Eenie, Meenie, Miney, Tau

Mike Webster, a celebrated Hall of Fame center for the Pittsburg Steelers, played in 245 NFL games, including his time with the Kansas City Chiefs, and was hit in the head thousands of times. “Iron Mike” died 24 September 2002 at the age of 50. Dr. Bennet Omalu, a neuropathologist, was assigned to perform the autopsy on the body and the brain. Omalu made a groundbreaking discovery, seeing something in Webster’s brain that had never been found in a football player’s brain before and should never have been present in the brain of a 50-year-old man (Breslow, 2013; Concussion Legacy Foundation [CLF], 2017).

 

 

If you’ve read at all about concussions you’ve probably come across the term Chronic Traumatic Encephalopathy (CTE). CTE is a progressive degenerative disease of the brain found in athletes, military veterans, and others with a history of repetitive brain trauma. The repetitive brain trauma causes a buildup of a protein called tau.  The aggregation of tau is toxic, slowly killing cells of the brain, as also seen in Alzheimer’s disease (CLF, 2017; Lerner, 2016; Mandelkow & Mandelkow, 2012).

cta.jpg

The tau protein in itself is not inherently dangerous. Tau is a protein in the brain which helps stabilize brain cell structure and internal transport system (CLF, 2017; Lerner, 2016). Tau links microtubules that run through axons of the brain, two tau proteins in each link; the heads of the tau proteins are each bound to a microtubule, and the tau tails meet in the middle and are bound together, but this bound isn’t permanent (Lerner, 2016). Because of its hydrophilic nature tau does not adopt the typical compact, folded structure of most proteins. Instead, it is “natively unfolded” and “intrinsically disordered”, meaning its highly flexible and mobile, kind of like pipe cleaners you use in arts and crafts  (Mandelkow & Mandelkow, 2012). Motion within the brain easily detaches the tail ends of the tau protein and causes them to reattach to a new tau protein tail. This binding and unbinding allow for easy sliding between microtubules without damage (Lerner, 2016).

repetitive trauma

However, repeated injury to the brain causes neurons to stretch and tear.  Rapid jolts in concussive episodes do not allow the bound portions of tau tails to untangle and bond with a new tau partner. High-velocity forces of a concussion do not allow to tail ends of the tau proteins to unbind and the forces are exerted on the microtubules instead, causing damage (Lerner, 2016). The tau protein then changes its shape, clumps together with another tau, and spreads while slowly killing neurons. In CTE, clumps of tau tend to first appear around blood vessels within the brain sulci (valleys between brain cortical folds), and then spreads to other areas of the brain (CLF, 2017).

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axons under stress

The danger of chronic brain injury is the guaranteed risk for memory loss, confusion, impaired judgment, paranoia, impulse control problems, aggression, depression, and eventually progressive dementia (CLF, 2017).

A study by Shahim et al. (2014) looked at blood biomarkers after a concussion in professional ice hockey players and found that the highest concentrations of total tau were measured immediately after injury, tau levels declined after the first 12 hours, and a second peak of tau levels occurred between 12-36 hours post-injury. Most importantly, tau levels 1 hour post-concussion concussion predicted the number of days it took for the concussion symptoms to resolve and the players to have safe return to play. This suggests that total tau levels may potentially be a way to monitor recovery in patients with brain injury (Shahim et al., 2014)Since diagnostic imaging is not able to help health care professionals predict concussion outcomes and recovery, perhaps these findings with help pave the way for more efficient, more informed, and

Since diagnostic imaging is not able to help health care professionals predict concussion outcomes and recovery, perhaps these findings with help pave the way for more efficient, more informed, and better-monitored recovery and return to play.

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Author: Alyssa Reidy, LAT, ATC, CCTP

References

Breslow, J. (2013). The Autopsy That Changed Football. [online] FRONTLINE. Available at: http://www.pbs.org/wgbh/frontline/article/the-autopsy-that-changed-football/

Concussion Legacy Foundation [CLF] (2017). What is CTE?. [online] Concussion Legacy Foundation. Available at: https://concussionfoundation.org/learning-center/what-is-cte

Lerner, E. (2016). Penn study determines breakaway protein is critical in concussions. [online] Penncurrent.upenn.edu. Available at: https://penncurrent.upenn.edu/2016-01-14/latest-news/penn-study-determines-breakaway-protein-critical-concussions

Mandelkow, E. and Mandelkow, E. (2012). Biochemistry and Cell Biology of Tau Protein in Neurofibrillary Degeneration. Cold Spring Harbor Perspectives in Medicine, 2(7), p.a006247

Shahim, P., Tegner, Y., Wilson, D., Randall, J., Skillbäck, T., Pazooki, D., Kallberg, B., Blennow, K. and Zetterberg, H. (2014). Blood Biomarkers for Brain Injury in Concussed Professional Ice Hockey Players. JAMA Neurology, 71(6), p.684

 

 

The Blue Light Spectrum Concussion

How many times have you stared at your cell phone screen since waking up this morning? How long will you look at after getting in bed tonight?

 

Patients with concussion present with varying symptoms: headaches, dizziness, and vertigo, amnesia, depression, irritability, word-finding difficulty, impulsiveness, difficulty sleeping, difficulty concentrating, sound sensitivity and visual symptoms. These visual symptoms might include photosensitivity and photophobia, wherein “photo-” equates to light. Photophobia translates to “fear of light”, but it is actually a neurological condition affecting how the light receptors in the eye transmit information to the brain. Generally, it refers to exposure to light that exacerbates pain (Digre & Brennan, 2012). Light and sound tolerance decrease in patients with head injuries compared to control subjects (Magone et al., 2013). Light sensitivity after a concussion in the absence of ocular inflammation is a common complaint and effects 40-50% of patients with brain injury.

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The increased sensitivity to light occurs in the subacute period (7-21 days) after a head injury, and although most patients/athletes report improved symptoms after 6 months, patients/athletes with post-concussive syndrome continue to report increased photosensitivity (Digre & Brennan, 2012). Research suggests the cause is cortical and subcortical lack of inhibitory control (Magone et al, 2013), as also seen in other brain disorders, such as migraines and epilepsy. These abnormal responses may include non-uniform cortical excitability and cortical hyper-responsiveness, which may interfere with visual perception to cause photophobia. A study of patients using resting state functional magnetic resonance imaging (fMRI) in patients with closed head injuries showed a cluster of increased functional connectivity in the right frontoparietal lobe as compared to and a matched control group (Shumskaya et al., 2012). This increased activity may cause increased awareness of one’s external environment resulting in cognitive fatigue with headache and increased sensitivity to light and sound. Digre and Brennan (2012) provide a more extensive description of the pathophysiology of photophobia. I have included the link below for your reading pleasure.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485070/

Computer Vision Syndrome occurs in 75% of computer workers who view a video display for 6-9 hours per day. Ocular complaints include eye fatigue, burning, redness, blurred vision, and dry eyes, as well as non-ocular symptoms (headache, neck/shoulder pain)(Loh & Redd, 2008; Lynch et al., 2015). Viewing a digital screen is different that reading printed material; the letters on a screen are not as sharply defined, contrast of letters to the background is reduced, and glare and reflection on the screen making it difficult to read, forcing increased visual demand by the reader (AOA, 217; Loh & Redd, 2008).The normal human blink rate of 10-15 times per minute is significantly reduced while using digital screens, causing poor tear film quality, stressing the cornea. Prolonged use of a digital screen (i.e. computers, cell phones, television, tablets, e-readers, etc.) causes transient deviation of phoria (visual alignment), transient myopia (nearsightedness), and diminished accommodation to changing visual stimuli (Loh & Redd, 2008; Lynch et al., 2015).

melatonin

Digital screens emanate a lot of low wavelength light, what the science world would call blue light. The eyes’ exposure to blue light suppresses the body’s ability to produce melatonin, the hormone produced by the pineal gland when light receptors in the eye detect darkness, helping to regulate the body’s circadian rhythm and make you fall asleep. Ergo, people who are glued to their digital screens, especially in the evening when the body should begin melatonin production, delay this mechanism or even prevent the body from making melatonin the entire night.

blue light frequency

Recent research supporting the use of bright light therapy in the morning to help improve sleep, cognition, emotion and brain function in patients with concussion (Stone, 2013).

Add all of that to concussion symptoms and an athlete/patient is guaranteed to hinder the healing process and delay their return to play/work.

big picture

Now, in a world that runs on screen time, it’s not realistic to completely cut out all electronics from our daily routines. What we as health care professionals can do it educate our athletes/patients and their parents/guardians on how to modify. First and foremost, limit screen time. The American Optometric Association recommends following the 20-20-20 rule for people without concussions; take a 20-second break to view something 20 feet away every 20 minutes (AOA, 2017).

202020

 

Again, it’s not realistic to micromanage one’s screen time when it’s dark outside, but we’re fortunate enough to live in a time where blue light is able to be eliminated without turning off our screens. Software engineers have created a plethora of apps and settings on our devices that automatically eliminate blue light from our devices at a set time, usually sunset, or a specified time set by the user. Below are just a few of many device applications that can be downloaded to help the concussed patient manage their light exposure.

 

flux

F.Lux (I personally use this for my computer) – this app reduces blue light after the sun sets in your specific location https://justgetflux.com/

 

twilight

Twilight – for Android users, this app is similar to f.lux, although it doesn’t have a particular blue light filter, you can control the color temperature and intensity https://play.google.com/store/apps/details?id=com.urbandroid.lux&hl=en

midnight

Midnight– you control the black, yellow, blue and red light, you can schedule to start and stop time of the filter, but it doesn’t automatically change based on your location’s sunrise/sunset. However, it can determine ambient light and dims the screen in dark environments.

This list is not exhaustive, all anyone needs is an internet search engine to compare and contrast apps.

 

Author: Alyssa Reidy, LAT, ATC, CCTP

 

 

References

American Optometric Association. (2017). Computer Vision Syndrome. Aoa.org. Retrieved 17 June 2017, from https://www.aoa.org/patients-and-public/caring-for-your-vision/protecting-your-vision/computer-vision-syndrome?sso=y

Digre, K., & Brennan, K. (2012). Shedding Light on Photophobia. Journal Of Neuro-Ophthalmology, 32(1), 68-81. http://dx.doi.org/10.1097/wno.0b013e3182474548

Greenbaum, D. (2017). 5 Best Android Apps that Reduce Eye Strain for Night Reading. Guidingtech.com. Retrieved 17 June 2017, from http://www.guidingtech.com/60491/best-android-night-filters/

Loh, K., & Redd, S. (2008). Understanding and Preventing Computer Vision Syndrome. Malays Fam Physician, 3(3), 128-130.

Lynch, J., Anderson, M., Benton, B., & Green, S. (2015). The Gaming of Concussions: A Unique Intervention in Postconcussion Syndrome. Journal Of Athletic Training, 50(3), 270-276. http://dx.doi.org/10.4085/1062-6050-49.3.78

Magone, M., Cockerham, G., & Shin, S. (2013). Visual Dysfunction in Combat-Related Mild Traumatic Brain Injury: A Review. US Ophthalmic Review, 06(01), 48.

Shumskaya E, Andriessen TM, Norris DG, Vos PE. (Jul 2012). Neurology, 10; 79(2):175-82.

Stone, P. (2013). Bright Light Therapy Relieves TBI Sleep Problems. Neurologic Rehabilitation Institute at Brookhaven Hospital. Retrieved 17 June 2017, from http://www.traumaticbraininjury.net/bright-light-therapy-relieves-tbi-sleep-problems/