History Of Chronic Traumatic Encephalopathy Psychology Essay

History Of Chronic Traumatic Encephalopathy Psychology Essay Chronic traumatic encephalopathy (CTE) is a syndrome of emotional lability, Parkinsonism, ataxia, and cognitive impairment suffered by athletes who undergo repetitive concussive and subconcussive blows to the head (Cantu 2007). Owing to its initial discovery in boxers, CTE has been various known as punch drunk, dementia pugilistica, and psychopathic deterioration of pugilist. This paper will discuss the history of research into this fascinating topic, starting with the first descriptions in the medical literature and covering the progress made in understanding the clinical presentation, epidemiology, neuropathology, and genetics of the disease. CTE was first described by the American pathologist Martland in a 1928 article on the punch drunk syndrome in boxers. Martland noted that for years boxing fans and promoters had observed cuckoo or goofy behavior in fighters. The fighters most often affected were poor boxers who would take considerable head punishment, seeking only to land a knockout blow. Punch drunk was also common among second rate fighters used for training purposes, who may be knocked down several times a day. Martland described the symptoms of punch drunk based on his examination of five boxers. The early symptoms of punch drunk were unsteady gait and slight mental confusion. Some boxers did not progress beyond this stage, while others went on to develop slow movements, hesitancy in speech, and hand tremors. In severe cases, boxers would develop a propulsive gait, Parkinsonian facies, and marked mental deterioration. Martland speculated that the mechanism of brain injury was traumatic cerebral hemorrhages follow ed by gliosis. This conjecture was based on his observation of multiple cerebral hemorrhages in people who died from acute traumatic head injury (Martland 1927). Building on Martlands work, researchers investigated the clinical course and epidemiology of CTE. Critchley observed that CTE can progress in many boxers even after they had retired, a phenomenon that to this day eludes explanation (1957). Corsellis noted that emotional lability and violent behavior tended to precede the Parkinsonian symptoms, ataxia, and cognitive decline mentioned by Martland (1973). Roberts studied the prevalence of CTE in retired professional boxers and found that 17% of subjects exhibited brain damage as determined by neurological exam and EEG abnormalities. Just as Martland observed that boxers who took more hits to the head were more likely to be punch drunk, Roberts showed that career length and number of professional fights were risk factors for CTE. Indeed, 47% of boxers whose careers were longer than 10 years suffered brain damage, compared with 13% of boxers with careers shorter than five years. Likewise, about 50% of boxers who had fought over 150 bouts had brain damage, compared with 19% of those with 50 to 150 bouts and 7% of those with less than 50 bouts (Roberts 1969). This idea of a dose-response relationship between repeated trauma and CTE was supported by the observation that amateur boxers did not suffer neuropsychological deficits due to boxing (Butler 1993). CTE is not unique to boxing, but has occurred in other sports with high rates of head trauma such as wrestling, horseracing, and parachuting as well as a case of battered wife syndrome (Corsellis 1976). Research into the gross neuropathology of CTE was spearheaded by Corsellis, who studied the brains of 15 deceased boxers, eight of whom were world or national champions (1973). Corsellis identified four common areas of brain damage and their associated clinical symptoms and signs. First, cavum septum pellucidum with fenestrations in the leaflets was a common finding. In addition, the lateral and third ventricles were enlarged and the frontal and temporal lobes were atrophied. These changes were associated with emotional lability and memory impairment. Second, degeneration of the substantia nigra, as evidenced by the loss of pigmented neurons, was associated with Parkinsonian symptoms like tremor, rigidity, and bradykinesia. Third, gliosis and neuronal loss in the cerebellar tonsils was associated with loss of balance and coordination. Fourth, diffuse neuronal loss was associated with an Alzheimers-like dementia. Eight of the fifteen cases Corsellis studied exhibited all four types of brain damage. The link between CTE and Alzheimers was strengthened when in 1967, Constantinidis showed the presence of neurofibrillary tangles in brains affected by traumatic injury (1967). Subsequent research showed that the microscopic pathology of CTE differed from that of Alzheimers in two important ways. First, CTE exhibited a unique distribution of neurofibrillary tangles in the neocortex. Neurofibrillary tangles in CTE were preferentially distributed in superficial layers of the neocortex layer II and the upper two thirds of layer III. In contrast, in Alzheimers they were located primarily in deeper layers the lower third of layer III and layer V (Hof 1992). Second, whereas beta amyloid plaques are an important feature of Alzheimers disease, they are not an essential part of CTE. One study showed that fourteen out of the fifteen brains studied by Corsellis stained positive for beta amyloid deposits (Roberts 1991). However, in a series of 51 CTE cases, McKee found that beta amyloid plaques were present in only 47% of cases (2009). The pattern of neurofibrillary tangles observed in CTE overlaps with the areas of neuronal loss identified by Corsellis. McKee observed neurofibrillary tangles and tau-immunoreactive astrocytes in parts of the neocortex, basal ganglia, cerebellum, brainstem and spinal cord. The density of neurofibrillary tangles was particularly high in the hippocampus, entorhinal cortex, and amygdala. This suggests involvement of the papez circuit and may explain the emotional lability observed in CTE. In addition, neurofibrillary tangles have been found in the substantia nigra and cerebellum. (McKee 2009). Recent research has suggested several mechanisms for brain injury in the setting of repeated trauma. Neurofibrillary tangles in CTE have a characteristic perivascular distribution, grouped around small intracortical vessels (Geddes 1999). This finding suggests that trauma may damage the blood-brain barrier, releasing neurotoxins that promote the formation of neurofibrillary tangles around blood vessels. In a similar vein, another study found that in many areas of CTE-affected brains the microvasculature was less dense and tortuous than normal. In addition, the distribution of this pathological microvasculature was highly correlated with the distribution of neurofibrillary tangles. The proposed explanation was that trauma damaged the microvasculature and led to the growth of neurofibrillary tangles. (Buee 1994). On a related note, neurofibrillary tangles in CTE were found to contain higher levels of iron and aluminum than those in Alzheimers disease, possibly due to damage to the bloo d-brain barrier (Bouras 1997). Diffuse axonal injury is a second possible mechanism of injury. After a concussion, disruptions in axolemma permeability and in axonal transport can lead to axotomy within 24 hours (Maxwell 1995). Indeed, in one study eighty percent of patients who died from acute head trauma showed immunocytochemical evidence of axonal injury (McKenzie 1996). A third mechanism of brain injury is the deposition of beta amyloid. Although beta amyloid plaques are present in only half of CTE cases, studies have shown that beta amyloid deposition increases after head trauma (Gentleman 1993). In addition, beta amyloid concentration in the brain is correlated with neurological recovery following head trauma (Brody 2008). Genetic studies suggest that the apolipoproteinE e4 allele predisposes to worse outcomes after traumatic brain injury. One study finds that patients with the APOE e4 allele have a two-fold higher risk of death, vegetative state, or severe disability compared to those without the allele (Teasdale 1997). The mechanism by which APOE e4 influences recovery from traumatic brain injury is unclear, though a role in neuronal repair has been suggested (Chen 1997). There are many unanswered questions regarding CTE. First, recent case reports indicate that CTE can occur in professional football players and soccer players (Omalu 2005, Matser 1998). The prevalence and risk factors for developing CTE in populations other than boxers are unknown and require further investigation. On this front, public awareness is increasing and more than 250 current and former NFL players have pledged to donate their brains to the Center for the Study of Traumatic Encephalopathy (CSTE) at Boston University School of Medicine (CSTE 2010). Second, the observation that CTE can present years after retirement from sports cannot be explained by current theories of CTE pathophysiology. Third, there has been no research into potential treatment options, though Parkinsons and Alzhemiers drugs have been used speculatively. Fourth, current preventative measures consist of return to play guidelines that sideline players who suffer concussions until their symptoms resolve. This is based on the finding that the risk of a second concussion is increased in the period following a concussion (Cantu 2003). However, no protocols for measuring degree of neurological impairment and reinjury risk in athletes have been developed. Chronic traumatic encephalopathy is a progressive neurodegenerative disease marked by emotional lability, Parkinsonism, ataxia, and cognitive decline. Since its first description by Martland, much has been learned about this disease. CTE occurs in professional athletes who suffer repeated head injury in a variety of sports, but has not been found in amateurs. Pathologically, CTE presents with neurofibrillary tangles in a distribution unique from Alzheimers and with beta amyloid deposits in about half of cases. Various mechanisms of injury have been proposed, though none have been proven. Genetic studies suggest that APOE e4 may promote CTE. Areas ripe for future research include the prevalence of CTE in sports other than boxing and the pathophysiology, treatment, and prevention of this disease.

Finally the Smoke Cleared and I Could See

Majbritt Dietrich 24/2/13 composition starting with â€Å"Finally the smoke cleared and I could see† Finally the smoke cleared and I could see what I think I’ve been looking for, for five years†¦ I saw a small, abandoned house, which was run down and you could see dead ivy along the tattered walls.It was a little haunting but I promised myself and my sister in law I would help find my two nieces that had made a giant mistake five years ago†¦ He drove out here, into the middle of no where and just dropped his two daughters off in this house and left them to live by themselves, they were no older than 3 years old†¦ He then just left and kept on driving, I’m guessing this was all planned as he then drove into a big truck at least twice the size of his car, and killed himself. We all were devastated. I walked into the house, not knowing what would expect me, I looked around and heard a noise.I stood completely still not even daring to breathe. I heard it again, it was like a soft whispering noise, I moved my shaking head, to see patterns developing on the wall, I was totally confused. A little girl peeped her head around the old wall and ran to attack me. I knew it was one of my nieces. The first thing I had noticed was she obviously hadn’t developed the way a normal girl her age would have. I called the police and managed to stutter the address. During the mean time I was studying the forever changing patterns on the wall. The two girls were running their hands along the wall as if the wall was a person.It was worrying me. I took pictures with my phone but when I went to look at them, the patterns that were on the wall had kind of disappeared†¦as if it were a ghost or a spirit, perhaps a soul stuck in the house? Either way it was scaring me. The police took a while; as the house was very difficult to find. It did take me five whole years to find it. But when the police finally were here they were as shocked as I was. They tried to catch the girls and put them in the back of the new police car, thankfully there was a cage splitting the front and back leather seats, as the girls were the complete opposite of calm.The girls were brought into a clinic and were examined by specialists. They were totally quiet and thought bad of my brother straight away. The girls were both kept in the clinic for a couple of weeks until an old specialist said to me there was nothing more they could do and it would be a good idea if the two girls stayed with me as they knew me. So the girls were brought to my house and process was made, both girls started to speak as the recognised things they had seen before when they had visited me. My partner Denise on the other hand was a bit afraid of them, but tried to act as motherly as possible.Both girls slept in the same room and got along fine with each other. They kept waking up at night, and spoke to the closet. It made absolutely no sense to Denise or me. One night both of us snuck up in front of their door and tried to listen to what they were saying but as soon as 1 second after we had arrived we heard a load screeching and immediately backed away and the screeching stopped. The girls ran out and screamed â€Å"you don’t know Mama, you’re not allowed to listen, she’ll get jealous! † but Denise and I were totally freaked out and slowly closed the door again and walked back to our bedroom, totally out of energy.The next morning Denise snuck into the girl’s room and wanted to look into the closet and she was so curious about what had happened last night. The same patterns that were on the walls in the house the girl were found in appeared on the walls of the girl’s bedroom here too. Whispering started again, the exact same whispering as in the house before too. One of the girls came in â€Å"don’t open it, Mama will get mad†¦Ã¢â‚¬  Denise started to get uncomfortable and walked back out and tal ked to her husband about it, the girl’s uncle.The girls were questioned about ‘Mama’ and said that she is a spirit that appears where ever she wants and can do what she wants. She takes care of the two girls apparently, but really what she wants is to get her child back. In 1485 she was accused of being a witch and was sentenced to death. Her baby was taken from her and was burnt. All she wants is to have her baby buried and to be with her†¦ one of the girls explained. Denise looked at her husband confused â€Å"okay†¦ girls are you sure she’s real? † the girls just looked at each other and said â€Å"don’t say she’s not, she really is real and will get mad if you talk bad about her! . The walls began to fill with the same patterns again and the screeching started too once again. â€Å"You made Mama mad! †. â€Å"Okay†¦Ã¢â‚¬  Denise began to shake. â€Å"What if we burry her baby? † the girls looked scar ed. The patterns began to disappear. The girls replied and said â€Å"maybe that could work†¦Ã¢â‚¬ . We walked to the woods where Mama was once burned at the stake. â€Å"Girls do you have any idea where her baby could be? † they both shook their heads, barely moving. Denise spotted an old ruin that could maybe have been the house where Mama could have lived. We got a priest and said the ceremony that would be said at a funeral.Patterns started fill the trees, and the ruin, they began to run along our bodies, it wasn’t a bad feeling; it was more of a thank you we thought. The two girls from then on were completely normal and were capable of going to a normal school nearby. They lived with Denise and their uncle and visited the graves of their father and mother, more their mother’s though as they couldn’t understand why their father had down that to them, but still knew there would have been a reason. But in the end they weren’t as damaged as the specialists had said, and it was only Mama who was in them.

Computer Industry And The World Of Mobile Phones - 1025 Words

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The Role Of A Mental Health Counselor - 1607 Words

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