From Axon to Action: The Devil of Brain Trauma Is in the Details
by David Castillo — Medical Instructor, HeadKickLegend.com
May 28, 2011 – 00:00
While it may seem intuitive to measure brain trauma, specifically the most intense trauma associated with contact sports (CTE: Chronic Traumatic Encephalopathy), in concussions, the current growing body of evidence suggests that the everyday, ostensibly ‘trivial’ trauma is causing this degenerative brain disease, as opposed to the accumulation of large, concussive trauma.
How does this affect behavior? Why is it that athletes in contact sports are statistically more likely to suffer depression? Why is it that people suffering from chronic pain (surely an occasional byproduct of CTE given that the symptoms of brain trauma can involve emesis, dizziness, motor impairment, photophobia, and memory loss) are six times more likely to report suicidal thoughts?
The case of Owen Thomas (diagnosed with CTE at age 21), prompts a closer look. Whether or not CTE caused his suicide is not the task of this essay, but perhaps emphasizing potential correlations are important enough. To explain why, scientists are looking at axons. Experiments with axons have been highlighted off the work of Douglas Smith at the University of Pennsylvania, where he builds miniature brains out of rat neurons, which are then ‘hit’ with controlled puffs of air to simulate brain trauma at a molecular level.
To recap from those static A&P lectures none of us enjoyed, the axon is like a paperboy, sending neurological news, referred to as neurotransmitters, to "homes" called dendrites. The findings show that as axons stretch upon trauma (vulnerable months after an initial stretch), like a worn rubber band, they lose their elasticity after swelling, where proteins then block the proper neural absorption until the axons fall apart (called Diffuse Axonal Injury).
This "traffic jam" of hoarded proteins, caused by the sudden acceleration/deceleration of the head, destroys axonal connections, which are important for the function of neurotransmitters that can do wonderful things: they inform sociability (seratonin), optimism, and persistence (dopamine), and even, as love expert and anthropologist, Helen Fisher has argued, the characteristics that model our capacity for romantic love, such as excessive energy, sleeplessness, loss of appetite, and the type of acute memory for new stimuli that allows us to keep from perceiving time spent with an intimate partner as trivial (associated with norepinephrine). CTE is a stark example of how intimate the connection between physiology and psychology is: a disorder that threatens the chemical constitution which helps define how we think.