CT scans do not show the changes associated with chronic traumatic encephalopathy (CTE). CTE is a progressive brain disease caused by repeated head trauma, often seen in athletes and others exposed to multiple concussions or subconcussive impacts over time. The hallmark of CTE is the abnormal accumulation of tau protein in the brain, which can only be definitively identified by examining brain tissue under a microscope after death. CT scans, which use X-rays to create images of the brain, are primarily useful for detecting acute injuries such as skull fractures, bleeding, or swelling but lack the sensitivity to detect the subtle, microscopic changes that characterize CTE.
CT imaging is the standard initial tool used in traumatic brain injury (TBI) cases because it quickly reveals fractures, hemorrhages, and other structural damage. It is excellent for acute settings where immediate decisions about treatment are needed. However, CT scans mainly show gross anatomical changes and cannot detect microscopic protein buildups or diffuse axonal injury, which are critical in CTE pathology. For example, CT can identify bleeding inside the brain or skull fractures but cannot visualize the tau protein deposits or the subtle brain tissue degeneration that occurs in CTE.
Magnetic resonance imaging (MRI) offers greater sensitivity than CT for detecting some brain injuries, especially in subacute or chronic phases. Advanced MRI techniques can reveal microbleeds, diffuse axonal injury, and other subtle brain abnormalities that CT misses. Still, even MRI cannot definitively diagnose CTE in living patients because it cannot directly visualize tau protein accumulations. Other emerging imaging methods, such as positron emission tomography (PET) scans using specialized tracers, are being researched for their potential to detect tau pathology in vivo, but these are not yet standard clinical tools.
The difficulty in detecting CTE during life stems from the fact that its changes are microscopic and biochemical rather than large-scale structural abnormalities. The disease progresses slowly, with symptoms like memory loss, mood changes, and cognitive decline appearing years after repeated head trauma. These symptoms overlap with other neurodegenerative diseases, making clinical diagnosis challenging without tissue confirmation.
In summary, CT scans are invaluable for acute traumatic brain injury assessment but do not show the chronic, microscopic changes of CTE. Diagnosis of CTE currently requires postmortem brain tissue analysis to identify abnormal tau protein deposits. Research continues into advanced imaging and biomarkers that might one day allow for diagnosis during life, but as of now, CT scans cannot detect CTE changes.
