The “Concussion” is the First Domino

We’ve all heard that about half the damage after a sprained ankle is caused by the swelling.

Swelling is a protective inflammatory response. Swelling is helpful for the sprained ankle because it immobilizes the joint and is associated with increased blood flow.

But the swelling itself can increase tissue damage, impair healing, and contribute to long-term dysfunction if not well controlled. That’s why it’s so important to ice as soon as possible.

It’s not surprising that “swelling” in the brain after an injury—called neuroinflammation—plays a significant role after a concussion. It impacts both injury progression and recovery.

We used to think about concussions as a single event. That event was a disruption in brain function caused by an external force to the head. But they aren’t compartmentalized like that. Now we know that the initial “jostling” is just the catalyst that sets a much larger process in motion.

Doctors use the terms primary and secondary injury mechanisms. The primary injury mechanism is the mechanical disruption of brain tissue. The secondary injury mechanism is the complex biochemical cascade that follows.

The disruption of brain tissues is the first domino to fall. It starts the chain reaction that causes other dominoes to fall.

One of these subsequent dominos is neuroinflammation. Neuroinflammation is joined by ischemia, hypoxia, excitotoxicity, calcium dysregulation, mitochondrial dysfunction, and apoptosis. An entire crew causing secondary injury.

Some of these secondary actors take a while to get going. They may not start affecting the brain for hours, days or weeks following the initial trauma. But once activated, they exacerbate the primary injury and cause additional neurological damage.

And even though both have a big impact, neither the primary injury or the secondary injury mechanisms are going to show up on an x-ray or CT scan.

It kills me when defense doctors try to exploit their knowledge to trick juries. They’re playing a shell game.

Their whole goal is to make the jurors look under the wrong shell and show there’s nothing there (while at the same time hiding the proof under a different shell).

I’m getting ready for a trial right now. Here are some of the ways the defense doctor is trying to run it (and these are typical):

• There’s modest damage to the car so there must not have been enough force to cause a brain injury.

• In the ER, doctors diagnosed a “closed head injury,” not a “concussion.”

• The CT scan shows no structural damage to the brain, so there much not have been an injury.

• The injured person reported symptoms days or weeks later that weren’t charted at the Emergency Room.

• The injured person suffers from somatic symptom disorder (meaning that their symptoms are real, but caused by their emotional reaction to the collision rather than an actual injury to their brain).

All of these “positions” taken by the defense doctor are classics. And they can all be defrocked.

The one I’ve underlined—that the collision must not have caused post-concussive symptoms because they were not reported right away—is completely explained by the cascade of secondary actors that cause injuries/symptoms hours, days or weeks after the primary disruption of brain tissue.