Chronic traumatic encephalopathy

CTE, Dementia pugilistica, DP


Chronic traumatic encephalopathy (CTE), a form of tauopathy, is a progressive degenerative disease found in people who have suffered repetitive brain trauma, including sub-concussive hits to the head that do not cause immediate symptoms. The disease was previously called dementia pugilistica (DP), i.e. "punch-drunk", as it was initially found in those with a history of boxing. CTE has been most commonly found in professional athletes participating in American football, association football, ice hockey, professional wrestling, stunt performing, bull riding, bicycle motocross, rodeo, and other contact sports who have experienced repetitive brain trauma. Its presence in domestic violence victims is also being investigated.

Individuals with CTE may show symptoms of dementia, such as memory loss, aggression, confusion and depression, which may appear years or many decades after the trauma. In the case of blast injury, a single exposure to a blast and the subsequent violent movement of the head in the blast wind can cause the condition.

In September 2015, researchers with the Department of Veterans Affairs and Boston University announced that they had identified CTE in 87 of 91 (96 percent) deceased NFL players that they had examined and in 79 percent of all football players.

Symptoms - Chronic traumatic encephalopathy

Symptoms of CTE generally begin 8–10 years after experiencing repetitive mild traumatic brain injury. First stage symptoms include deterioration in attention as well as disorientation, dizziness and headaches. Further disabilities appear with progressive deterioration, including memory loss, social instability, erratic behavior, and poor judgment. Third and fourth stages include progressive dementia, slowing of muscular movements, hypomimia, impeded speech, tremors, vertigo, deafness, and suicidality. Additional symptoms include dysarthria, dysphagia, ocular abnormalities, such as ptosis.

Currently, CTE can only be definitively diagnosed by direct tissue examination, including full autopsies and immunohistochemical brain analyses.

The neuropathological appearance of CTE is distinguished from other tauopathies, such as Alzheimer’s disease. The four clinical stages of observable CTE disability have been correlated with tau pathology in brain tissue, ranging in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions.

Research performed at the Cleveland Clinic and at the University of Rochester has shown that sub-concussive head hits also produce measurable changes in athletes' MRI. The MRI changes reported in this study were causally related to the presence in serum of players of auto-antibodies against the brain protein S100B. These auto-antibodies may be pathogenic as shown for example in epileptic human brain

Causes - Chronic traumatic encephalopathy

Initial injury

The main cause of CTE is repetitive head trauma. Football players have been the focus of most CTE studies. However, athletes participating in other sports, including soccer, ice hockey, rugby, boxing, wrestling, basketball, field hockey, cheerleading, volleyball and lacrosse, may experience repeated head impacts and also have high rates of concussion.

Blast injuries to military personnel also can result in CTE.

However, not all athletes and not everyone who experiences repeated concussions, including military personnel, go on to develop CTE.

Effect of injury

CTE causes the wasting away (atrophy) of many parts of the brain. Injuries to the section of nerve cells involved in conducting electrical impulses (axons) interfere with cell-to-cell communication. Other changes include deposits of the proteins tau and TDP-43, and changes in white matter — the part of the brain made up of nerve fibers. Unlike in Alzheimer's disease, deposits of beta-amyloid, another protein, are not common.

More than one-third of people with CTE also have signs of another neurodegenerative disease, including Alzheimer's disease, motor neuron disease, Parkinson's disease or frontotemporal lobar degeneration.

Prevention - Chronic traumatic encephalopathy

Investigators have demonstrated that immobilizing the head during a blast exposure prevented the learning and memory deficits associated with CTE that occurred when the head was not immobilized. This research represents the first case series of postmortem brains from U.S. military personnel who were exposed to a blast and/or a concussive injury. However, the protein tau which binds microtubules of brain axons, was found to have an elastic limit which is speed dependent; when breached, the microtubules become undone and cause brain swellings due to backups of information transport.

Diagnosis - Chronic traumatic encephalopathy

The lack of in-vivo techniques to show distinct biomarkers for CTE is the reason CTE cannot currently be diagnosed during lifetime. The only known diagnosis for CTE occurs by studying the brain tissue after death. Concussions are non-structural injuries and do not result in brain bleeding, which is why most concussions cannot be seen on routine neuroimaging tests such as CT or MRI. Acute concussion symptoms (those that occur shortly after an injury) should not be confused with CTE. Differentiating between prolonged post-concussion syndrome (PCS, where symptoms begin shortly after a concussion and last for weeks, months, and sometimes even years) and CTE symptoms can be difficult. Research studies are currently examining whether neuroimaging can detect subtle changes in axonal integrity and structural lesions that can occur in CTE. Recently, more progress in in-vivo diagnostic techniques for CTE has been made, using DTI, fMRI, MRI, and MRS imaging; however, more research needs to be done before any such techniques can be validated.

Positron Emission Tomography (PET) using a newly developed radiopharmaceutical [18F]FDDNP is being investigated as a tool to allow in-vivo diagnosis of CTE. In late 2013, breaking research was completed by the University of California Los Angeles in which, for the first time ever, Chronic Traumatic Encephalopathy was reportedly found in living-retired National Football League players. Prior to this breakthrough study conducted by UCLA, Chronic Traumatic Encephalopathy could only be found posthumously through autopsies of diseased athletes, however, this study found the brain disease in numerous living athletes. The scan lit up for tau in all five former players, according to the study. The protein was concentrated in areas that control memory, emotions and other functions—a pattern consistent with the distribution of tau in CTE brains that have been studied following autopsy, according to the researchers. A small study of 5 patients has been reported to show accumulation of tau protein in the brains of suspected CTE patients seen on PET scan. This finding is also noted in a number of other dementing disorders such as Alzheimer's disease, Pick's disease, progressive supranuclear palsy, corticobasal degeneration and familial frontotemporal dementia and Parkinsonism linked to chromosome abnormality. At the current time PET scanning is not widely used in screening due to the perceived high cost of the study.

A putative biomarker for CTE is the presence in serum of auto-antibodies against the brain. These may enter the brain by means of a disrupted blood-brain barrier, and attack neuronal cells which are normally protected from an immune onslaught. Given the large numbers of neurons present in the brain, and considering the poor penetration of antibodies across a normal blood-brain barrier, there is an extended period of time between the initial events (head hits) and the development of any signs or symptoms. Nevertheless, autoimmune changes in blood of players may consist the earliest measurable event predicting CTE.

Robert A. Stern, one of the scientists at the Boston University CTE Center, said in 2015 that "he expected a test to be developed within a decade that will be able to diagnose C.T.E. in living people.

Prognosis - Chronic traumatic encephalopathy

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Treatment - Chronic traumatic encephalopathy

CTE is a progressive, degenerative brain disease for which there is no treatment. Currently, the best approach is to prevent head injury and stay informed about the latest recommendations for proper detection and management of mild traumatic brain injury.

Patients who have symptoms typically associated with CTE, may benefit from supportive care similar to that provided for people with other kinds of dementia.

  • Calming environment. Reducing clutter and distracting noise can make it easier for someone with dementia to focus and function. It may also reduce confusion and frustration.
  • Reassuring responses. A caregiver's response to a behavior can make the behavior, such as agitation, worse. It's best to avoid correcting and quizzing a person with dementia. Reassuring the person and validating his or her concerns can defuse many situations.
  • Modified tasks. Break tasks into easier steps and focus on success, not failure. Structure and routine during the day help reduce confusion in people with dementia.
  • Regular exercise. Help with activities such as a daily 30-minute walk to improve mood and maintain the health of joints, muscles and heart. Exercise can also promote restful sleep, prevent constipation, lessen symptoms of depression, help retain motor skills and create a calming effect. Someone who has trouble walking may still be able to use a stationary bike or participate in chair exercises.
  • Games and thinking activities. Participating in games, crossword puzzles and other activities in which people are using thinking (cognitive) skills may help slow mental decline in people with dementia.
  • Nighttime rituals. Behavior is often worse at night. Try to establish going-to-bed rituals that are calming and away from the noise of television, meal cleanup and active family members. Leave night lights on to prevent disorientation.

Resources - Chronic traumatic encephalopathy

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by Abidemi Uruejoma
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