How Cte Progresses Is Still Unknown

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

This brain injury also includes the “production of harmful chemicals called free radicals, inflammation, impaired transport of molecules within nerve cells, and imbalances of key ions needed for nerve function” (Menon 1). Memory is also effected by a concussion. Short term memory is often “individuals complain that they cannot remember something they just saw, or things that were just said. This is the most common type of memory problem” (French 1). Long term memory impact is viewed as “individuals who suffer a head injury are able to remember things that occurred in the past, but may struggle with things that happened recently” (French 1). When a concussion happens it is mostly common to only be effective to short term memory. Concussions not only potentially bruise your brain but produces harmful chemicals. A concussion causes “injury to the nerves in the scalp or larger nerves in the face and upper neck from the trauma can result in head discomfort” (Zasler 1). Head discomfort includes piercing headaches and lasting head pain. The nervous system is effected in negative ways because at the moment of impact to the brain, the nerve tissues are stretched and teared causing great pain.

The author of “Ahead of the Hit” is Jeff Wheelwright a contributing editor at Discover. Most non-professional literature also contains graphic and illustrations with appealing colors. On every page of “Ahead of the Hit” there is at least one picture. Most of the pictures are football related, there is only one picture that pertains to CTE specifically; located on page 19. Non-professional literature is meant to inform or entertain,“Ahead of the Hit” was written to inform readers about the debate in sports of whether head injuries lead to CTE (Wheelwright, 18). “Ahead of the Hit” is written in an easy to read non-technical style. Technical terms used in the article are defined and explained in the article. “Among the evidence, they pointed to amyloid plaques, which are unnatural deposits of amyloid protein, and neurofibrillary tangles and threads, which are microscopic aggregations of another protein called tau, rarely found in healthy brains”(Wheelwright, 19). “ Ahead of the Hit” doesn’t have a bibliography, which is another characteristic of non-professional literature.

How an injury to the head can do damage to the brain varies. Brain swelling and disruption of blood supply are some direct causes of damage (Kolb & Whishaw, 2009). However, neurological damage develops after (also known as secondary injuries) the immediate moment of impact (Ghajar, 2000). In other words even minor head injuries can lead to lasting disabilities and that the injuries are amassed. Meaning that a minor injury can result in a major impairment (Ponsford, Sloan, & Snow, 2012).

Chronic Traumatic Encephalopathy, or better known as CTE has gained momentum in areas of public awareness and scientific involvement in recent years due to the popularized sport on American Football. During recent years, the media has been swaying and educating the public on the adverse outcomes that CTE can initiate. However, the first discovery of this disease was diagnosed by pathologist Harrison Martland and can be related back to the late 1920’s; the first true cases were identified in the physical sport of boxing. During that time, CTE was commonly known as dementia pugilistica meaning “punch drunk” from the wobbly nature of boxers during repetitive hits to the head.1,2 It was determined that dementia pugilistica (also known as boxer’s

As we all know, the human brain is the most insubstantial and vital organ in the human body as it is the command center for every other body part (newscientist.com). Any slight wound to this organ could lead to severe consequences usually encountered at that very moment. It may be an extremely low chance of a major head injury, but it does happen to millions of people annually. One single concussion, provided with the lack of healing, could lead to short-term and long-term memory loss, depression,

With the latter of the two of them all being the more frequent causes of brain injury. It has never been clear exactly on how much damage is done and how the symptoms are caused when the injury happens. There has been reported that there is cellular damage that happens in the concussed brain. Currently it is thought that structural and neuropsychiatric factors may be responsible for these effects.

Concussions are complex cerebral injuries that result in a series of metabolic events within the brain. The changes are seen in the fragile neuronal homeostatic balances where changes in the elevations of glutamate and potassium have been identified. The effects of concussions have also been seen in the functioning of the brain rather than in the structure of the brain itself. Being identified as mild traumatic brain injuries, occurring due to a bump or jolt to head or neck, concussions can result in both short-term and long-term effects. Although most individuals are able to recover from these head injuries, a small but relevant portion of individuals have been found to suffer from chronic long-term effects including early onsets of Alzheimer disease, clinical depression and other cognitive complications. The occurrence of a secondary concussion during the recovery phase of a primary concussion, also recognized as the second impact syndrome, has been shown to increase the risk for long-term effects of cerebral and neurological failure as the neurons have become incapable of experiencing normal functions after an initial traumatic brain injury. The recoveries from these initial concussions are critical to prevent the onset of long-term effects.

Concussions are minor traumatic brain injuries caused by bumping the head. The action taking place that causes a concussion is when the brain bounces around in the skull causing minor to major bruising. This causes chemical changes in the brain and leaves the damaged areas in the brain vulnerable to permanent damage if injured again. Symptoms involve “impairments of memory and attention, headache, and alteration of mental status, are the result of neuronal dysfunction mostly caused by functional rather than structural abnormalities” ( Signoretti, 2011). According to Signoretti, the symptoms occur because of the trauma causes the neurons to fall out of homeostasis causing a chain reaction of metabolic events such as temporary

Not long before his death, Hoffman told a news reporter who had become interested in his story, “something is wrong with me. I don’t know what it is, but I used to be normal. ” Hoffman and his family believed football -related brain injuries were at least partly to blame for the tragic unravelling of his life. Hoffman’s family plans on keeping a promise they made to Hoffman that when he died they would have his brain tested for C.T.E. – there is currently no test for C.T.E. that can be done while someone is still living. Now, after years of not knowing, his family will finally be able to know the

This “involves either the head striking a hard surface or a rapidly moving object striking the head. The dura mater remains intact and brain tissues are not exposed to the environment”(McCance & Huether, 2014, p. 582). Closed (blunt) trauma can be classified as primary (injury results from the initial anatomical and physiological insult usually direct trauma to the head) and secondary (results from hypotension, hypoxia, acidosis, edema, or factors that can secondarily damage brain tissue)(Rangel-Castilla, 2014, p. 2). It can also cause mild concussion (characterized by immediate but transitory clinical manifestations) and classic cerebral concussion (any loss consciousness accompanied by retrograde and anterograde amnesia)(McCance & Huether, 2014, p. 587). The degrees of concussions

Chronic Traumatic Encephalopathy formally known as CTE is a progressive degenerative disease that forms in the brain. CTE isn't something you get over night or after a few visits to the hospital for headaches, It's a disease usually found in athletes or regular people with a history of brain trauma, severe blows to the head or concussions (temporary unconsciousness caused by a blow to the head. The term is also used loosely of the aftereffects such as confusion or temporary incapacity).

The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.

Here they concentrate more on the iron and aluminum mass in the hippocampus. According to this studied the Alzheimer’s disease has similar symptoms to dementia pugilstica .Patients with punch drunk (dementia pugilistica) showed sign such as aggressive behavior. The similarities between the syndromes between Alzheimer’s disease and Punch drunk, and also between the deficits may suggest that this two diseases have similar etiological mechanism which means the reasons caused these two are the same. The symptoms such as having an aggressive behavior is explained by having smaller amount of Purkinje cells, also ventricles are becoming bigger than normal size. The reason for those symptoms are repetitive brain injuries in case of boxing getting repetitive hits on the heads of boxers. Bur the most important problem in punch drunk syndrome is that neurofibrillary tangles (NFT) are being developed. The statement about NFT again brings to the ide about similarities between Alzheimer’s disease and punch drunk syndrome but there is difference between distributions of it in both cases. In AD (Alzheimer’s disease) it has been seen in deeper levels. But however NFT had higher level of Al and Fe in punch drunk syndrome than in Alzheimer’s

In 1906 a physician, named Alois Alzheimer, cared for a fifty-one year old patient with severe dementia. Upon her death, he was able to examine her brain at autopsy. Dr. Alzheimer was able to take advantage of recent innovations in microscopy and histological techniques that allowed him to study in detail the cellular components in nervous tissue. He found that the brain of his patient had severe cortical atrophy and described the neurofibrillary bundles and plaques that are now the hallmark for definitive diagnosis of what he at that time called “presenile dementia”. An account of his first patient was published in 1907. It is a little ironic that reevaluation this case has lead some to believe that this first patient did not suffer from the Alzheimer’s disease at all. Instead they believe she suffered from a different, rare disease called metachromatic leukodystrophy (Izenberg, 2000).