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Chronic Traumatic Encephalopathy: symptoms, causes and treatment

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There is no question that sport has a ton of benefits, both physical and mental. However, a little known aspect, especially of contact sports, is the damage that can be caused to the brain.

These injuries would be due to, for example, punching in boxing or tackling in American football, generating damage at the neuronal level that cause cognitive deterioration, emotional instability and problems motor skills.

Chronic Traumatic Encephalopathy is a neurodegenerative disease associated with impacts on the brain. It has been related to both athletes and victims of some type of head injury. Let's take a closer look at what it entails.

  • Related article: "The 15 most common neurological disorders"

What is Chronic Traumatic Encephalopathy?

Chronic Traumatic Encephalopathy, formerly called pugilistic dementia or "punch drunk syndrome", is a neurodegenerative disease, mainly caused by repeated head injuries. This syndrome has been linked to many contact sports, including boxing, football, hockey, and the arts. martial arts, although it has also been seen in victims of domestic violence and blast survivors, as personal military.

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It affects the brain, causing various symptoms at a cognitive, psychomotor and mood level. Despite the severity of his symptoms, which involve planning problems, memory lapses, slow movements and changes in abrupt moods, these do not begin to appear until several years after the injuries were suffered, this being their main trouble.

Chronic Traumatic Encephalopathy cannot be diagnosed in life, except for the rare cases of individuals with high-risk exposures. This neurological disease is still being studied and its exact frequency in the population is not known, in addition to the fact that the causes can be multiple. There is no known cure for chronic traumatic encephalopathy.

Symptoms

Although several symptoms have been linked to Chronic Traumatic Encephalopathy, it can be said that the fact that can only be diagnosed post-mortem makes, really, it is not very clear what all its symptom.

Likewise, it has been seen that people who have practiced professions in which the repeated blows to the head were present manifest, after a few years, the following problems.

  • Cognitive impairment: trouble thinking.
  • Impulsive behavior and substance abuse.
  • Emotional instability: depression, anger, sudden mood swings.
  • Aggression, both physical and verbal.
  • Short-term memory loss, especially that related to daily tasks
  • Difficulties in executive functions: planning problems.
  • Emotional instability.
  • Suicidal thoughts and behaviors.
  • Generalized apathy: lack of expressiveness and emotional interest.
  • Motor problems: begins by being clumsy and progresses to slowness, stiffness and coordination problems.

It looks to be relationship between the severity of this brain disease and the time spent in contact sportalong with the number of blows to the head or number of traumatic injuries. Likewise, it must be said that it may be the case of receiving only a single traumatic injury and that this is so strong enough that, after a few years, the disease appears, being the case of survivors of explosions.

The clinical deterioration of this disease is gradual, appearing after a few years since the injuries occurred, or even after several decades. This deterioration occurs in three phases:

1. Early phase

The first symptoms of cognitive impairment begin to appear, as a result of the blows. Although a clear onset has not been established, the disease is usually latent in the early years.

It is in this early phase that affective disorders and psychotic symptoms begin to appear.

2. Advanced phase

This phase occurs between 12 and 16 years from when the contact sport began or when the traumatic injury occurred, although it can vary from person to person.

Social instability, erratic behavior, memory loss appear and symptomatology related to the first stages of Parkinson's disease. The symptoms are already seen more clearly, although it cannot yet be classified as dementia.

  • You may be interested: "Parkinson's: causes, symptoms, treatment and prevention"

3. Dementia phase

The symptoms are more serious, being well established and affecting the functionality of the subject in all areas of his life. He loses mental faculties, such as memory and reasoning, in addition to speech and gait abnormalities.

Diagnosis

At present, there is no definitive clinical diagnosis for Chronic Traumatic Encephalopathy, due to the lack of specificity in the symptoms attributed to this neurological disease. Nevertheless, the study of brain tissues once the patient has died allows us to confirm whether the individual had the disease.

In any case, attempts have been made to use neuroimaging techniques to see if it is possible to make a safe diagnosis while the patient is still alive.

The possibility of using Fluorine 18 Positive Emission Tomography to be able to detect the pathology in the living brain has been developing. Given the the disease is not associated with a particular injury to the brain It is not possible to diagnose it simply by looking at images of the brain without understanding how damaged the brain tissue is.

What happens to the brain in this disease?

When a blow is received, the white matter in our brain suffers the most. This matter is a part of the central nervous system composed of myelinated nerve fibers, which acts as a transmitter and coordinator of communication between different nervous regions.

The brain has a constitution similar to that of jelly, which means that in case of receiving an impact a lot of pressure is put on its nerve fibers, being able to break and causing damage both in the short and long term.

Although the skull is a great protector of the brain and cerebrospinal fluid is the substance that cushions the impacts, if the blow is very strong the brain bounces against the cranial walls, giving the damage. This can lead to unconsciousness, bruising, bleeding, and sudden death.

The damage behind this disease is not a particular injury to one area of ​​the brain, but rather a progressive damage to brain tissue. The brain loses some of its weight, associated with atrophy of the cerebral lobes: the frontal lobe (36%), the temporal lobe (31%), the parietal lobe (22%) and, to a much lesser extent, the occipital lobe (3%). In addition, the lateral ventricle and the third ventricle are dilated. The fourth ventricle rarely does.

The corpus callosum thins and the cavum septum pellucid shows fenestrations. The brain tonsils are losing neurons, the substantia nigra and the locus coeruleus are damaged. The olfactory bulbs, the thalamus, the mammillary bodies, the brain stem and the cerebellum atrophy and, as As the disease becomes more severe, the hippocampus, entorhinal cortex, and amygdala.

Similar to what happens in the Alzheimer disease, in Chronic Traumatic Encephalopathy large number of neurofibrillary tangles of Tau protein appear. Neuropil threads and glial tangles can also be found.

Risk factor's

The main risk factor is the practice of contact sports, along with being a victim of domestic violence, having experienced an explosion or being part of military personnel.

The deterioration is the result of the various injuries that are received in the head, very common in sports such as boxing, kick-boxing, motor racing sports, and martial arts. Other risk factors are the practice of a contact sport from a young age, not using the proper protection and not using injury prevention strategies.

Protection factors

The main protection factor is the most obvious: protecting your skull when doing contact sports, especially those where repetitive head blows are unavoidable, such as boxing or kick boxing. This is why the use of helmets is so important, in addition to reducing the number of matches or matches per season. and make sure the contestants don't do more damage than is necessary.

It is very important to see a doctor, whether or not you have cognitive, emotional and psychomotor symptoms associated with the disease. Although they have not yet been presented, it is possible to perform tests that assess cognitive impairment, stability emotional and psychomotor skills that allow to have an objective proof that the first phase of the illness. Medical follow-up in people at risk You can prevent further damage through early intervention techniques.

Treatment

There is no cure for Chronic Traumatic Encephalopathy. The main intervention measure is to avoid risk factors. In the event that a contact sport is carried out, an attempt should be made to avoid any risk, using the proper protection measures.

If symptoms of the disease are already showing, there are two general ways to treat it. The first is medicalization, using drugs that act on specific symptoms, while the second is rehabilitation, which, as in dementias such as Alzheimer's and Parkinson's, it should be as early as possible, taking advantage of brain plasticity to make the most serious symptoms of the disease appear more late.

Bibliographic references:

  • Neighborhood. J; Small. G; Wong. K; Huang. S; Liu. J; Merrill. D; Giza. C; Fitzsimmons. R; Omalu. B; Dances J; Kepe. V.. (2015). In vivo characterization of chronic traumatic encephalopathy using [F-18] FDDNP PET brain imaging. In PNAS (E2039 – E2047). Washington University in St. Louis: Marcus E. Raichle.
  • Ling, H., Hardy, J., Zetterberg, H., 2015. Neurological consequences of traumatic braininjuries in sports. Molecular and Cellular Neuroscience.
  • Garret. W; Kirkendall. D; Contiguglia. R. (2005). Soccer Medicine. Spain: Editorial Paidotribo.
  • Saffary, R. (2012). From Concussion to Chronic Traumatic Encephalopathy: A Review. Journal of Clinical Sport Psychology: 315–362.
  • McKee, A. C., Stern, R. A., Nowinski, C. J., Stein, T. D., Alvarez, V. E., Daneshvar, D. H., Lee, H. S., Wojtowicz, S. M., Hall, G., Baugh, C. M., Riley, D. O., Kubilus, * C. A., Cormier, K. A., Jacobs, M. A., Martin, B. R., Abraham, C. R., Ikezu, T., Reichard, R. R., Wolozin, B. L., Budson, A. E.,… Cantu, R. C. (2013). The spectrum of disease in chronic traumatic encephalopathy. Brain: a journal of neurology, 136 (Pt 1), 43–64. https://doi.org/10.1093/brain/aws307
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