Diffuse Axonal Injuries in a Traumatic Brain Injury

It is now well accepted that all traumatic injuries involve both a mechanical and neurochemical changes within the brain. Diffuse Axonal Injuries is the term used to explain the mechanical injury that results from a traumatic brain injury.

Diffuse Axonal Injuries are the result of mechanical trauma to the long thin extensions of neurons, which disrupt complex neural networks with devastating functional consequences but frequently do not show an abnormality on MRI or CT because the area of damage is too small to image. Diffuse Axonal Injury can occur without any direct impact on the head, as it requires only the condition of rapid acceleration / deceleration such as takes place in motor vehicle crashes, due to acceleration / deceleration resulting in rapid flexion-extension movement of the head. It is not the contact phenomenon which causes DAI, but rather the change in momentum. Studies have found that 85.2% of all Diffuse Axonal Injuries are caused by motor vehicle crashes.

The brain is made up of many different layers of matter, each which have a different density from each other. When the brain is subjected to acceleration/deceleration forces, the different layers are accelerated/decelerated at different speeds. The most obvious differences in density of the brain are between the cerebral cortex (the gray matter) and the subcortical regions (the white matter.) As these different layers of the brain have different densities, and are located at varying distances from the center of the given axis of rotation, they will be accelerated and decelerated at different speeds when a rapid acceleration / deceleration occurs. This results in different layers of the brain sliding across each other, which puts unnatural stress on the axons, which extend across these layers. A neuron may stretch from the gray matter through the white matter, or out of the brain and into the brain stem or spinal cord.

When axons are torn or stretched as a result of the different layers moving at different speeds, this is called “shearing.” This shearing damage is microscopic. Unlike what typically occurs with an impact injury, where bleeding and swelling can often be seen on a CT or MRI, shear injury occurs at the cellular level, as a result of damage to the brain’s central cell, the neuron. It is for this reason that conventional imaging techniques have little diagnostic value with such injuries. In fact, CT and MRI are read as “normal” in nearly 100% of mild traumatic brain injuries.  This is particularly true when a standard resolution (1.5T) MRI is done with standard slice width (5mm).  The resolution of these imaging methods, and the width of the slices make it almost impossible to find microscopic areas of damage.  Despite this, autopsy studies demonstrate that MRIs and CTs miss nearly 100% of mild traumatic brain injuries, and also miss a high percentage of other injuries including small fractures and small internal bleeds.

While these injuries are microscopic in nature, their effects and long term consequences are significant. The majority of neurological sequela and vegetative states following severe head injury are thought to be due to DAI.   More importantly, it is now well known by medical researchers that brain trauma increases the risk for developing Alzheimer’s Disease later in life. Diffuse Axonal Injury is the primary vector of Alzheimer’s according to these researchers. “Such injury is enough to cause microscopic damage throughout the brain that, in turn, initiates a cascade of biochemical events that leads to the subsequent formation of Alzheimer’s-like plaques.” Researchers have observed that damaged axons, caused by automobile accidents, produce a sticky substance called A-beta that sets the stage for the later development of Alzheimer-like plaques. In a report presented at the recent World Alzheimer Congress, Steven T. DeKosky, MD, and colleagues at the University of Pittsburgh Medical Center reported findings from neocortical samples taken from brain injury patients one and three days after head injury showing that these changes had already started to take place.

Alzheimer’s disease, the most common form of dementia in elderly people, is a progressive, degenerative brain disease that results in cognitive decline, impaired memory and thinking, behavior changes, loss of language, motor skills and a decline in the ability to perform basic activities. Head trauma expert John Q. Trojanowski, MD, PhD, Professor of Pathology and Laboratory Medicine at the University of Pennsylvania states that there is “very strong evidence that there is a connection between head trauma and at least some of the pathology of Alzheimer’s disease.” In fact, the American Journal of Epidemiology noted that a person who sustained a head injury in a car accident were 350% more likely to get Alzheimer’s that they were prior to the accident. Based on the strength of this research there is a greater than reasonable medical probability that people injured in a Motor Vehicle Collision have already started the development of Alzheimer’s Disease as a result of their collision.

A substantial amount of research has been done in this area which shows profound cognitive, behavioral, developmental, social and emotional damages to children injured in collisions. Contrary to the insurance industry’s position that children are not injured in car accidents, and don’t require treatment, kids need to be evaluated and treated where appropriate by a child psychologist and/or neurologist.

Where is the head injury located? Only a doctor, or neuropsychologist can tell. But, consider the following symptoms that can arise with injuries to specific areas of the brain:

Frontal Lobe:

  • Loss of simple movement of various body parts (Paralysis).
  • Inability to plan a sequence of complex movements needed to complete multi-stepped tasks, such as making coffee (Sequencing).
  • Loss of spontaneity in interacting with others.
  • Loss of flexibility in thinking.
  • Persistence of a single thought (Perseveration).
  • Inability to focus on task (Attending).
  • Mood changes (Emotionally Labile).
  • Changes in social behavior.
  • Changes in personality.
  • Difficulty with problem solving.
  • Inability to express language (Broca’s Aphasia).

Parietal Lobe:

  • Inability to attend to more than one object at a time.
  • Inability to name an object (Anomia).
  • Inability to locate the words for writing (Agraphia).
  • Problems with reading (Alexia).
  • Difficulty with drawing objects.
  • Difficulty in distinguishing left from right.
  • Difficulty with doing mathematics (Dyscalculia).
  • Lack of awareness of certain body parts and/or surrounding space (Apraxia) that leads to difficulties in self-care.
  • Inability to focus visual attention.
  • Difficulties with eye and hand coordination.
  • Occipital Lobes:
  • Defects in vision (Visual Field Cuts).
  • Difficulty with locating objects in environment.
  • Difficulty with identifying colors (Color Agnosia).
  • Production of hallucinations.
  • Visual illusions - inaccurately seeing objects.
  • Word blindness - inability to recognize words.
  • Difficulty in recognizing drawn objects.
  • Inability to recognize the movement of object (Movement Agnosia).
  • Difficulties with reading and writing.

Temporal Lobes:

  • Difficulty in recognizing faces (Prosopagnosia).
  • Difficulty in understanding spoken words (Wernicke’s Aphasia).
  • Disturbance with selective attention to what we see and hear.
  • Difficulty with identification of, and verbalization about objects.
  • Short term memory loss.
  • Interference with long term memory.
  • Increased and decreased interest in sexual behavior.
  • Inability to catagorize objects (Categorization).
  • Right lobe damage can cause persistent talking.
  • Increased aggressive behavior.
  • Brain Stem:
  • Decreased vital capacity in breathing, important for speech.
  • Swallowing food and water (Dysphagia).
  • Difficulty with organization/perception of the environment.
  • Problems with balance and movement.
  • Dizziness and nausea (Vertigo).
  • Sleeping difficulties (Insomnia, sleep apnea).
  • Cerebellum:
  • Loss of ability to coordinate fine movements.
  • Loss of ability to walk.
  • Inability to reach out and grab objects.
  • Tremors.
  • Dizziness (Vertigo).
  • Slurred Speech (Scanning Speech).
  • Inability to make rapid movements.

The complex part of brain injuries is that axon injury in one part of the brain can impact functions in other parts of the brain because each axon can connect with thousands of others, which means all of those connections can be disrupted by damage to one very small area and certain skills are reliant upon cells in multiple areas of the brain.

If you have a traumatic brain injury case, you will need a Diffuse Axonal Injury lawyer who fully understands these injuries. Please feel free to call us today at (503) 227-1233 to set up your free consultation.

About the

Aaron DeShaw is a personal injury lawyer at DeShaw Trial Lawyers, a law firm representing injured people with serious injuries including brain injuries and other catastrophic injuries. He has individually, and in association with other law firms, obtained over $1 Billion for his clients. Learn more about Aaron and the Firm.