Chronic Traumatic Encephalopathy (CTE)
VAIBHAV MESTRY
THADOMAL SHAHANI ENGINEERING COLLEGE
vaibhavmestry45@gmail.com
Concussion – The Gateway to Neurological Disorders
A concussion is a commonly occurring term in recent days. We frequently hear about Athletes suffering from a concussion when they receive a blow to the head. There can be several accidents to cause a concussion too. The mechanism of injury involves either a direct blow to the head or forces elsewhere on the body that are transmitted to the head. This is believed to result in neuron dysfunction, as there are increased glucose requirements, but not enough blood supply. A concussion can be the starting point for several neurological and mental disorders. The severity of a concussion cannot be underestimated, and hence Sports Organizations across all sports around the world and other Healthcare associations are paying special attention to trauma on the head to mitigate the effects of a concussion or other related neurological problems. But why are we discussing concussions? Well, the potential complications associated with Parkinson’s, Alzheimer’s, and Chronic Traumatic Encephalopathy are quite severe.
What is Chronic Traumatic Encephalopathy?
Chronic Traumatic Encephalopathy or CTE is a degenerative brain disorder associated with repeated blows to the head. The symptoms include mood swings, behavioral problems, and thinking problems. The condition can worsen and lead to dementia.
The limited research on this disorder makes it quite mysterious and dangerous. The exact amount of trauma required to cause the condition is unknown, and the diagnosis can only be done during an autopsy. There is no specific treatment for the disease, and only supportive treatment is offered to mitigate the symptoms. Hence, it has been proposed that rules of certain sports be changed as a means of prevention.
The usual occurrences of this condition are documented in contact sports like wrestling, boxing, mixed martial arts, rugby, football, American football, etc. Other factors include accidents, being in the military, domestic violence, or any repeated banging to the head. CTE is classified as Tauopathy which is a class of neurodegenerative disorders involving aggregation of tau protein in neurofibrillary or gliofibrillary tangles in the human brain.
Stages and Symptoms of CTE
Signs of CTE occur in 4 stages, which appear after 8-10 years of repeated brain traumas. First stage symptoms are confusion, disorientation, dizziness, and headaches. The second stage includes memory loss, impulsive behavior, social instability, and poor judgement. The third and fourth stages include dementia, movement disorders, hypomimia, tremors, vertigo, depression, sensory processing disorders, and even suicidal tendencies.
Diagnosis
Diagnosis of CTE cannot be made in living individuals. Although there are symptoms that can be associated with CTE, there is no definitive test to prove its existence. Signs can also be confused with other neurological disorders. The lack of distinct biomarkers is the reason why CTE cannot be diagnosed in living humans. Concussions are non-structural injuries and do not lead to brain bleeding, hence neuroimaging tests like CT or MRI cannot detect most concussions. PET tracers that bind to tau proteins aid in the detection of CTE. The tracer [18F] FDDNP, is retained in certain sites in an individuals’ brain which can be used to associate with various neurological disorders. The sites where the tracer is retained, however, were not distinctive with the neuropathology of CTE.
The presumed biomarker for CTE is the presence of a serum of antibodies against the brain. These autoantibodies were detected in football players who received blows to the head but displaying no signs of a concussion, which suggests that even sub-concussive episodes may be brain-damaging. The autoantibodies may enter the brain using a disrupted blood-brain barrier, and attack neuronal cells, which over time can lead to the development of signs and symptoms of CTE. These autoimmune changes may be a measurable event to predict CTE.
Prevention and Cases
The use of helmets and mouthguards is promoted as a preventive measure. Although there is no significant research to support the use of helmets to reduce the risk of concussions, there is evidence that helmet use reduces impact forces. Mouthguards have shown to decrease dental injuries but again have not shown significant evidence to reduce concussions. Efforts are being made to change the rules of contact sports to reduce the frequency and severity of blows to the head.
In 2005, Bennet Omalu, a forensic pathologist along with his colleagues from the Department of Pathology at the University of Pittsburgh, published a paper titled “Chronic Traumatic Encephalopathy in a National Football League Player”, in the Journal of Neurosurgery, based on the analysis of the brain of deceased former NFL player Mike Webster was one of the first and most influential studies in reporting the potential damage of CTE. In February 2011, Dave Duerson committed suicide, leaving messages to loved one’s asking that his brain be donated for CTE research. The family got in touch with the Boston University center studying the case. Robert Stern, the co-director of the research group, studied the case and reported the possibility of someone who committed suicide might be potentially linked to CTE. Stern and his colleagues found high levels of the protein tau in Duerson’s brain. These elevated levels were abnormally clumped and pooled along the brain sulci, indicating CTE. Further, the mysterious double homicide and suicide of professional wrestler Chris Benoit were potentially linked to CTE due to numerous concussions sustained due to repeated hits to the head throughout his professional wrestling career. There are plenty of such reports and investigations associated with erratic behavior and self-harm in professional athletes, which all indicate some signs of Chronic Traumatic Encephalopathy. Therefore, several athletes have committed their brains after death for further research on this neurological disorder.
Reference (Apr-21-A4)
