Essay about Brain Injuries : Long Term Effects Of Damaged Neuron And Glial Cells

Essay about Brain Injuries : Long Term Effects Of Damaged Neuron And Glial Cells

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Traumatic brain injuries: long term effects of damaged neuron and glial cells
Concussions due to head or neck injuries are common in athletics, in some instances these type of injuries can be misdiagnosed as post-traumatic stress syndrome, or PTSD in military personnel, due to the similarity of its symptoms. For the most part, many individuals’ means of damaging their cell to cell communication pathways, are due to common accidents. Research shows that damage to neurons, specifically glial cells could possibly be related to the long term effects of traumatic brain injuries or TBI, among other degenerative diseases. Most individuals with mild injuries recover without incident, however a subgroup of people develop persistent post-concussive symptoms which often include headaches. Such post-traumatic headaches vary in proliferation and may progress to become chronic and in some cases debilitating. Leading some individuals to the take their own lives to relieve their symptoms. There is little known of the pathogenesis of post-traumatic headaches, nevertheless shared pathophysiology with that of the brain injury is suspected.
By first visualizing the injury at the molecular level, one can begin to understand how a shocking change of environment in these highly functional cells could likely result in prolonged side effects associated with brain injuries. According to Reece (2014), the brain consists of many neurons, which are supported and outnumbered by glial cells. Neurons carry out integration from the central nervous system or CNS, meanwhile those relaying information in and out of the CNS form the peripheral nervous system PNS. Some of the functions of glial cells include, nourishing neurons, insulating the axons, the signaling ...

... middle of paper ... According to Schultz and colleagues (2015) sodium selenate is a pharmacological compound that activates the protein phosphatase of PP2A/PR55, which decreases hyper phosphorylated tau, may be a novel therapeutic approach to improve the outcome following TBI (introduction). Another possibility for treatment could be a pioneering method called, low intensity focused ultrasound pulsation which was recently used to reactivate the brain of a comatose patient.
Based on the research conducted I can conclude that brain injuries happen at the cellular level, from there a series of cascading events lead to the degeneration of neurons, partially due to the damage and immune response of glial cells following trauma. However, promising techniques to treat brain injuries and stop the degenerative process gives light to people who often suffer from these invisible injuries.

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