From the Guidelines
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that can only be prevented, not treated, and thus, individuals with a history of repetitive head trauma should be monitored for cognitive and behavioral changes and seek medical attention if symptoms develop. The development of CTE is closely linked to the accumulation of tau protein in the brain, which is a result of repetitive head trauma and concussions, as discussed in the study on the current state of biomarkers of mild traumatic brain injury 1. This condition primarily affects individuals who participate in contact sports, such as football, boxing, and hockey, as well as military personnel exposed to blast injuries. The symptoms of CTE typically appear years or decades after the trauma and include:
- Memory problems
- Confusion
- Impaired judgment
- Impulse control issues
- Aggression
- Depression
- Eventually, dementia
As noted in the study on biomarkers of mild traumatic brain injury, there is a critical need for the identification of biomarkers for mild traumatic brain injury (mTBI) to aid diagnosis and to inform the establishment of more effective clinical guidelines for treatment based on objective findings rather than subjective symptom complaints 1. However, currently, CTE can only be definitively diagnosed after death through brain tissue examination. Management of CTE focuses on symptom control using medications for depression, anxiety, or behavioral issues. Prevention is crucial and involves reducing head impacts through proper technique in sports, following concussion protocols, limiting contact in practices, and using appropriate protective equipment. The study highlights the importance of discovering biomarkers that relate to the effects of and recovery from concussion/mTBI, which could potentially aid in the diagnosis and treatment of CTE 1.
From the Research
Definition and Pathology of Chronic Traumatic Encephalopathy
- Chronic Traumatic Encephalopathy (CTE) is a neuropathological disease defined by perivascular hyperphosphorylated tau protein depositions in a patchy distribution at the depths of cortical sulci in the brain 2.
- It is histologically identified by the presence of tau-immunoreactive NFTs and NTs with some cases having a TDP-43 proteinopathy or beta-amyloid plaques 3.
- Neuropathological findings are marked by abnormally phosphorylated tau accumulations at the depth of cerebral sulci, as well as TDP43, Aβ and α-synuclein positive staining 4.
Clinical Presentation and Diagnosis
- CTE has an insidious clinical presentation that begins with cognitive and emotional disturbances and can progress to Parkinsonian symptoms 3.
- It has been described 3 clinical variants: the behavioural/mood variant, the cognitive variant and the mixed behavioural/cognitive variant 4.
- Diagnosing CTE during life with sensitive and specific biomarkers is the next critical step, and currently, it cannot be precisely diagnosed or differentiated from other neurodegenerative diseases 2.
- Cerebral MRI revealed signs of diffuse atrophy with abnormal axonal findings using the diffusion tensor imaging methods, and cerebral PET tau revealed increased standardised uptake value ratio (SUVR) levels in various brain regions of CTE patients compared to controls 4.
Risk Factors and Prevention
- Risk factors include head trauma, presence of ApoE3 or ApoE4 allele, military service, and old age 3.
- Prevention and education are currently the most compelling way to combat CTE, and the best way to prevent CTE in athletes is to put in place strict and appropriate measures by physicians 3, 4.
- An individual with concussion should not be allowed to play again immediately (and sometimes never) in cases of abnormal neurological symptoms or imaging abnormalities 4.
Current Research and Controversies
- The study of CTE remains in its infancy, and current research focuses on methods of diagnosing the disease during life, examination of CTE risk factors, and description of the clinical presentation of CTE 5.
- The incidence of CTE is unknown, the clinical diagnostic criteria have not been agreed upon, and the current neuropathological characterization of CTE is acknowledged as preliminary 6.
- Disagreement continues about the neuropathological aspects that make CTE unique, and evidence suggests that a single moderate or severe traumatic brain injury can also induce progressive neuropathological changes 6.