Mild Brain Injury Neuropathology
Mild Brain Injury Neuropathology – Shearing Injury Time Delayed
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I believe that to understand the Mild Brain Injury Neuropathology, that it is important to understand the basics of brain anatomy and neuropathology. I have taken a detailed approach to those topics on BrainInjuryHelp.com under our severe brain injury pages. Here is an outline of the severe brain injury anatomy and pathology pages:
- Understanding Normal Brain Anatomy
- Neuropathology – Understanding Severe Brain Injury Pathology
Most of the outlined discussion on severe brain injury also applies to mild traumatic brain injury. Thus, this discussion of Mild Brain Injury Neuropathology will be more abbreviated and focused on what is different in Mild Brain Injury Neuropathology.
It may seem that I spent too many pages on Amnesia and relatively few words on Mild Brain Injury Neuropathology. I did so because mild brain injury treatment and outcome usually are dependent upon whether the concussion was identified on the date it was suffered. What the medical community gets most wrong is the triage for concussion. If the magnitude of the concussion is identified in the acute stage, proper treatment with the best chance for recovery, is likely to come. My goal here is not just to teach, but to guide future concussion protocols. Whether I am sufficiently a neuroscientist to do so, I will let the user decide.
There are many events which create force against the brain. These events would include a blow to the head, the head striking an object, gunshot wounds. This type of mechanism of injury creates “impact” force. The event which does not get enough credence despite its relevance to auto accident cases and mild brain injury neuropathology is the rapid acceleration and deceleration of the brain. The brain can be injured from such acceleration forces in a whiplash, without striking the head. The injury occurs in whiplash because of the internal stress of brain’s different parts, being differentially accelerated or decelerated around the fulcrum of rotation. A fulcrum is the point in a lever, that the lever pivots upon. As all motion around a fulcrum is in a circle, this type of mechanism is called “rotational” force.
While we just introduced the concepts of impact and rotational forces as separate, both types of injury can occur from either an impact or rotational event. A blow to the head may cause the brain to spin or twist on some internal axis. A rotational type snapping of the head, may involve a blow to the brain delivered by the carton intended to protect it, the skull.
Damage from impact tends to be focal, that is concentrated in specific parts of the brain. Damage from rotational forces tend to be diffuse, meaning occurring throughout widespread portions of the brain. Thus, the term “Diffuse Axonal Injury“ is used to mean widespread injury to the axons, the long thin protrusion of the neuron.
Mechanisms of Mild Brain Injury Neuropathology
It is not the blow or the whiplash, but what happens inside the skull, which causes the Mild Brain Injury Neuropathology. The two most significant causes of brain injury are the “contact” of the head with a blunt object and the “inertia” as a result of a rapid acceleration or deceleration of the brain. The terms “impact” and “shear” are also often used to differentiate the internal mechanisms of injury between the contact and inertial sources of injury. The term “contact phenomenon” is used to describe what occurs when the energy of the impact of the head with something is transferred to the brain.
Diffuse versus Focal Injuries:
Brain injuries can be either diffuse or focal (meaning to a specific spot or structure of the brain). When the term “contact phenomenon“, is used, it is usually in context of a”focal” brain injury. The term “diffuse” is used when the pathology is distributed throughout the brain. Diffuse is a bit of a misnomer, however, as most of what is referred to as diffuse brain injury, is in fact multi-focal, meaning that it is in multiple places within the brain, but in specific places. Typically the term multi-focal brain injury that is called diffuse, is brain injury labeled diffuse axonal injury. The reason it is more often multi-focal is because that diffuse axonal injury is known to occur most often in the areas where the fiber tracts are most likely to see radical shifts during a traumatic event. One such place is in the corpus callosum, the fiber tracts which connect the two hemispheres of the brain.
Unlike injury to axonal tracts, focal injuries are typically large enough that they can be seen on CT and MRI. Such injuries are “macroscopic” (meaning they can be seen without the use of a microscope). Diffuse or multi-focal injuries are typically microscopic as these injuries typically occur on the cellular level. A microscope is typically only used to examine brain cells after death. Autopsy is rarely done on those with documentation of concussion, although the CTE movement with NFL players is reversing this trend.
Diffuse brain injury exists in four principal forms.
- Diffuse swelling,
- Diffuse hypoxic/anoxic/ischemic injury;
- Diffuse vascular injury
- Diffuse axonal brain injury;
Diffuse axonal injury (DAI) gets the most discussion. The reason for the attention on DAI is undoubtedly its relationship in its less severe forms, to the concussion or MTBI. Diffuse hypoxic/anoxic/ischemic brain injury is often catastrophic, and outside the discussion of MTBI. The effects of diffuse brain swelling can span the spectrum of severity, with little being understood about the interplay of subtle increases in swelling, or swelling that occurs on the microscopic level, upon long term recovery.