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 whiplash injuries due to acceleration/deceleration resulting in rapid flexion-extension movement of the neck.
However, the likelihood of significant diffuse axonal injury increases when the head hits something, such as a windshield, as the change in momentum is greater because of the sudden stopping of the head. But in a shearing mechanism, it is not the contact phenomenon which cause the injury, but the change in momentum.
The axons within the brain are long thin nerve fibers that may extend across different layers of the brain, from example the cerebral cortex (the gray matter - on the outside of the brain) to the subcortical region (the white matter - deep inside the brain.) As these different layers of the brain have different densities (weight), and are located at varying distances from the center of a given rotation, they will be accelerated and decelerated at different speeds when a whiplash mechanism occurs. This results in different layers of the brain, sliding across each other, which can put unnatural stress on the axons, which extend across these layers.
Cells are Like Electrical Connections:
The diagram below demonstrates the similarity (although of course on a much different scale) of the structure and purpose of a brain cell and that of an electrical connection. The cell body is similar to the switch. The axon is similar to the wires that connect the switch to the light socket and the terminal end of the axon (the spot where the nerve impulse leaves one cell and enters another), is similar to the end of the wire that connects to the light socket.
Axons are Similar to Electrical Wires:
The axon is the part of the nerve cell that transmits the nerve impulse from one nerve cell to another, in a similar way that electrical impulse are transferred down a wire. Like a wire, if the axon is torn or broken, the nerve impulse will not be transmitted. And like a wire, axons may have insulation, which when it becomes damaged as a result of forces placed against the axon, may cause serious problems to the nerve cell, even if the axon is not actually torn.
Microscopic damage to axons can be caused by:
Cell Miscommunication,
Neurotoxins and
Inflammatory Effects.
"The delayed consequences of primary injury have only recently begun to be understood. These are various events that have been triggered by the primary injury and include neurobiological processes involving cellular dysfunction such as free radical formation, receptor mediated mechanisms, calcium and inflammation mediated damage."
Cell Miscommunication A series of electrical and chemical changes developing over a period of hours, result in changes to blood flow, the metabolism and the ionic balance in the brain.
Brain cells communicate with each other both electronically and chemically. Trauma can disrupt the electrical and chemical balance, with the result that brain cells set off the wrong signals, which can damage or destroy the cell.
Neurotoxins Trauma can also result in the release of chemicals which are toxic to brain cells.
What ability the brain cell has to protect itself from these toxins, may also be reduced by the effects the trauma had to the physical structure of the cell. Brain cells have protective coatings, much like the insulation on a wire or the paint on a car.
Micro Inflammation Other damage is related to the inflammation of the cell, as chemicals accumulate within the cell.
Such swelling can cause an increase in pressure at the cellular level, which results in secondary brain damage.
The common conception of brain injury seems to be that real world brain injuries are like those we observe in the boxing ring. When a fighter is knocked down, we wait to see if he gets up. If he gets up, we realize that he is particularly vulnerable at first. But our experience with boxing matches tell us that if he can survive for even thirty seconds or to the end of the round, he may shake off the effects of the blow and have a chance to win the fight.
This view of a brain injury is prevalent in the focus on loss of consciousness as the litmus test. But what this conception of brain injury ignores is that while at the same time the part of the brain that governs consciousness is improving, the brain cell may be in the middle of the fight of it's life.
Orientation at the scene or the emergency room does not tell us that the brain has not been injured, for brain injury is a process that may escalate for many hours after the injury. Despite our images of the sporting concussion, brain damage does not peak at the moment of the event, but much later. The escalation of brain damage over time can be caused by brain swelling, which cuts off circulation of blood and oxygen within the brain, by hemorrhage or bleeding within the brain and by damage on the microscopic level to brain cells. The combination of these factors can result in significant cell death up to 72 hours after the trauma. Any expert would acknowledge this in a severe case, where hematoma or hemorrhage can be seen on the CT scan. Yet this is clearly the case in non-coma injuries as well. As difficult as cellular level neuropathology may be to absorb, I believe it is important to understand the pathological explanation of what is happening to the part of the brain that cannot be seen on imaging studies.
Equally as important is to revisit our examination of the injured brain, 12 hours after trauma. In my experience, in those cases with persisting problems, the neurological and cognitive function may have actually gotten worse the next day, than it was during the time window of the ER visit. While a much shorter time frame than 12 hours, the persistence of symptoms after 15 minutes to distinguish between a Grade One and Grade Two concussion, also focuses on the cascade of events, not the moment of injury.
The Defense Argues
The Plaintiff was able to say: "Yes, I'm fine. I'm okay. I was wearing my seat belt," to various questions.
When he exchanged information: "Look in my briefcase. There's my business card."
He knew where it was.
Cellular Damage
"In various combinations and various severities, the resultant cellular dysfunction (of brain injury) defines the nature and extent of the primary injury, the outcome of which may not become apparent for several days or even weeks after injury." (Graham, Gennarelli, Greenfield's Neuropathology, 1996, page 197.)
Cellular damage occurs predominantly to the axons.
Shear Can Cause Delayed Effects
Immediate Cell Death
Delayed Cell Death
"It appears that ionic changes at cell membranes initiate events that cause a progressive cascade that can be potentially deleterious. Therefore, most TBI is not immediate. Brain damage is a process, and not an event, that is set into motion by the ionic fluctuations that occur immediately.
Why did this Person have a Bad Result?
Age Over 40
Prior History of Brain Injury
Extraordinary Demands on Brain
High Achiever
Far too much of the focus in the study of what the researchers always call "mild" brain injury, is trying to predict how serious a brain injury will become, based upon the way in which the patient interacts with medical professionals in the acute stage. * Personally, I think this misses the point. Certainly, if there was no concussion, there isn't likely to be a brain injury. But once there has been a concussion, the focus should not be on categorizing how serious the concussion was, but on what deficits the person is left with, after a healing period, and what we can do to minimize the disruption of those deficits upon this person's life.
But as initially the focus of this page has been devoted to explaining why concussion can cause permanent brain damage, a discussion of why some people have apparent full recoveries, while others, are profoundly effected by a similar injury, is tantamount. To begin this discussion, we must again summarize our theory of the pathology of subtle brain injury.
Diffuse Axonal Injury. Concussion results in organic injury to the brain, in most cases, by the mechanism of diffuse axonal injury.
Process not an Event. This injury is more likely as a result of strain to axons than actual tearing, which over a period of 12-72 hours results in a cascade of events which can disrupt a significant number of neural connections, either because of the death or damage to the axons which connect the neuron bodies.
Regeneration isn't Total Recovery. Our current research into neuropathology indicates that significant regeneration of these neural connections can occur, but that the extent of such regeneration falls off considerably with age (with over 40 being a meaningful line of demarcation) and that the regenerated neural connections are less efficient than premorbid.
High Achiever Problems. For this reason, individuals in professions which place a high demand on processing speed, are more likely to experience deficits than others, and that most people who have suffered more than a Grade I concussion, will have some measurable deficits, if sufficient demands are made upon their brains.
*(The sport and concussion guidelines
Concussion does indicate the beginning of a cascade of events, that may or may not damage sufficient neural connections to cause noticeable changes in the injured persons behavior over the first 12-72 hours. We cannot predict a "full recovery", as opposed to an "apparent full recovery" based upon any snap shot of an injured persons function over such time frame. It may be that they were fully oriented during the period from one minute post trauma to time they left the ER, but that their cognitive and neurological function deteriorated thereafter.
If we were to require everyone with a concussion to return to the ER the next day, we would probably get a much better picture of who was having persisting problems than we get in the in the first hour or two after trauma. Unfortunately, in most concussion cases, the only time during the first 72 hours that a person is seen by a medical professional is in the first hour or two after trauma. Thus, we clearly cannot make any determination about severity from what is recorded in such person's medical records.
We have known, far longer than we have known why, that certain individuals were significantly more at risk for less than apparent full recovery. Research has demonstrated, that even though almost all young people appear to have "apparent full recoveries", that if their brains are put under sufficient stress, they have materially different performances than uninjured persons. See the treatment of Measuring Attentional Problems elsewhere on these pages. What these findings have explained is why those who are in particularly challenging professions, or who put exceptional demands on their brains ability to attend and process information, are at risk for noticeable deficit, even at a young age.
We have also known that anyone over 40 was unlikely to have an "apparent full recovery." Until recently, the reason for this wasn't entirely clear, but with the discovery of the brains ability to regenerate damaged neuroconnections, we have learned that the growth factor which allows for such regrowth, has largely disappeared by the age of 40. Thus, what recovery that occurs is slower and apparently "incomplete".
We also have known that people with a history of previous concussion, are at far greater risk for a poor outcome. Again, our recent advances in neuropathology are pointing us to the explanation that the regeneration of neuroconnections that does occur, is more fragile than the original connections. Thus, it takes less to cause more damage than it did with the first concussion.
"Computed tomography, magnetic resonance imaging, electroencephalogram, or routine neurological evaluations may be normal."*
Subtle brain injury can only be identified by a triangulated evaluation of these three things:
The patients acute history,
The patients long term symptomatology; and
A detailed neuropsychological assessment.
Thus, when considering the relevancy of scanning in the diagnosis of brain injury, it is important to understand what each of the below diagnostic tests can tell us about brain damage.
CT
MRI
EEG
PET
ENG and Vestibular Testing
*Source: Definition of Mild Traumatic Brain Injury Developed by the Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine.
J Head Trauma Rehabil 1993:8(3):86-87
Normal CT and MRI scans do not rule out brain injury. Both of these tests are macroscopic. Axonal and neuronal brain injury are microscopic.
50% of those who are in a coma have normal MRI and CT scans.
In such cases, "it is usually concluded that the patient has sustained diffuse brain damage, but even with improved imaging, its precise type may not be identifiable during life." Greenfield's Neuropathology, page 209.
So so much to read and so much to take in...wow!
The 'scary part' is how the chemical imbalance can cause further brain damage. I am aware of how MRI, CT's can seem normal with BI. I wonder if this can cause seizures? and I hope they go away at some point. I'm hoping.
We are all so vulnerable to so much, yet we are so resiliant.
I believe I have some mild BI. We'll see..my neuro is still treating me as he sees; as he is the dr-there is a protocol of how. My family members ask, "why can't the drs know--how long will it take to know"; when you tell them, it takes time, I hear: oh, they know! I am learning that this is a process: the healing, the understanding--all of it. It's so disheartening.
Last year my sister fell off her bike and aquired a brain injury(head); she had 'subdural hemotoma' and she is completely better now a 1.5 yr later...miracles do happen.
health and happiness(and serenity)
Vee
IT's snowing like crazy here in CO *
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