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Writer's pictureSierra Corbin

Understanding Concussion






Since professional football players have brought to light the problem of concussion, and the NFL has controversially denied it, we have heard more about this subject than ever before and most states have passed laws because of it.  Players are suffering from concussions and chronic traumatic encephalopathy, a progressive disease that is caused by a severe brain injury or multiple blows to the head.  During Super Bowl 50, two players endured a concussion.  Concussions are mild traumatic brain injuries (MTBI).  Similar to the old term, “shell shock”, which is more appropriately named, post traumatic stress disorder (PTSD), “concussion” seems to be a less intimidating term than “traumatic brain injury” (TBI).  The truth is, 1.7 million people sustain a TBI each year in the U.S. and the more we beat around the bush about it, the more we ignore people effected.  A mild head injury’s outcomes may last only a few months, but any severity level can have lifelong symptoms. 


Our brains, vital to our well being and functioning, are actually quite vulnerable to damage.  TBI occurs from a:  

• translational or rotational force that displaces the brain from its original position (e.g. whip lash)

• blow to the head (e.g. ground level fall or being punched)

• puncture (e.g. gun shot)

• extreme pressure change (e.g. from explosives used in war)


Upon closer look, damage is caused by:


• axonal shearing (tearing the neural axons)

• lack of or insufficient supply of oxygen 

• cavitation effects (bubbles in cerebral fluid, created by a jolt, burst and damage neurons)


Brain injuries have three recognized severity levels, mild (MTBI), moderate, and severe, that are determined by objective measurement through neurological imaging and standardized assessments.  However, computer imaging cannot always show damage done to axons after injury and keen observation is required to assess a TBI, especially MTBI. Some of the symptoms experienced after just a MTBI are:

• headache

• decreased concentration

• depression

• slower processing speed

• poor sleep quality

• aggression 

• degenerative disease

• inability to process complex visual stimuli

• Second Impact Syndrome: severe TBI or death in young adults under 23 who sustain a second TBI before an initial TBI’s signs and symptoms resolve


People who sustain moderate and severe brain injuries experience these symptoms more intensely and for longer (or like I said, a lifetime), as well as a range of other problems, some involving the inability to communicate, take care of oneself, or walk. 


Statistics of TBI (annually):

• 1.7 million people sustain a TBI 

• 275 million people are hospitalized for TBI

• Medical costs estimate 60 billion dollars

• Toddlers, young men, and senior citizens sustain the most TBIs

• Falls and motor vehicle accidents are the most common causes of TBI


As a speech-language pathologist, I study brain injury and treat people who are effected.  Some of the scariest outcomes I have seen after a TBI are personality changes, inability to initiate tasks, memory loss, mood swings, and inability to express emotions.  These outcomes change the life of not only the person who sustained the injury, but family and friends as well.


We don’t have to be NFL players to make a difference in how brain injuries are detected and treated.  Currently, millions of people are suffering from the consequences of TBI and don’t have the support in place to be treated with restorative therapy.  Whether your children or nieces and nephews play school sports, you watch football or soccer, have a toddler or care for an aging parent, with this information, you can advocate for people who have sustained TBIs. 


These signs and symptoms are taken from The Brain Injury Association of America website, a great resource on TBI.  Recognize these after an accident and get the appropriate support.

• Spinal fluid (thin water-looking liquid) coming out of the ears or nose

• Loss of consciousness; however, loss of consciousness may not occur in some concussion cases

• Dilated (the black center of the eye is large and does not get smaller in light)or unequal size of pupils

• Vision changes (blurred vision or seeing double, not able to tolerate bright light, loss of eye movement,

blindness)

• Dizziness, balance problems

• Respiratory failure (not breathing)

• Coma (not alert and unable to respond to others) or semicomatose state

• Paralysis, difficulty moving body parts, weakness, poor coordination

• Slow pulse

• Slow breathing rate, with an increase in blood pressure

• Vomiting

• Lethargy (sluggish, sleepy, gets tired easily)

• Headache • Confusion

• Ringing in the ears, or changes in ability to hear

• Difficulty with thinking skills (difficulty “thinking straight”, memory problems, poor judgment, poor

attention span, a slowed thought processing speed)

• Inappropriate emotional responses (irritability, easily frustrated, inappropriate crying or laughing)

• Difficulty speaking, slurred speech, difficulty swallowing

• Body numbness or tingling

• Loss of bowel control or bladder control


References

About brain injury.  (2012, Oct 12).  Brain Injury Association of America.  Retrieved from  http://www.biausa.org/about-brain-injury.htm 

Ahmed F.A., Kamnaksh, A., Kovesdi, E., Long, J.B., Agoston, D.V. (2013).  Long-Term         Consequences of Single and Multiple Mild Blast Exposure on Select Physiological Parameters and Blood-Based Biomarkers.  Electrophoresis.  doi: 10.1002/elps.201300077

Brosseau-Lachaine, B., Gagnon, I., Forget, R., & Faubert, J. (2008).  Mild traumatic brain injury induces prolonged visual processing deficits in children.  Brain Injury, 22(9), 657-668.  

Cantu, R.C & Gean, A.D. (2010).  Second-impact syndrome and a small subdural hematoma: An uncommon catastrophic result of repetitive head injury with a characteristic imaging appearance.  Journal of Neurotrauma, 27(9), 1557-1564. 

Dixon, C.E., Clifton G.L., Lighthall J.W., Yaghmai A.A., & Hayes R.L. (1991).  A controlled cortical impact model of traumatic brain injury in the rat (Abstract).  Journal of Neuroscience Methods. 39(3). 253-262. 

Hayempour, B.J., Rushing, S.E., & Alavi, A.  (2011).  The role of neuroimaging in assessing neuropsychological deficits following traumatic brain injury.  Journal of Psychiatry and Law, 39, 537-566.

Lundin, A., Boussard, C., Edman, G., Borg, J. (2006).  Symptoms and disability until 3 months after mild TBI.  Brain Injury, 20 (8), 799-806. 

McKee, A. C., Stern, R.A., Nowinski, C.J., Stein, T.D., & Alvarez, V.E. (2013).  The Spectrum of Disease in Chronic Traumatic Encephalopathy.  Brain, 136 (1), 43-64. doi: 10.1093/brain/aws307

Omalu, B.I., Bailes, J., Hammers, J.L., Fitzsimmons, R.P.  (2010).  Chronic traumatic encephalopathy, suicides and parasuicides in professional american athletes: the role of the forensic pathologist.  American Journal of Forensic Medicine & Pathology, 31 (2), 130-132.

Teasdale, G., & Jennett B. (1974).  Assessment of coma and impaired consciousness. A practice scale.  The Lancet, 304(7872), 81-84.

Wetjen, N.M., Pickelmann, M.A., & Atkinson J.L. (2010). Second impact syndrome: concussion and second injury brain complications.  Journal of the American College of Surgeons, 211, 553-557.


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