Published by A Mckee and colleagues in 2013 in Brain.
Written by Amy Lynch (Medical Student, Trinity College Dublin), edited by Dr Lucia M Li
Introduction
In the 1920’s ‘punch drunk’ was a term used to describe the decline seen in some boxers. This syndrome consists of progressive change in personality, memory decline, mood problems and eventual dementia. It was thought to be caused by the repetitive brain trauma boxers sustained throughout their career. Athletes from other high contact sports were also displaying similar symptoms and the condition was renamed Chronic Traumatic Encephalopathy (CTE).
CTE is a progressive neurodegenerative condition associated with repetitive ‘mild’ traumatic brain injury (for example from repeated knocks to the head over a number of years during contact sports). The symptoms usually appear slowly and progress 8-10 years after the damage happens. Currently, CTE can only be diagnosed after death, and depends on finding abnormal protein in brain tissue. A protein called p-tau escapes its normal location within the brain and becomes damaging to the brain and the nervous system. In later stages of CTE, this abnormal tau protein spreads to more areas of the brain and nervous system.
This study studied the brains, donated after death, from 85 people thought to be at high risk of CTE. This group included athletes, military veterans and civilians that all experienced some form of mild traumatic brain injury. The study compared these brains to the brain donated from 18 people with no known history of mild traumatic brain trauma (a control group). The results were compared with clinical information regarding symptoms of CTE that they gained from interviewing the families of those at risk of CTE.
The aim of the study was to describe the clinical symptoms and brain tissue findings at different stages of CTE.
Results
From the 85 brains of at risk subjects, 68 (80%) had abnormal p-tau protein in the nervous system. Abnormal p-tau was found in more widespread areas of the brain with later stages of CTE. Of the 68 at risk subjects, there were 64 contact sport-playing athletes and 4 individuals with no history of contact sports (3 army veterans and one individual with self-injury from repeated head banging tendencies). Any subjects that had other neurological diseases were excluded. 51 cases were left.
As can be seen, the average age increased with the increasing stages.
Special attention was paid to the American footballers in the study. Residual brain damage due to the numerous hits over years of playing American football is very topical at the moment. For this group, the average age of onset of symptoms was 54 years.
Discussion
In CTE, the evidence suggests that the spread of this abnormal p-tau protein begins in a small number of places and spreads slowly throughout the brain and nervous system over decades with an average rate of 11-14 years between stages. We can see this progression with the increase of the average age in the groups with the advancing stages. In future studies on CTE, it may be interesting to look more into the subjects that incur repetitive mild brain trauma but don’t show evidence of CTE. Among other things this may show the threshold of the amount of Mild trauma needed to trigger CTE.
While this study defines very well the different stages of CTE based on the amount of disease seen in the brain, it is not useful for diagnosis of living patients. Therefore the clinical criteria for the diagnosis of CTE needs to be established. Although this study described certain symptoms as being particularly associated with each ‘stage’ of CTE, the more common situation described by doctors is that these symptoms are seen in head injury in general.
Better diagnosis in living patients would lead to better management in the future. Although many factors are to be determined in the cause of CTE, this study clearly shows that for some athletes and soldiers, repetitive trauma to the head that is considered mild at the time can have major consequences on the brain in the long run.
Written by Amy Lynch (Medical Student, Trinity College Dublin), edited by Dr Lucia M Li
Introduction
In the 1920’s ‘punch drunk’ was a term used to describe the decline seen in some boxers. This syndrome consists of progressive change in personality, memory decline, mood problems and eventual dementia. It was thought to be caused by the repetitive brain trauma boxers sustained throughout their career. Athletes from other high contact sports were also displaying similar symptoms and the condition was renamed Chronic Traumatic Encephalopathy (CTE).
CTE is a progressive neurodegenerative condition associated with repetitive ‘mild’ traumatic brain injury (for example from repeated knocks to the head over a number of years during contact sports). The symptoms usually appear slowly and progress 8-10 years after the damage happens. Currently, CTE can only be diagnosed after death, and depends on finding abnormal protein in brain tissue. A protein called p-tau escapes its normal location within the brain and becomes damaging to the brain and the nervous system. In later stages of CTE, this abnormal tau protein spreads to more areas of the brain and nervous system.
This study studied the brains, donated after death, from 85 people thought to be at high risk of CTE. This group included athletes, military veterans and civilians that all experienced some form of mild traumatic brain injury. The study compared these brains to the brain donated from 18 people with no known history of mild traumatic brain trauma (a control group). The results were compared with clinical information regarding symptoms of CTE that they gained from interviewing the families of those at risk of CTE.
The aim of the study was to describe the clinical symptoms and brain tissue findings at different stages of CTE.
Results
From the 85 brains of at risk subjects, 68 (80%) had abnormal p-tau protein in the nervous system. Abnormal p-tau was found in more widespread areas of the brain with later stages of CTE. Of the 68 at risk subjects, there were 64 contact sport-playing athletes and 4 individuals with no history of contact sports (3 army veterans and one individual with self-injury from repeated head banging tendencies). Any subjects that had other neurological diseases were excluded. 51 cases were left.
- 7 of the subjects fell into the Stage 1 category, the average age being 28.5. There were usually a small number of isolated areas of the brain with the abnormal tau protein. One subject had no symptoms. Headaches, loss of concentration, short-term memory loss, aggressive tendencies and depression were commonly reported symptoms.
- 14 subjects were classed as being in Stage 2 with the average age being 44.3. 4 Subjects had no symptoms. The commonest presenting symptoms were similar to stage 1 with additional, less common symptoms being executive dysfunction (issues with how the brain processes everyday information and organises it into tasks that are then acted upon), impulsivity and difficulties both with speech and understanding and processing what others say. Some of the at risk subjects also reported some suicidal thoughts in this stage.
- 15 subjects were deemed to be Stage 3 with the average age being 56. In contrast to the earlier stages, most of the brains examined had other larger-scale changes including a decrease in size of the brain. The areas with the abnormal tau proteins were more widespread. The symptoms were similar to those described in Stage 1 and 2 but were more severe with 75% of the symptomatic subjects being classed as cognitively impaired (meaning they had a sufficient deficit in their speaking, memory, judgement and thinking to warrant this classification).
- 15 of the Subjects were at Stage 4 with the average age being 77.4. In stage 4 there was a more dramatic decrease in size of the brain seen along with severe p-tau abnormalities seen throughout much of the nervous system. ALL subjects were symptomatic with executive dysfunction and memory loss being the most common symptoms. All subjects had developed severe memory loss that progressed to dementia at some stage during this stage of their disease.
As can be seen, the average age increased with the increasing stages.
Special attention was paid to the American footballers in the study. Residual brain damage due to the numerous hits over years of playing American football is very topical at the moment. For this group, the average age of onset of symptoms was 54 years.
Discussion
In CTE, the evidence suggests that the spread of this abnormal p-tau protein begins in a small number of places and spreads slowly throughout the brain and nervous system over decades with an average rate of 11-14 years between stages. We can see this progression with the increase of the average age in the groups with the advancing stages. In future studies on CTE, it may be interesting to look more into the subjects that incur repetitive mild brain trauma but don’t show evidence of CTE. Among other things this may show the threshold of the amount of Mild trauma needed to trigger CTE.
While this study defines very well the different stages of CTE based on the amount of disease seen in the brain, it is not useful for diagnosis of living patients. Therefore the clinical criteria for the diagnosis of CTE needs to be established. Although this study described certain symptoms as being particularly associated with each ‘stage’ of CTE, the more common situation described by doctors is that these symptoms are seen in head injury in general.
Better diagnosis in living patients would lead to better management in the future. Although many factors are to be determined in the cause of CTE, this study clearly shows that for some athletes and soldiers, repetitive trauma to the head that is considered mild at the time can have major consequences on the brain in the long run.