Neuroanatomy and Traumatic Brain Injury
The human brain is the most complex, mystifying, and elegant object in the known universe. Our brains are responsible for virtually every aspect of our functioning from controlling hair growth to the origins of the universe. The human brain is truly a remarkable organ. It is estimated that the human brain contains over 100 billion neurons and several times that number in supportive cells. Each neuron, in addition, assesses between 30,000 and 50,000 branches which connect to both itself and other neurons. Thus, in one cubic millimeter of particle tissues there are literally billions of synapses or connection points between neurons. Furthermore, to support this complex system of neuronal connections the vascular system must function at a highly complex level in order to supply oxygenated blood to each of the neuronal cells. Thus, the vascular system in the human brain and the neurons it serves form a complex and interrelated matrix of extremely delicate vessels. The sensitivity and complexity of such a system leaves one to easily comprehend the results of high velocity impact injury to such a delicate system. Any stretching, compression, twisting, or other physical forces to the brain have the potential to negatively impact these delicate, physical structures. And this does not even address the changes which take place at a metabolic or chemical level. As noted by Bigler (2001) in describing the complexity of the human brain and the effects of trauma on that structure, “complex systems achieve complex functions only with efficient, well integrated, and fast recruitment of constituent parts, followed by a rapid response. Anything that disrupts this complex system, even subtly, will render the system less efficient and prone to errors in processing and responding.”

To further expand on this concept let us look at the individual neuro cell. Each cell in the brain has a specified length, width, and breadth and is held in position by other cells. As such, consistent with the physical constraints inherent in any component, the cell has limited elasticity. In other words, as with almost anything, neuro cells are limited in the amount they can be stretched, twisted, rotated, or compressed before there is an associated negative result. And the human brain is subjected to such physical motion damage may be identified using neuroimaging techniques such as computerized tomography (ct), magnetic resonance (mr), single photon emission computed tomography (spect), and magneto encephalography (mag). It is important to remember, however, that the entire brain is affected by such physical forces. Thus, when a legion is identified by any of the above methods it is erroneous to conclude that the brain has been subjected to damage in only that area identified by the imaging study. Thus, damage to the brain is always beyond just the visually identified legion. In essence, brain injuries resulting from traumatic forces are often diffuse in nature rather than specific to localized areas. Differences in brain injury, thus, should be viewed on a continuum ranging from minimal damage to a few selected neurons to progressively greater damage involving more neuronal injury.

Diffuse axonal injury has been described as a term involving injury to the cerebrial white matter of the brain. Neurons are comprised of a cell body, an axon or long trunk, and dendrites or connective branches. DAI identifies injury to the axonal section of the neurons. Three levels of DAI have been identified. Grade 1 represents wide spread non-specific axonal damage without focal abnormalities. Grade 2 incorporates the injuries in grade 1 but also includes focal abnormalities. Grade 3 again assumes levels 1 and 2 and includes brain stem injury. Very mild DAI has been objectively identified on autopsy as a result of a trauma involving as little as 60 seconds recorded loss of consciousness. Onset of DAI occurs anywhere from 6 to 72 hours following injury. And delayed cell death can occur for as long as up to one month post injury. Researchers have suggested that neuronal death can continue to occur for up to 3 years post injury!

The brain has been found to be most vulnerable if it is moved laterally. That is, trauma that occurs from a side impact has been found to result in the greatest degree of wide spread axonal damage.

Three stages of axonal injury have been suggested. In stage 1 a rapidly stretched axon which does not tear can undergo biochemical changes that may be transient. Studies have found that a minimum of a 5% increase in axon length from its resting length is sufficient to produce a transient disruption of the membrane of the neuron. This results in the neuron being unable to fire. Neuronal function may fully return within minutes after such an injury. Stage 2 axonal injury results from a 5 to 10% increase in axonal length resulting in swelling and enlargement of the injured axon resulting in disruption of neuronal functioning. Stage 3 occurs with a 15% or greater stretching and results in a high likelihood of permanent damage. With such a level of injury the neuron is believed to be unable to self-repair. Stage 4 injury in which stretching is in excess of 20% of the resting length produces immediate and irreversible damage.

In addition to neuronal injury as a result of physical forces impacting the human brain, the vascular system can also be compromised given the delicate lattice work of blood vessels supplying the billions of neurons in the brain any injury to the vascular system resulting in damage to that system can have a profound impact on the ability of that system to deliver nutrients to neurons. Swelling and compromised blood flow drop resulting in a reduction of glucose and oxygen delivery below the need the energy demands of the neuronal cells. With such a drop in glucose and oxygen there is a corresponding metabolic response in the neuron. This finding has been demonstrated most readily with SPECT and MAG imaging. The result of reduced glucose and oxygen delivery to neurons results in neuronal death and can be demonstrated by reduced brain volume. Experimental studies of even mild TBI have demonstrated hemorrhagic contusions at the gray-white matter interface.

*** studies have found that mild cases of TBI which include simple concussions, typically do not demonstrate depictable abnormalities using traditional MR imaging techniques. This does not mean, however, that there is an absence of injury to the brain. In fact, a recent series of articles published in the Journal of the American Medical Association demonstrated that concussion can produce mild but persistent neurocognitive deficits despite the absence of complete cell death resulting from such injuries. It is considered that a concussion can result in a disruption in the “efficiency” of the neurofunctioning of the brain. This finding clashes with other researchers who have consistently found in their studies that persistent post-concussion symptomatology is more likely due to psychological rather than neurologic injury. It has been suggested by other researchers, however, that as greater sophistication develops in the area of neuroimaging that argument will be found to be untenable.

In conclusion, the complexity of the human brain cannot be understated and the extent to which that delicate structure can be negatively impacted as a result of trauma should not be minimized. Most confident assessing such injury should involve sophisticated neuroimaging techniques and neuropsychological and comprehensive and sophisticated neuropsychological testing conducted by a well-trained and experienced Neuropsychologist.
 
 

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