More on CTE

That’s Chronic Traumatic Encephalopathy.  There have been several previous healthy memory posts on this important topic (see “Chronic Traumatic Encephalopathy,” and “Watching Football, Feeling Guilty”.  The March 5, 2016 edition of “The Economist” contains two articles on this topic.

The first part of this post is taken from the article “Bang to Rights.”  The road to CTE starts with concussions.  About one instance in five of these then leads  to post-concussion syndrome, which is a period of cognitive impairment the may last months, in which sufferers have headaches, unsteadiness, and other problems.  It seems likely that repeated concussions can lead to CTE.

The underlying biology  is becoming apparent. It begins with the release of certain chemicals  when axons, the connections between nerve cells, are damaged.  Concussion is caused by the internal movement and distortion of the brain as it bounces around inside the cranium upon impact.  This bouncing stretches and deforms bundles of axons that connect different regions of the brain.  This defamation shears some axons directly, releasing their protein contents, including tau, which with time can form abnormal tangles similar to those found in Alzheimer’s disease.  It also causes abnormal inflows of sodium and calcium ions in unsecured but damaged axons. These trigger a process which releases protein-breaking enzymes that destroy the axon, further disrupting the brain’s internal communication.  The blood-brain barrier is also damaged.   This barrier is a system of tightly joined cells that surround the capillaries that service he brain.  The purpose of the blood-brain barrier is to control what enters and exits the central nervous system.  One consequence of damaging the blood-brain barrier is that a brain protein called S100B is released into general circulation.  The body’s immune system mounts a response against this protein, and the antibodies it generates can find their way back into the brain and damage healthy brain cells.  Researchers think that repeated damage could set the stage for a continuous autoimmune attack on the brain.

This connection between concussion, post-concussion syndrome and CTE itself is still an hypothesis and is yet to be established.  This connection is important as it provides a basis for assessing the long term consequences of an injury.  Another protein released  during concussion, SNTF, is also of interest.  Research on concussed ice-hockey players suggests its level in the blood after a blow to the head  predicts the severity of the concussion.  Presumably, a test for SNTF or S100B might be a means to determine the prognosis of an injured individual.

Most coaches and players do not appreciate the damage caused by concussions.  Many return to the field before  before the brain’s physical healing is complete.  A survey of university athletes fond that 20% believed  they had suffered a concussion, but almost 80% of those decided to continue to play rather than to seek medical attention.

Research continues to find an objective measure of the damage a concussion  causes.  A rugby club in London is having it players wear impact sensors to monitor collision and provide  samples at the end of every game.  The researchers hope to find chemical associated with brain injury that could be used to develop a blood test.  Translational Genomics Research Institute in Phoenix is conducting a similar project  to study football players at Arizona State University.

Brain scanning is also being used to reveal reduced brain flow in the brains of athletes who have suffered concussions.  There are also commercially available apps called Headcheck and Braincheck, which are intended  to help athletes  asses their baseline brain performance and allow the tracking of the brain’s health.  These are not approved as medical devices, so they cannot be used to diagnose concussions.

Children are of special concern, as their brains are more vulnerable.  In 2012 an article by Andrew Mayer at the University of New Mexico reported that subtle brain changes in children who have sustained a concussion press for months after the injury, even when thee are no longer obvious symptoms.  Work by Charles Hillman of the University of Illinois found that children who had sustained a single sports-related concussion still had impaired brain function  two years later.  Ten-year-olds with a history of concussion  performed worse on tests of working memory, attention, and impulse control  that did their uninjured counterparts.  Among children with a history of concussion, those injured earlier in life  had larger deficits.

The second Economist article, “Schools and hard knocks,” addressed this children issue further.  The risks of concussion are even greater in rugby than they are in American football.  Rugby now has “head-injury assessment” rules that look players who have suspects-concussions to be substituted  temporarily  so they they can be checked by medical staff.  All 50 American states have “return to play” laws that require medical clearance before younger athletes who have sustained a concussion can return to the field again.  Of course, the obvious issue here is whether it is safe to play a game whose rules require people to slam into each other.  Remember that the purpose of athletics is to promote health, primarily, and sometimes to promote team building.  It is doubly ironic when schools, who should have the objective of building minds, promote activities that injure the primary organ underlying the mind.  At least the American football coaches at Ivy League universities have agreed to get rid of “full contact” training sessions during the playing season.

Children still remain a special case.   Research at the University of Illinois  have found that children who had sustained a singe sports-related concussion still had impaired brain function two years later.  The governing body US Soccer has banned headers for children aged ten and under, and restricted then for 11-to-13-year olds.

Clearly, much more needs to be done.

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