells due to the brain repairing the injured area with scar tissue. This can result in abnormal discharges causing seizures.

The onset of epilepsy following brain trauma is called posttraumatic epilepsy (PTE). There is a difference between PTE and posttraumatic seizures (PTS), which is a broader-spectrum term and signifies seizures that occur as a sequel to brain injury. Seizures that occur within 24 hours after brain injury are called immediate PTS. PTS that occur within 1 week after injury are termed early PTS and seizures that occur more than 1 week after injury are termed late PTS. About 20% of people who have a single late posttraumatic seizure never have any further seizures, and these people should not be labeled as having PTE.

Patient factors that increase susceptibility to PTE include the following:
  1. Age younger than 5 years or older than 65 years.
  2. Chronic alcoholism[2] .

Apolipoprotein E epsilon4 genotype has been proposed as a risk factor, but there is conflict within the literature. [9.10]
Injury-related factors that increase the risk of PTE are as follows:
  • Severe trauma
  • Penetrating head injuries
  • Intracranial hematoma
  • Linear or depressed skull fracture
  • Hemorrhagic contusion
  • Coma lasting more than 24 hours
  • Early PTS
  • Focal neuroimaging or electroencephalographic abnormalities in the acute postinjury period.[3] [4]

Cognitive and Perceptive Defects as a Result of Brain Damage

An important brain function is facial recognition. The brain identifies the human face’s proportions and expressions in order to recall emotions, health qualities and sometimes, social recognition. Studies have identified that major neural activations of the brain in order to be able to recognize faces occur in the extrastriate areas, particularly in the fusiform, gyri and in the inferior temporal gyri. The fusiform and the gyri are responsive to faces whereas the parahippocampal region is responsive towards structures.[5] [6] Since birth, this form of perception is important to the individual’s social interaction.[7] Damage to the brain such as a concussion, would cause impairment in understanding faces or what we call prosopagnosia.[8]
Prosopagnosia is a disorder in which the brain’s ability to recognize faces is impaired while the ability to recognize other objects may be relatively intact. This condition is usually associated with the acute brain damage characteristic of football. The damage to the brain is localized to the fusiform gyrus and extensive damage occurs in both the occipital and temporal lobes.[9]

There are three types of prosopagnosia but only two that stem from brain trauma:
  1. Apperceptive prosopagnosia.
    • One of the first disorders in the earlier processes of the face perception system. This disorder stems from a heavy blow, thus damaging the occipital lobe.
    • Incapable of making sense of faces or make same-different judgement when presented with pictures of different faces.
    • Incapable of working out attributes such as gender or age.
  2. Associative prosopagnosia.
    • Impairment to the links between early face perception processes and the semantic information in brain memory.
    • May be able to recognize and produce such information if information came from non-facial reception.
Personality Change due to Neural Death from Brain Trauma

Brain related injuries are the most common, specified type of injury in the NFL games, states the NFLS health care data report (2011) and the most minor and common example of brain related injuries as stated above are concussions. The National Institute of Health (2011) further points out that brain trauma in general and experienced by NFL players, can lead to secondary injury which could start within hours, a day or even minutes, leading to injuries like neural death, stroke, edema , infections, intracebral haematoma and many more.

diffuse_axonal_injury_mr_flair.jpg
Figure 2: A CT scan revealing diffuse axonal injury.


Neurotrauma (injury to the nerve) is a primary injury arising from numerous factors besides the NFL games such as accidents, missile’s, violence, falls and so on (Mudaliar and Burke, 1998). Diffuse axonal injury (DAI) is the most common type of primary traumatic injury found in patients with severe neurotrauma and tends to occur in three major anatomical areas namely the lobar white matter, corpus callosum and the dorso lateral aspects of the upper brain stem (Muduliar, 1998). DAI is triggered by focal intra-axonal change involving neurofilament subunits, resulting from either mechanical failure of axonal cytoskeleton or disruption of the axolemma increasing membrane permeability to calcium ions and sodium levels. The microscopic changes in DAI are characterised by multiple intra-axonal retraction balls, caused by the breakage of the cytoskeleton. This leads to a build up of transport products and swellings. When swellings become large enough they can tear the axon at the site of cytoskeleton breakage (axonal degeneration) causing a draw back towards the cell to form a bulb (Bullock, 2011). Breakage and misalignment of the cytoskeleton often leads to tearing of axon and eventually death of neurons, which can be classified as a secondary type of injury.





axon-shear.jpg
Figure 3: Axonal Shearing due to Injury



Personality changes, emotional problems and problem behaviours that may result from traumatic brain injury include :
  • Anxiety
  • Depression
  • Apathy
  • Anger
  • Confusion
  • Agitation
  • Mood swings
  • Lack of inhibition
  • Childish behaviours
  • Emotional outburst

Analysis


There is no doubt that the intention of the selected media item is to completely satirize the condition of your average NFL player. It dehumanizes the players by giving them base, animalistic characteristics brought up in the first point of the article where ‘playing dead’ would save your average person’s life. For its intent it can be justified that the information is indeed, extremely biased.

The article itself originates from a website based on satirizing general news coverage. The Onion is an American satire organization that releases print media- newspapers and web articles that publish satirical articles that feature both real and fictional issues. Judging by the varied content of the articles and the language used particularly in the media item, The Onion targets a range of viewers from ages 18 to 50; and those who are able to appreciate the value of the satirical content published.

The media item Keep Safe: What To Do If You See A Brain-Damaged Former NFL Players targets a 18-50 year old target audience that probably have a minimal interest the sport and may understand only base terminology relating to the sport.

So what neuroscientific content is actually presented in the article? Not a great deal. In fact one could argue that there is no neuroscientific information at all presented by this article. But the ‘symptoms’ of an ex-NFL player presented do seem to have a neuroscientific basis behind them. As mentioned in the neuroscientific content section, there is in fact statistical evidence to support a player may be more susceptible to epileptic fits due to brain trauma, and that a player may be more prone to aggression post-NFL career as a secondary side effect of strokes induced by neural trauma resulting from their games. Neural damage and death may occur in the frontal lobe of the cerebrum, causing irreversible personality changes.


In conclusion, can it be said that the article presented loses neuroscientific credibility because it has no immediate or appropriate neuroscientific content and is published by a satirical network? Well its content certainly cannot be taken for face value as a work of infallible fact relating to the condition of NFL players. However the points it does bring up do have a solid neurological base and on further study, positively relate to the neurological status of NFL players after trauma.

Search Process


The media item we selected to analyse is from 'The Onion News Network' a satirical news site which publishes humerous stories on popular topics.

When we were selecting a media item we first discussed a range of topics which appealed to each group member and a large range of topics were suggested. As our group members are from a range of backgrounds it was going to be difficult to find a topic which we all felt somewhat comfortable with yet would still be challenged to research and write about.
This particular item was in the form of an advice blog and was selected after a group member stumbled across it when browsing 'The Onion News'. This article was suggested to the group when we were sharing ideas and potential media items. We were immediately attracted to the large range of topics which were addressed. We selected this article because of the varied topics each group member would be able to research and address. It was also a very humorous piece which we felt would give us great scope for analysis and commentary on various misconceptions outlined.

This was a media article that succeeded in capturing the interests of everyone in the group. It addressed various topics which the group members could divide to research and then collaborate their results to provide more fact to the fiction.


References


Amen, D. G., Newberg A., Thatcher, R., Jin, Y., Wu, J., Keator, D. and Willeumier, K. Impact of Playing American Professional Football on Long-Term Brain Function. 2011. J Neuropsychiatry Clin. Neurosci. 23:1. 98 - 106.

Casson, I. R., Pellman, E. J. and Viano, D. C. Concussion in the National Football League: An Overview for Neurologists. 2008. Neurol Clin. 26. 217 - 241.

Drake, R. L., Vogl, A. W. and Mitchell, A. W. M. Gray's Anatomy for Students. 2005. Churchill Livingstone, Philadelphia.

Kelly, J. P., Nichols, J. S., Filley, C. M., Lillehei, K. O. and Rubinstein, D. Concussion in Sports. 1991. Journal of the American Medical Association. 266:20. 2867 - 2869.

Mendelow, A. Burke,L. Primary and Secondary Brain Injury. Neurotruama Society, 4:2, 70-88.

National Institute of Health .2011.Retrieved from 7 September 2011, http://www.ninds.nih.gov

Pangilinan, H and Muduliar,P.2011.Classification and Complications of Traumatic Brain Injury .Medscape, 41:6,976-80 .


Randolph, C. and Kirkwood, M. W. What are the real risks of sport-related concussion and are they modifiable? 2009. Journal of the International Neuropsychological Society. 15. 512 - 520.

Ropper, A. H. and Gorson, K. C. Concussion. 2007. N Engl J Med. 356:2. 166 - 172.

Rowson, S. and Duma, S. M. Development of the STAR Evaluation System for Football Helmets: Integrating Player Head Impact Exposure and Risk of Concussion. 2011. Annals of Biomedical Engineering. 39:8. 2130 - 2140.

The NFL Lockout's Health-Care Data .2011. Retrieved September 10, 2011, from http://www.esquire.com/the-side/feature/nfl-lockout-2011

The stroke foundation committee .2011. National Stroke foundation, Retrieved September 13, 2011, from __http://www.strokefoundation.com.au/what-is-a-stroke__

Dam, M. 
The Patient with Recently Diagnosed Epilepsy. 1983. Medical Aspects.
 Acta. Neurol. Scand. 93:67. 47.

Dam, A. M., Fuglsang-Frederiksen, A., Svarre-Olsen, U., Dam, M. 
Late-Onset Epilepsy: Etiologies, Types of Seizure, and Value of Clinical Investigation, EEG, and Computerized Tomography Scan. 1985.
 Epilepsia 26. 227

Frey, L. C. Epidemiology of Post Traumatic Epilepsy: A Critical Review. 2003. Epilepsia. 44:10. 11-7.
  1. ^ Dam, M. 
The Patient with Recently Diagnosed Epilepsy. 1983. Medical Aspects.
 Acta. Neurol. Scand. 93:67. 47.
  2. ^ Dam, M. 
The Patient with Recently Diagnosed Epilepsy. 1983. Medical Aspects.
 Acta. Neurol. Scand. 93:67. 47.
  3. ^ D'Ambrosio, R., Perucca, E. Epilepsy After Head Injury. 2004. Curr Opin Neurol. 17:6. 731-735.
  4. ^ Diaz-Arrastia, R., Gong, Y., Fair, S., Scott, K. D., Garcia, M. C., Carlile, M. C., et al. Increased Risk of Late Post Traumatic Seizures Associated with Inheritance of APOE Epsilon4 Allele. 2003. Arch Neurol. 60:6. 818-822.
  5. ^
    Nelson, C. A. The Development and Neural Bases of Face Recognition. Infant and Child Development. 2001. 10:1-2. 3–18.
  6. ^ Andreasen, NC., O'Leary, DS., Arndt, S., et al. Neural substrates of facial recognition. 1996. J Neuropsychiatry Clin Neurosci. 8:2. 139-146.
  7. ^ Bruce V, Young A (August 1986). "Understanding face recognition�. Br J Psychology 77(Pt 3): 305-327.
  8. ^ Kanwisher, N., McDermott, J., Chun, MM. The Fusiform Face Area: A Module in Human Extrastriate Cortex Specialized for Face Perception. 1997. J. Neurosci. 17:11.
  9. ^
    Pauley, Poul-Erik. Brain Function, Locomotion and Disorders. 1999-2000. Textbook in Medical Physiology and Pathophysiology Essentials and Clinical Problems. Copenhangeen Medical Publishers. 4.