Chronic traumatic encephalopathy: symptoms, causes and treatment

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

These injuries are believed to be due, for example, to punches in boxing or tackling in American football, causing neural damage that leads to cognitive impairment, emotional instability and motor problems.

Chronic traumatic encephalopathy is a neurodegenerative disease associated with impacts on the brain. It has been linked to both athletes and victims of certain types of head injuries. Let’s take a closer look at what this entails.

    What is chronic traumatic encephalopathy?

    Chronic traumatic encephalopathy, formerly known as drunk punch syndrome, is a neurodegenerative disease, produced mainly by repeated head trauma. This syndrome has been linked to many contact sports, such as boxing, football, hockey, and martial arts, although it has also been seen in victims of domestic violence and survivors of explosions, such as military personnel.

    It affects the brain, causing various cognitive, psychomotor and mood symptoms. Despite the severity of their symptoms, which involves problems with planning, memory problems, slow movements, and sudden mood swings, they don’t start to appear until several years after injury, which is their main problem.

    Chronic traumatic encephalopathy it cannot be diagnosed in life, With the exception of rare cases of individuals at high risk. This neurological disease is still under study and its exact frequency in the population is not known, in addition to which the causes may be multiple. There is no known cure for chronic traumatic encephalopathy.


    Although several symptoms have been linked to chronic traumatic encephalopathy, it must be said that the fact that it can only be diagnosed after death really doesn’t make it very clear what all of its symptoms are.

    Likewise, yes, we have seen that people who worked in professions in which repeated blows to the head were present they manifest, after a few years, the following problems.

    • Cognitive impairment: thinking problems.
    • Impulsive behavior and drug addiction.
    • Emotional instability: depression, anger, sudden mood swings.
    • Aggression, both physical and verbal.
    • Short-term memory loss, especially related to daily tasks
    • Difficulties in executive functions: problems to be expected.
    • Emotional instability.
    • Suicidal thoughts and behaviors.
    • Generalized apathy: lack of expressiveness and emotional interest.
    • Motor Problems: Begins to be awkward and progresses in slowness, stiffness and coordination problems.

    seems to have relationship between the severity of this brain disease and the time spent in contact sport, With the number of blows received to the head or the number of traumatic injuries. Likewise, it must be said that it is possible to receive only one traumatic injury and that it is so strong that after a few years the disease appears, when it comes to survivors of explosions.

    The clinical worsening of this disease is progressive, Appearing a few years after the injuries, or even after several decades. This deterioration occurs in three phases:

    1. Early phase

    The first symptoms of cognitive impairment begin to appear, following the beatings. Although no clear onset has been established, the disease is usually latent in the early years.

    It is at this early stage that emotional disturbances and psychotic symptoms begin to appear.

    2. Advanced phase

    This phase occurs between the ages of 12 and 16 from when contact sport first started or when the traumatic injury has occurred, although it can vary from person to person.

    Social instability, erratic behavior, memory loss appear and the symptoms associated with the early stages of Parkinson’s disease. The symptoms are already visible more clearly, although it cannot yet be classified as dementia.

      3. Phase of dementia

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


      There is currently no definitive clinical diagnosis for chronic traumatic encephalopathy, due to the lack of specificity of symptoms attributed to this neurological disease. however, the study of brain tissue after the patient has died confirms whether the individual had the disease.

      However, attempts have been made to use neuroimaging techniques to see if it is possible to make a sure diagnosis while the patient is still alive.

      The possibility of using positive emission tomography with fluorine-18 to be able to detect pathology in living brain has been developed. since the disease is not associated with a particular brain injury it is not possible to diagnose it just by looking at pictures of the brain without understanding how damaged the brain tissue is.

      What happens to the brain in this disease?

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

      The brain has a constitution similar to that of gelatin, Which means that in case of shock, a lot of pressure is put on their nerve fibers, which can break and cause short and long term damage.

      While the skull is a great protector of the brain, and cerebrospinal fluid is the substance that cushions impacts, if the blow is very strong, the brain bounces against the cranial walls, harming itself. 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 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 dilate. The fourth ventricle rarely does this.

      The corpus callosum is thinned and the septum of the hairy cavum presents fenestrations. The cerebral tonsils lose neurons, the substantia nigra and the locus coeruleus are damaged. The olfactory bulbs, thalamus, mammary bodies, brainstem and cerebellum are atrophied, and as the disease worsens, the hippocampus, entorhinal cortex, and amygdala are also damaged.

      Similar to how it happens in Alzheimer’s disease, in chronic traumatic encephalopathy a large number of neurofibrillary tangles of the Tau protein appear. Neuropil threads and glial buds can also be found.

      Risk factors

      The main risk factor is participating in contact sports, in addition to being a victim of domestic violence, having suffered an explosion or being in the military.

      The deterioration is the result of various head injuries, very common in sports such as boxing, kickboxing, motor racing and martial arts. Other risk factors are practicing contact sport from a young age, not using adequate protection and not using strategies to prevent injuries.

      Protective factors

      The main protective factor is the most obvious: to protect the skull when playing contact sports, especially in those where repeated blows to the head are inevitable, such as boxing or kickboxing. This is why the use of the helmet is so important, besides reducing the number of fights or matches per season. and make sure the suitors don’t get hurt more than they need to be.

      It is very important to see a doctor whether or not you have cognitive, emotional, and psychomotor symptoms associated with the disease. Although they are not yet presented, it is possible to perform tests that assess cognitive impairment, emotional stability and psychomotor skills that allow objective tests that can pass through the first phase of the disease. Medical monitoring of people at risk it can prevent significant damage through early intervention techniques.


      There is no cure for chronic traumatic encephalopathy. The main intervention measure is to avoid risk factors. In the case of contact sports, every attempt must be made to avoid any risk, using the appropriate protective measures.

      If the symptoms of the disease are already manifesting themselves, there are two general ways of treating 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 disease, must be done as early as possible, taking advantage of plasticity. the disease occurs later.

      Bibliographical references:

      • District. J; Small. G; Wong. K; Huang. S; Liu. J; Merrill.D; Giza. VS; Fitzsimmons.R; Omalu. B; Bailes. J; Kepe. V .. (2015). In vivo characterization of chronic traumatic encephalopathy by [F-18]Brain image PET PET FDDNP. At PNAS (E2039 – E2047). Washington University at St. Louis: Marcus E. Raichle.
      • Ling, H., Hardy, J., Zetterberg, H., 2015. Neurological consequences of traumatic brain injury in sport. Molecular and cellular neurosciences.
      • Attic. W; Kirkendall. RE; Contiguglia. R. (2005). Football medicine. Spain: Editorial Paidotribo.
      • Saffary, R. (2012). From concussion to chronic traumatic encephalopathy: a review. Journal of Clinical Sports Psychology: 315-362.
      • McKee, AC, Stern, RA, Nowinski, CJ, Stein, TD, Alvarez, VE, Daneshvar, DH, Lee, HS, Wojtowicz, SM, Hall, G., Baugh, CM, Riley, DO, Kubilus, * CA, Cormier, KA, Jacobs, MA, Martin, BR, Abraham, CR, Ikezu, T., Reichard, RR, Wolozin, BL, Budson, AE, … Cantu, RC (2013). The spectrum of disease in chronic traumatic encephalopathy. Brain: Journal of Neurology, 136 (Pt 1), 43-64.

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