Differences
This shows you the differences between two versions of the page.
| Both sides previous revision Previous revision Next revision | Previous revision | ||
|
group_4_presentation_2_-_cte [2018/11/02 16:11] markovif [Introduction] |
group_4_presentation_2_-_cte [2018/11/04 01:21] (current) kimr1 |
||
|---|---|---|---|
| Line 27: | Line 27: | ||
| ===== Risk Factors ===== | ===== Risk Factors ===== | ||
| - | The major risk for developing CTE is trauma to the central nervous system, therefore individuals who experience more head trauma are at a higher risk (DeKosky, Blennow, Ikonomovic & Gandy, 2013). Other factors such as the age at first head trauma and the length of the exposure to the head trauma also need to be taken into account and can increase risk to developing the disorder. Studies show that individuals who experience their first head trauma before the age of 12 are at a higher risk for developing CTE and have worse outcomes (Stamm et al., 2015). Furthermore, individuals who have a career with longer exposures to head trauma have a higher risk for CTE than those with a shorter career (Lakhan & Kirchgessner, 2012). Further research needs to be done on the genetic risk factors of CTE, as several have been proposed but remain to be established (DeKosky, Blennow, Ikonomovic & Gandy, 2013). | + | The major risk for developing CTE is trauma to the central nervous system, therefore individuals who experience more head trauma are at a higher risk (DeKosky, Blennow, Ikonomovic & Gandy, 2013). Other factors such as the age at first head trauma and the length of the exposure to the head trauma also need to be taken into account and can increase risk to developing the disorder. Studies show that individuals who experience their first head trauma before the age of 12 are at a higher risk for developing CTE and have worse outcomes (Stamm et al., 2015). Furthermore, individuals who have a career with longer exposures to head trauma have a higher risk for CTE than those with a shorter career (Lakhan & Kirchgessner, 2012). Further research needs to be done on the genetic risk factors of CTE, as some have been proposed but not yet confirmed (DeKosky, Blennow, Ikonomovic & Gandy, 2013). |
| {{ :screen_shot_2018-10-25_at_10.14.54_pm.png?300 |}} | {{ :screen_shot_2018-10-25_at_10.14.54_pm.png?300 |}} | ||
| Line 66: | Line 66: | ||
| ===== Pathophysiology and Mechanisms ===== | ===== Pathophysiology and Mechanisms ===== | ||
| + | |||
| Currently, the neurological effects of chronic traumatic encephalopathy (CTE) can only be studied post-mortem. The pathophysiology of the disease is unclear as there is a lack of clinical evidence and the symptoms can also be attributed to other factors such as aging, medications, and other diseases (Petraglia et al., 2014). | Currently, the neurological effects of chronic traumatic encephalopathy (CTE) can only be studied post-mortem. The pathophysiology of the disease is unclear as there is a lack of clinical evidence and the symptoms can also be attributed to other factors such as aging, medications, and other diseases (Petraglia et al., 2014). | ||
| - | To be diagnosed with CTE as opposed to other neurological diseases such as Alzheimer’s disease, the following four criteria need to be present in the brain tissue: the presence of perivascular foci of phospho-tau (p-tau) immunoreactive astrocytic tangles and neurofibrillary tangles, presence of irregular cortical distribution of p-tau immunoreactive neurofibrillary tangles and astrocytic tangles (with a predilection for the depth of cerebral sulci), groups of subpial and periventricular astrocytic tangles in the cerebral cortex, diencephalon, basal ganglia and brainstem, and finally the presence of neurofibrillary tangles in the cerebral cortex located preferentially in the superficial layers (McKee et al., 2013). Other pathological findings from individuals diagnosed with CTE are general atrophy (with greatest concentration in the frontal and temporal lobes, somewhat in parietal lobe, and nearly none in occipital lobe), scarring of cerebellar tonsils, a fenestrated cavum septum pellucidum, and enlargement of the ventral and third ventricles (Yi, Padalino, Chin, Montenegro, and Cantu, 2013). | + | To be diagnosed with CTE as opposed to other neurological diseases such as Alzheimer’s disease, the following four criteria need to be present in the brain tissue: the presence of phospho-tau (p-tau) around the brain's blood vessels, irregular cortical distribution of p-tau immunoreactive neurofibrillary tangles and astrocytic tangles (with a preference for the cerebral sulci), groups of subpial and periventricular astrocytic tangles in the cerebral cortex, diencephalon, basal ganglia and brain stem, and finally the presence of neurofibrillary tangles located preferentially in the superficial layers of the cerebral cortex (McKee et al., 2013). Other pathological findings from individuals diagnosed with CTE are general atrophy (with greatest concentration in the frontal and temporal lobes, somewhat in parietal lobe, and nearly none in occipital lobe), scarring of cerebellar tonsils, a fenestrated cavum septum pellucidum, and enlargement of the ventral and third ventricles (Yi, Padalino, Chin, Montenegro, and Cantu, 2013). |
| {{:cte_1.jpg?300|}} {{:cte_2.jpg?300|}} | {{:cte_1.jpg?300|}} {{:cte_2.jpg?300|}} | ||
| - | **Figure 5: ** (Left to right) Degeneration of brain tissue associated with each stage of CTE | + | **Figure 5: ** (Left to right) Degeneration of brain tissue associated with each stage of CTE (McKee et al., 2013) |
| In one study, researchers evaluated the development of CTE by exposing unanesthetized mice to closed head impacts. There were three groups in this study: control, single-hit, and repetitive. The study found increased p-tau immunoreactivity in the single-hit mice group and the repetitive-hit group after one month. Both groups also had elevated inflammatory cytokine levels, mediated by microglial and astroglial cells. However, after six months, the single-hit group recovered substantially while the repetitive-hit group’s p-tau immunoreactivity increased significantly. The repetitive-hit group also had substantial and widespread microglial and astroglial activation, indicating a major neuroinflammatory response (Petraglia et al., 2014). | In one study, researchers evaluated the development of CTE by exposing unanesthetized mice to closed head impacts. There were three groups in this study: control, single-hit, and repetitive. The study found increased p-tau immunoreactivity in the single-hit mice group and the repetitive-hit group after one month. Both groups also had elevated inflammatory cytokine levels, mediated by microglial and astroglial cells. However, after six months, the single-hit group recovered substantially while the repetitive-hit group’s p-tau immunoreactivity increased significantly. The repetitive-hit group also had substantial and widespread microglial and astroglial activation, indicating a major neuroinflammatory response (Petraglia et al., 2014). | ||
| Line 79: | Line 80: | ||
| {{ :cte_3.jpg?300 |}} | {{ :cte_3.jpg?300 |}} | ||
| - | **Figure 6: ** Comparison of brains taken from a control mouse and a repetitive-hit mouse | + | **Figure 6: ** Comparison of brains taken from a control mouse and a repetitive-hit mouse (Petraglia et al., 2014) |
| Line 86: | Line 87: | ||
| {{ :cte_4.jpg?300 |}} | {{ :cte_4.jpg?300 |}} | ||
| - | **Figure 7: ** Illustration of the neurotoxic effects of proinflammatory cytokines and chemokines acting together with amino acids (mainly glutamate). | + | **Figure 7: ** Illustration of the neurotoxic effects of proinflammatory cytokines and chemokines acting together with amino acids (mainly glutamate) (Blaylock and Maroon, 2011) |
| Line 96: | Line 97: | ||
| Another crucial aspect of prevention is the improvement of protective gear worn by athletes (Saulle & Greenwald, 2012). It has been shown that properly fitting and padded helmets as well as mouthguards function well in protecting players from severe head injury (Saulle & Greenwald, 2012). A study conducted by Viano and Halstead has shown that newer American football helmets are heavier, more padded, and larger than older helmets, and were better at absorbing impacts (Saulle & Greenwald, 2012). | Another crucial aspect of prevention is the improvement of protective gear worn by athletes (Saulle & Greenwald, 2012). It has been shown that properly fitting and padded helmets as well as mouthguards function well in protecting players from severe head injury (Saulle & Greenwald, 2012). A study conducted by Viano and Halstead has shown that newer American football helmets are heavier, more padded, and larger than older helmets, and were better at absorbing impacts (Saulle & Greenwald, 2012). | ||
| - | Despite being untreatable, the symptoms of CTE can be treated and managed. According to the Alzheimer's Association, treatment of CTE symptoms is similar to treatment of the symptoms of Alzheimers. An example is the treatment of aggression using behavioral methods, or the treatment of depression using medication and therapy. Furthermore, as with Alzheimer’s and dementia patients, a calming environment helps the patient to maintain focus and function and modified tasks help section tasks into easier steps. | + | Despite being untreatable, the symptoms of CTE can be treated and managed. According to the Alzheimer's Association (n.d.), treatment of CTE symptoms is similar to treatment of the symptoms of Alzheimers. An example is the treatment of aggression using behavioral methods, or the treatment of depression using medication and therapy (Alzheimer's Association n.d.). Furthermore, as with Alzheimer’s and dementia patients, a calming environment helps the patient to maintain focus and function and modified tasks help section tasks into easier steps (Alzheimer's Association n.d.). |
| ===== Research ===== | ===== Research ===== | ||
| Line 108: | Line 110: | ||
| ===== References ===== | ===== References ===== | ||
| + | Alzheimer's Association (n.d.). Chronic Traumatic Encephalopathy (CTE). Retrieved from https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/chronic-traumatic-encephalopathy-(cte) | ||
| + | |||
| Asken B., Sullan M., DeKosky S., Jaffee M., Bauer R. (2017). Research Gaps and Controversies in Chronic Traumatic Encephalopathy: A Review. JAMA Neurology. 74 (10): 1255–1262. doi:10.1001/jamaneurol.2017.2396. PMID 28975240 | Asken B., Sullan M., DeKosky S., Jaffee M., Bauer R. (2017). Research Gaps and Controversies in Chronic Traumatic Encephalopathy: A Review. JAMA Neurology. 74 (10): 1255–1262. doi:10.1001/jamaneurol.2017.2396. PMID 28975240 | ||
| Line 117: | Line 121: | ||
| Chronic Traumatic Encephalopathy. (2016). Retrieved October 26, 2018, from https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921 | Chronic Traumatic Encephalopathy. (2016). Retrieved October 26, 2018, from https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921 | ||
| - | |||
| - | Chronic Traumatic Encephalopathy (CTE). (n.d.). Retrieved from https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/chronic-traumatic-encephalopathy-(cte) | ||
| DeKosky, S., Blennow, K., Ikonomovic, M., & Gandy, S. (2013). Acute and chronic traumatic encephalopathies: pathogenesis and biomarkers. Nature Reviews Neurology, 9(4), 192-200. doi: 10.1038/nrneurol.2013. | DeKosky, S., Blennow, K., Ikonomovic, M., & Gandy, S. (2013). Acute and chronic traumatic encephalopathies: pathogenesis and biomarkers. Nature Reviews Neurology, 9(4), 192-200. doi: 10.1038/nrneurol.2013. | ||
