Traumatic Brain Injury Research Paper

Traumatic brain injury (TBI) is a complex brain injury that is produced by a sudden damage to the brain, resulting in a wide range of symptoms and infirmities. There are multiple different causes of TBIs, but damage to the brain comes in two forms: primary brain damage and secondary brain damage. Primary brain injury occurs at the time of impact. Secondary brain injury is the type of damage that progresses over time after the initial insult, leading to seizures, brain swelling and the like. This subsequent deterioration of the brain and its cellular processes is not the result of mechanical damage; instead, it signifies the successive pathological developments initiated with the primary injury. Secondary insult may be a potential focus

This causes the breakdown of phospholipids, proteins, and lipids, ultimately pushing a self-destruction button on biological membranes. Scar tissue results after inflammatory reactions act to remove the debris that is left behind. While TBI may cause cell death in the form of necrosis, it may also cause programmed cell death, or apoptosis. Neurons that are affected by this kind of automated destruction are physically unabridged at the beginning stage of injury and are reasonably functional, but the effects of injury are seen several hours or days after the primary event. Membrane deterioration, including nuclear membrane lysis, and DNA fragmentation take place, with apoptotic bodies cleaning up the subsequent rubble. As a result of the delayed action of apoptosis, it presents great potential for therapeutic

This reduction in NAA is followed by an increase at 3 and 6 months, suggesting a resolution from metabolic impairment. The elevation in Cho levels also supports this, as it is indicative of neuronal damage and elimination, which in turn initiates inflammatory processes, glial propagation and edema. While Cho levels are elevated at 1.5 months, they were reduced to near normal levels in the following 3 and 6 months. This Cho reduction may indicate a recovery after the reactive processes produced by TBI-induced tissue damage. Elevated levels of WM mIns may also suggest volatile reactions, which initiate the propagation of glial cells and/or cerebral edema. GM Cho does not show the same decline and maintains higher levels throughout the 3-6 month time period, indicating slowly dying neurons, as macrophages have been present in the human brain after 240 days of the primary injury. This incessant inflammation represented by elevated GM Cho and mIns levels at the 3-month time period is associated with poorer outcome with the TBI patients. The differences observed between the WM neurometabolies and GM neurometabolites demonstrate a possible metabolic uncoupling of the two types of tissue following TBI, as there appears to be a lag-effect on the cell body in the