The science around concussion has been a pretty big story for the last two decades or so thanks largely to the increased attention that American football players have received, especially the younger players who have not even reached brain maturity yet. As a teen playing rugby, I received some “mild” concussions and witnessed several of my peers suffer some serious blows to the head that made them forget what they had eaten for lunch that day. For a long time, the medical community saw concussions as an acceptable risk in the sporting world, one that can be recovered from with time. But, how do concussions work in the brain and how bad for us are they really?
Concussion as a medical condition has been recognized as a distinct phenomena from brain trauma as far back as a thousand years ago, and was the topic of discussion in the 1900s due to how often it was seen in professional boxing (for more on that, see this brain basics article). The medical definition for concussion highlights its observable symptoms, namely the alteration to memory and orientation, and even the possibility of losing consciousness. Although loss of consciousness is rare, the neurobiological cascade that causes the rest of the symptoms is relatively well understood from animal models. When the brain is damaged by the sudden, violent movement of head trauma, there is a burst of excitatory neurotransmitters released. This may sound counterintuitive, but the sudden increase in the concentration of glutamate results in it binding with NMDA receptors, which triggers a release of potassium ions from neurons into the extracellular space. Consequently, sodium ions flood into the cell through the ion channels in the neuronal membrane. The brain attempts to recover from this event by activating membrane pumps to restore the homeostasis between the sodium and potassium ions, but this requires energy, thus the region sees an increase in blood pressure and drop in glucose concentration. Naturally, the high demand for ATP results in increased lactate concentrations, causing neuronal function to be impaired and reducing blood flow in the region.
For an analogy of this, imagine a bustling city with a complex network of roads and vehicles representing the neurons in your brain. In this analogy, head trauma is like a sudden, violent collision between two cars, causing a disruption in the flow of traffic. When the collision occurs, there is chaos and confusion. Excitatory neurotransmitters, acting as traffic signals, are released in large amounts. These neurotransmitters, like green lights, tell the neurons to become active. However, due to the collision, the normal traffic control mechanisms are disrupted. The sudden increase in excitatory neurotransmitters is like an excessive number of green lights turning on at once. This leads to a surge of cars leaving and entering the roads, causing congestion. To restore order, the brain tries to balance the situation. It activates "traffic pumps" that work like emergency traffic controllers. These pumps try to restore the balance between sodium and potassium ions, which are like cars and trucks moving in and out of the neurons. But this recovery process requires a lot of energy, similar to the effort needed to get the traffic flowing smoothly again. The brain needs to increase blood pressure, like bringing in more traffic police, and use up glucose, which is like reducing the fuel available to the vehicles. As a result, there is an increased demand for ATP, the energy currency of cells, similar to how more fuel is needed to power the traffic pumps and police officers. This high demand for energy leads to a buildup of lactate, which is like exhaust fumes accumulating on the roads, impairing the functioning of neurons and reducing blood flow in the affected region.
On average, the recovery time from such a traumatic brain event is quoted as 7-10 days, by which time the symptoms of post-concussion syndrome, namely the headaches, should have diminished. However, research has shown that the metabolic and blood flow imbalance in the traumatised brain can take several weeks to recover, during which time the brain is very sensitive to further damage. During concussion diagnosis, if a severe injury is suspected, a CT or MRI scan is usually the recommended course of action. These methods provide a structural image of the brain that informs doctors of the presence of inflammation, that could be indicative of severe brain trauma, and would have to be monitored closely. However, structural imaging is too weak to look at small scale damage that can occur at the level of, say, the axon of neurons. Consequently, most cases of long-term post-concussion symptoms are either undiagnosed or largely ignored due to lack of structural damage. Such long-term symptoms can be impactful and include physiological effects, such as headaches, or cognitive effects, such as mood disorders or difficulty concentrating, that go on for several months after the impact occurred.
Recently, a team at the University of Cambridge published a study on post-concussion syndrome that showed not only that just under half of patients experienced symptoms six months after the event, but also attempted to understand why. Given the cognitive changes and the ineffectiveness of structural scans, the team looked to functional MRI to investigate the changes in the patients. Looking at data from 108 volunteers and 76 controls, they found that those who had been concussed in the past had abnormal connectivity in the thalamus compared to the controls. The thalamus, found in the midbrain, serves mainly as a relay of information from the senses to the cerebral cortex. Additionally, it has also been implicated in levels of consciousness, such as sleep and wakefulness, as well as in learning and memory. Conversely with expectations, those that suffered the most from post-concussion syndrome had improved connectivity between the thalamus and the rest of the brain. This finding may imply that the increased connectivity is an over-compensation for adaptation to the mild brain trauma. Further investigations shone a light on the long-term cognitive symptoms too. Positron emission tomography showed that patients suffering from memory problems had increased connectivity between the thalamus and brain regions with higher concentrations of noradrenaline. Meanwhile, those with mood problems had higher connectivity to brain regions high in serotonin.
Limited as we are with current structural neuroimaging technology, imaging the changes in brain networks is an enormous step in the direction of not only understanding the damage that concussion wrecks on the brain, but also how the brain heals from damage. With an improved comprehension of the long-term chemical and physical changes we could even have targeted drugs that improve our mental wellbeing following brain trauma.
Author: Thomas von Rein