Delayed, Progressive Brain Injury Symptoms Following Head Trauma

Brain Injury
Delayed Brain Injury Symptoms

Traumatic Diffuse Axonal Injury / Neuron Suicide and Murder         

On any given day dozens, if not hundreds of individuals suffering from “mild” TBIs are turned away as they seek help from personal injury attorneys across the country. Who could blame the attorneys for turning these people away. After all, the facts associated with these cases are something like this: 1) no initial symptoms or complaints of neurocognitive involvement, 2) no complaints of neurocognitive symptoms until weeks or months after the traumatic event, 3) no evidence of brain injury on traditional brain imaging studies (CT or MRI), 4) progression of neurocognitive symptoms for months or even years after the traumatic event.

Perhaps many of the attorneys turned away these individuals because the attorneys were unable to appreciate and recognize the above-described pattern of delayed onset and progression of neurocognitive symptoms without evidence of injury on imaging studies is a classic presentation pattern, well documented in medical literature. Other attorneys may have recognized the pattern of symptoms, but may have felt unable to effectively prove these neurological symptoms were “real” and/or directly related to some traumatic event.

Regardless of why these TBI victims were initially turned away, many sought out other attorneys who were able to help them. If personal injury attorneys possess the knowledge of pathophysiology associated with the aforementioned pattern of TBI injuries, they can avoid turning away TBI victims, instead helping them or referring them to an attorney who can.

The fact that individuals sustaining traumatic brain injuries (TBIs) often exhibit delayed or worsening symptoms over time is well documented in medical literature. A narrated animation that very effectively demonstrates this process can be seen at the following link Despite this fact, insurance company representatives and their attorneys will often argue that this delayed pattern of symptoms is instead, proof that an individual did not sustain a brain injury as a result of a particular event.  Instead of acknowledging the delay in development and progressive worsening of symptoms are consistent with TBIs, the insurance companies will argue that the symptoms should have been immediately evident and at their most severe immediately following a traumatic event. Because of the delay and worsening of symptoms, insurance companies and their representatives may argue that the victim is malingering or that the symptoms must be related to some other injury or disease process. It is a challenge for an attorney representing the victim of a TBI to overcome the jurors' and other decision makers' predisposition to believe that symptoms should be at their most severe immediately following a traumatic event and improve over time (like most other wounds).

Scientific research, has revealed that not only is there an initial stage of injuries to neurons that result in immediate symptoms, there is also a second stage of gradual death of neurons that progresses over a prolonged period of and results in significant worsening of those injuries in scope and severity. The literature describes this progression and worsening of symptoms as continuing for months, years, or even for the TBI survivor's entire lifetime. Many refer to a TBI as a "process" not an "event".

Trauma to the head doesn't have to be particularly severe to begin the insidious chain of events that can devastate the lives of victims of TBIs and their loved ones. The onset begins with tears of scattered axons (long extensions of neurons that carry chemical and electrical impulses to other neurons). A partial tear of just the outer membrane may heal, or it may allow an influx of calcium ions (necessary for transfer of impulses, but very harmful if allowed to uncontrollably flow into the axon through the membrane tears). 


Figure 1: Calcium ions flowing uncontrollably into a small tear in the membrane of an axon.

If the influx of calcium is too great, the mitochondria within the axon begin a process of self-destruction (referred to as "apoptosis" or "suicide"). This process involves the excretion of substances from the mitochondria that breakdown the cell. The destructive substances also escape to create small openings in the cell membranes of nearby axons, resulting in uncontrolled influx of calcium ions in the nearby axons as well. 


Figure 2:  Release of self-destructive substances from injured axon into surrounding fluid where they are transported to; and begin to break down nearby healthy, functional axons.

Injured axons may partially heal and form terminal bulbs. During the attempted healing processes, the injured axons continue to receive and carry excitatory impulses. Unfortunately, as these impulses reach the injured end of the axon (the terminal bulb), the impulses are unable to continue across the site of disruption and the chemical and electrical impulses are arbitrarily released. Via a process referred to as "excitotoxicity", these substances are toxic to nearby axons that may have been unharmed and perfectly functional prior to this "attack". 


Figure 3: Destructive electrical and chemical impulses being discharged from a terminal bulb.

When combined with the destructive substances from the axons undergoing apoptosis (suicide), nearby axons are similarly destroyed (murdered). As they are "murdered" they too release their internal destructive substances. Combined with excitotoxicity of the newly injured axons as well, the breakdown of other nearby axons continues in an ongoing cascade.

Just as with most disease processes, different people are more susceptible to the process than others and the speed and longevity of the destructive process can vary from weeks to months, years, or even over the course of a person's entire lifetime.


Figure 4: "Island" of spreading injured axons and terminal bulbs.

Islands where these injury processes occur can be spread throughout the brain. These multiple widespread lesions are often referred to as "traumatic axonal injury" or "diffuse axonal injury". Each island of injury may involve only a few axons, to thousands, or even tens of thousands. Because typical MRIs can only detect lesions that are about the size of the head of a pin and tens of thousands of axons can fit through an area the size of the head of a pin, MRIs are typically interpreted as negative for injury even though hundreds of thousands or millions of axons could be injured in the scattered areas of "traumatic axonal injury".


Figure 5:  Multiple microscopic islands of injured axons, each consisting of hundreds, thousands or even tens of thousands of axons - all too small to be visible on typical MRIs.

This article was submitted by MediVisuals. For more information, contact MediVisuals at

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