Home » Causes - Disorders » Brain Injury by degenerative diseases » Chronic Traumatic Encephalopathy

Chronic Traumatic Encephalopathy

Since the beginning of last century it is known that in certain sports in which a lot of head trauma occurs, there is a great chance that in later life a progressive neurological deterioration of the brain occurs.

 

The sports in question are: boxing, American football, wrestling, rugby, hockey, soccer, lacrosse and skisport. It is known that it occurs that athletes who practice these sports have more than 1000 clashes with their head in a single sport season.

These clashes do not always lead to a concussion, but it seems that in later life they can lead to a degeneration of the brain tissue and a decrease of the brain functions.

Because there were not always multiple concussions, the relationship with this neurological decline was not made before. Only recently has the relationship been established as a result of scientific research.

Previously, this deterioration of the brain functions was called 'dementia pugulistica'.

CTE has already been demonstrated in boxers, professional football players, soccer players, a wrestler. It is also demonstrated in people with epileptic seizures who fall, in headbangers and in victims of violence. The syndrome that is seen in people with repeated concussions, Post-Commital Syndrome or PCS, is seen in rugbyers, karate practitioners, people who ride horses and para-jumpers. For them there is an increased risk of developing CTE. Veterans are also more at risk.

 

The main risk factors for developing CTE are:

  • The accumulation of repeated head injuries with or without obvious symptoms as a concussion,
  • The duration of exposure to the repeated head injuries (for example the duration of the sport career).

The exact relationship between concussions in the past and this neurodegenerative disorder CTE must still be demonstrated by future research.

 

Consequences of CTE

  • Memory disorders, attention and concentration disorders, cognitive decline, executive dysfunction, 
  • behavioral disorders such as emotional instability, unpredictable behavior, problems with impulse control, including in the sexual sphere (hitting, kicking, shouting), reduced empathy, (However, there are  people who become more gentle)
  • Personality changes,
  • Parkinsonism; complaints of Parkinson's disease, problems with speech and walking, difficulty in swallowing, ataxia,
  • Depression, manic depression, bipolar disorder
  • Dementia
  • Problems with seeing, visuospatial problems.

 

Diagnosis

CTE resembles Alzheimer's disease, frontotemporal dementia (FTD) and psychiatric disorders. However,  scans show that there is a decrease (atrophy) in the brain tissue of cerebrum, thalamus, brainstem and a dilation of the lateral and third brain cavities.
The brain bar (the corpus callossum) is thinner than normal.

The decrease in brain weight is generally mild and was seen in the frontal lobe (36%), the temporal lobe (31%), the parietal lobe (22%) and less frequently in the occipital lobe (3%).

On a microscopic level, stacks of the Tau protein can be seen. Tau is a kind of protein in the axon (spine of the cranial nerve) that is important for the function of the nerves. Without Tau nerves can not transmit impulses. Also, the TAR DNA-binding protein (TDP-43) was found with relatively little beta-amyloid.

 

Differences with other Tau disorders

In contrast to other Tau-protein disorders such as Alzheimer's, ALS and Parkinson's dementia, the accumulations of Tau protein at CTE mainly occur in the superficial cerebral cortex layers of the temporal and frontal lobe.

 

During autopsy researchers found several 'plaques' under the microscope, in less than half the number of people studied.
Because of the causes and the differences with other tau protein disorders, CTE has become a new condition that can be diagnosed separately.


At this moment there is no treatment for CTE.

 

Sources, more information

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945234/