The Effect Of Calcium On The Contribution Of Calcium Uptake Of The Vesicular Glutamate Released Into The Extracellular Space

The pathophysiology of traumatic brain injuries can be slightly different depending on the type of injury that has occurred. For example, injuries can result from

At the molecular level of explanation these processes are dependent on the interplay between glutamate receptors, Ca2+ channels, the increase of intracellular Ca2+ levels, Ca2+-dependent proteins like Akt, ERK, mTOR and neurotrophins such as brain derived neurotrophic factor (BDNF) (24, 25).

Brain trauma can cause a build -up of abnormal types of protein called tau, which slowly kills brain cells. Once started, these changes in the brain appear to continue and

It is amazing to me how people’s brains are so small compared to the whole body, yet it is an exceedingly complex organ that deals with so many mental and physical functions that help regulate our body. The brain is one of our main sources of operation, and so when a person’s brain is harmed or damaged in any way, there can be major consequences for that individual. One detrimental brain injury that has recently been heavily researched and talked is chronic traumatic encephalopathy (CTE), which is a progressive degenerative disease in the brain (Comer, 2014). More light has been showed on CTE in order to raise more awareness and seek solutions in helping prevent and fix the disease. In the following paragraphs, I will explain more in detail about CTE, specifically the causes, symptoms and outcomes, and the importance of being aware of CTE.

1.5 million people in the United State of America have a traumatic brain disorder (TBI). These disorders have symptoms of memory dysfunction, depression and anxiety; Dr. Byrnes and her team at the Uniformed Services University have examined mouse models to find the cellular mechanisms for these symptoms.

Traumatic brain injuries, or TBI, are the leading cause of death in children and young adults globally. Of the people who survive, most live a drastically

The brain is a complex and curious organ; despite extensive research, scientists still know little about it. William Allman described the brain as “a monstrous, beautiful mess.” He went on to say that “its billions of nerve cells – called neurons – lie in a tangled web that display cognitive powers far exceeding any of the silicon machines [scientists] have built to mimic it” (faculty.washington.edu). Imagine this mess of neurons experiencing a simple disruption, one that creates a domino effect that effortlessly damages this intricately created organ. Some of the most disastrous disruptions to this complex organ, traumatic brain injuries, most commonly occur in the frontal lobe. Injuries to

Traumatic brain injury affects people from all walks of life. Form military personal to the elderly that get injured when they fall or even athletes in relation to the injuries they acquire. Traumatic brain injury progressively leads to complex pathophysiological events that may lead neurodegenerative complications. For those that have experienced traumatic brain damage are more susceptible for the development of diseases such as Alzheimer’s, dementia, epilepsy, posttraumatic stress disorder, and neuropsychiatric disorder. The progression of these diseases can occur in a span of a few weeks, months, or even decades after trauma, so it is important to look over the underlying pathophysiology that traumatic brain injury can cause after the injury

Traumatic brain injury (TBI) occurs when there is a damage in the brain a result of physical trauma. TBI may be caused by a penetrating (open) head injury, in which an object pierces the skull and enters the brain tissue, or a closed head injury, in which the skull is not breached, and frequently results in the major long-term disability of individuals surviving head injuries.(7) Cranial firearm wounds often result in severe injury to the brain and related central nervous system (CNS) structures.(17). Although penetrating head trauma is less prevalent than closed head trauma, PBI carries a worse prognosis with high morbidity and mortality rates. Understanding of the mechanisms of injury and aggressive medical management with rapid surgical intervention may lead to improved outcomes.(8)

The brain is split into different compartments, each of which has it’s own functions that it carries out (like: memory, judgment and movement). When brain cells in a particular compartment is damaged, it can’t carry out its functions as is normally would.

The article, Concussive brain injury enhances fear learning and excitatory processes in the amygdala by Maxine L. Reger, Andrew M. Poulos, Floyd Buen, Christopher C. Giza, David A. Hovda, and Michael S Fanselow took a close look into the fears and behaviors generated in rats two days after suffering trauma to the brain. This particular article was discovered by searching the keywords: brain injury and amygdala, in the PubMed database. By searching those keywords, the database was able to pull up numerous articles discussing the two topics, but I felt that Reger et al (2012) demonstrated a clear association between the topics. The article brings about a question of whether or not there is a link between brain injuries, posttraumatic stress disorder, commonly referred to as PTSD, and the changes involved in the excitatory and inhibitory processes involved in the amygdala. In order to examine such a link, the authors performed a number of tests on adult Sprague-Dawley rats to test their hypothesis as well as to investigate the neurobiological correlation between concussion and PTSD. To further assess these correlations, it is imperative to explore the methods used to conduct this study.

The awareness of Traumatic Brain Injuries (TBI) has increased and the information available is better now than it was in the past. I believe many people are aware of concussions and traumatic brain injuries but not how it can affect their brain. Traumatic Brain injuries are a very complex injury with a broad spectrum of symptoms and disabilities. Many healthcare professionals in the field of brain injury often say, “If you’ve seen one concussion, you’ve seen one concussion.” Even a mild case of a concussion should not be taken lightly. People do not realize the impact it can have on a person and his/her family, it can be devastating. One of the leading causes of Brain Injuries is concussion as this has been brought to light by

Secondary injuries can manifest from hours to weeks after the primary injury. The secondary brain injury involves numerous metabolic processes that result from the interruption of blood flow and lack of oxygen to undamaged cells, which causes anaerobic metabolism to occur. Once anaerobic metabolism has started this causes a disruption in the energy producing mechanisms in the body, which causes inadequate synthesis of adenosine triphosphate (ATP) (Tran,

In the military setting, wide decompression carries the benefit of reducing malignant brain edema and elevations in ICP in the first several hours after the TBI (intro 15,16). However, the patients with large cranial defects and complex brain injuries remain as a challenge, and the outcome at severe primary or secondary blast injuries of children varies from adult one. Therefore, conclusive evidence of whether it has a beneficial or adverse effect on outcome is lacking (Intro4, trat 9). Children have more shearing and diffuse damage than adults. Even the definition of normal ICP and CPP varies with age (intro19). The differences in bio-structure of children’s brain from adult including more edema, hypotension, cardiac output, and less antioxidative capacity and basement membrane glycoproteins. Better outcome in children would be explained by several factors such as low level of chondrotin sulfate proteoglycan glycoproteins, which is responsible for rigidity and support of parenchyme (intro18,

AMPA receptors are localized at a postsynaptic level and under normal condition transduce responses to glutamate, released before the junction across which a nerve impulse passes from an axon terminal to a neuron, muscle cell, orgland cell. In the brain, AMPA receptors are the most represented ionotropic glutamate receptors and mediate excitatory neurotransmission. Hypersensitivity and overexpression of AMPA receptors in human epileptic hippocampal and neocortical tissue has been reported and an excessive glutamate release has been observed during seizure activity. (Zaccara et al., 2013) studies Suggest that reducing the overstimulation of AMPA receptors via AMPA receptor antagonism can have an anticonvulsant effect and inhibit seizure generation and spread. In addition to their anticonvulsant effects, AMPA receptor antagonists could play an important neuroprotective role by preventing neuronal death and could elicit an anti-epileptogenic effect (Franco et al.,