traumatic brain injury

Mild traumatic brain injury can cause post-concussion syndrome (PCS) when lasting over three months. This can lead to chronic traumatic encephalopathy, but the risk of developing chronic traumatic encephalopathy is poorly known. It was found that patients with PCS had an increased level of neurofilament light protein and a decrease of amyloid beta in the cerebrospinal fluid, which are neurodegenerative biomarkers, and therefore can be used as a tool to assess a PCS patient’s risk of developing chronic traumatic encephalopathy.

 

Mild traumatic brain injury (mTBI) is one of the leading causes of death in the world. Symptoms usually resolve themselves within a few days or weeks, however, 10% to 15% of patients have symptoms that are persistent, lasting for over three months. This is known as post-concussion syndrome (PCS). Patients with PCS are at risk of developing chronic traumatic encephalopathy (CTE), which is a disorder that is characterized similarly to neurodegenerative disorders like Alzheimer’s disease.  The histopathological changes involved in such disorders include the involvement of neurofibrillary tangles and the deposition of plaques. The relationship between PCS and CTE is unknown. Therefore, Shahim et al. conducted a study to characterize what neurodegenerative processes are activated after repeated mTBI. The study investigated the biochemical markers in the cerebrospinal fluid, which can assess the damage of axons in white matter, the deposition of amyloid beta, and synaptic loss. These are also known to cause tangles and plaques.

The study was a cross-sectional study using a total of 31 male patients enrolled between January 2014 and February 2016. 16 of these patients were professional Swedish ice hockey players who have had a past of repeated mTBI with PCS symptoms for over three months, 9 of which had PCS for over a year. The remaining patients were healthy individuals used as controls. Concentrations of various proteins that were known to be involved in CTE were measured in the cerebrospinal fluid, including neurofilament light protein and amyloid beta.

It was found that there were increased levels of neurofilament light protein in patients who had PCS for over a year, when compared to patients with PCS that was resolved within a year and to healthy patients. Furthermore, it was found that patients with PCS had a reduced level of amyloid beta when compared to healthy patients. This proved that PCS is associated with injury to axons in white matter and the deposition of amyloid beta. This can eventually lead to the development of neurofibrillary tangles and plaques, confirming that patients with PCS for over year are at risk of developing CTE. Therefore, the biochemical markers assessed in this study are an objective tool that can be used to evaluate future injuries to the central nervous system and the risk of a patient with PCS in developing CTE.

The main limitations of this study were the small sample size and the exclusion of the appraisal of the relationship between the biochemical markers and the behavior, cognitive, and neurological changes of the patients. The assessment of this relationship should be further studied.

 

 

 

Written By: Unaisa Bhayat, BMedSc

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