A standard MRI scan cannot diagnose chronic traumatic encephalopathy. CTE is caused by a specific pattern of abnormal tau protein deposits deep in the brain’s folds, and those microscopic clumps are invisible on the kind of MRI you would get at a hospital or imaging center. The only confirmed way to diagnose CTE remains examination of brain tissue after death. That said, researchers are using advanced MRI techniques to detect a growing list of brain changes linked to repetitive head impacts, and some of those findings are edging closer to something that could serve as a living biomarker for the disease.
Why a Routine MRI Misses CTE
The signature lesion of CTE is an accumulation of hyperphosphorylated tau protein around small blood vessels at the depths of the brain’s sulci, the grooves between folds of cortex. These deposits are microscopic. A conventional MRI, even a high-resolution one, captures the brain’s overall structure, but it does not have the resolution or contrast to pick out clumps of misfolded protein scattered in specific pockets of tissue. A neurologist reviewing a standard MRI of someone with early- or even moderate-stage CTE might see a scan that looks entirely normal.
This is not a failure of the machine so much as a mismatch between what MRI was designed to do and what CTE looks like at the cellular level. MRI excels at showing tumors, strokes, large areas of tissue loss, and fluid buildup. CTE’s pathology is diffuse, patchy, and protein-based. Even at ultra-high magnetic field strengths used in research settings, the connection between tau deposits and standard MRI contrast has been difficult to establish. One study using an extremely powerful 11.7-Tesla research scanner on ex vivo brain tissue diagnosed with Stage III or IV CTE found no relationship between tau burden at the sulcal depths and any of the diffusion-based measures typically used to assess tissue integrity, though it did find signs of white matter disruption beneath those sulcal depths that were unique to CTE compared to Alzheimer’s disease or frontotemporal dementia tissue.
Brain Shrinkage That MRI Can Measure
While MRI cannot see tau directly, it can measure something tau eventually causes: tissue loss. As CTE progresses, neurons die and brain regions shrink. Volumetric MRI, which quantifies the size of specific brain structures over time, has picked up these patterns in people with histories of repetitive head trauma. In professional fighters, increasing exposure to head impacts was associated with smaller volumes in the thalamus and caudate, two deep brain structures involved in processing speed and movement control.1PubMed. Repeated head trauma is associated with smaller thalamic volumes and slower processing speed: the Professional Fighters’ Brain Health Study These are not regions that typically shrink first in Alzheimer’s disease, which tends to hit the hippocampus early, so the pattern offers at least a hint that something different is happening.
Longitudinal studies tracking fighters over time have made the case even more specific. Active boxers showed measurable yearly declines in the left thalamus and parts of the corpus callosum compared to controls, while retired boxers showed the steepest declines in the amygdala and hippocampus.2PubMed Central. Longitudinal change in regional brain volumes with exposure to repetitive head impacts A case report of a former high school football player found progressive focal gray matter loss on serial MRI scans, suggesting that even non-professional athletes may develop a measurable volumetric signature.3American Journal of Geriatric Psychiatry. Progressive Focal Gray Matter Volume Loss in a Former High School Football Player: A Possible Magnetic Resonance Imaging Volumetric Signature for Chronic Traumatic Encephalopathy
The catch is that brain shrinkage on its own is not specific to CTE. Many conditions cause atrophy, including normal aging, heavy alcohol use, Alzheimer’s, and depression. What researchers are trying to do is identify a pattern of regional volume loss distinctive enough to separate CTE from the rest. That work is still early, but the thalamus and corpus callosum findings in fighters, combined with the regional specificity, are among the more promising structural leads.
White Matter Signals Worth Watching
Beyond overall volume, MRI can also pick up abnormalities in the brain’s white matter, the bundles of nerve fibers that connect different regions. A type of MRI sequence called T2 FLAIR is commonly used in clinical practice to spot white matter hyperintensities, which appear as bright spots on the scan. These bright spots show up in many conditions and even in healthy aging, but researchers have proposed that people exposed to repetitive head impacts develop a distinctive pattern: small, round, non-confluent spots located close to the boundary between gray and white matter. This pattern has been termed RHI-associated white matter hyperintensities, and initial observations suggest it may be visually different from the more typical periventricular pattern seen in vascular disease or aging.4PubMed Central. Does white matter and vascular injury from repetitive head impacts lead to a novel pattern on T2 FLAIR MRI? A hypothesis proposal and call for research This is still at the hypothesis stage, but it illustrates how even existing, widely available MRI sequences might hold clues if clinicians know what to look for.
Susceptibility-weighted imaging, another MRI technique sensitive to iron deposits and blood products, has revealed microbleeds in active elite rugby players. In one study, roughly a quarter of the players showed evidence of either diffuse axonal injury or deep vascular injury on their scans, while microbleeds were found in a small number of players, including two who were sub-acutely injured.5Brain Communications. White matter abnormalities in active elite adult rugby players Microbleeds are not unique to CTE either, but their presence in young, otherwise healthy athletes is notable because it shows the brain is sustaining vascular damage that a standard clinical read of an MRI might overlook or attribute to something benign.
Diffusion MRI and What It Reveals in Younger Athletes
Diffusion tensor imaging, often called DTI, is a specialized MRI technique that tracks how water molecules move through brain tissue. In healthy white matter, water moves preferentially along the direction of nerve fibers. When those fibers are damaged, water movement becomes more random, and that change shows up as a measurable shift in a metric called fractional anisotropy. DTI is not part of a routine clinical MRI, but it has become a workhorse in research on repetitive head trauma.
A systematic review of diffusion imaging studies in athletes found a consistent story: contact sport athletes experienced greater changes in white matter integrity over the course of a season compared to controls. In some studies, athletes who sustained more impacts, as measured by helmet-mounted accelerometers, showed larger shifts in their diffusion metrics. High-strain football players showed significant pre-to-post-season changes compared to controls, while low-strain players did not, suggesting a dose-response relationship between head impact exposure and white matter disruption.6PubMed Central. Diffusion Imaging of Sport-related Repetitive Head Impacts—A Systematic Review
These findings matter because they show that measurable brain changes can appear even from subconcussive impacts, hits that do not produce a diagnosed concussion. Many of the athletes in these studies were college or high school players, not professionals with decades of exposure. The changes were sometimes reversible after a period of rest, which complicates the picture. Are these transient fluctuations, or are they early signs of cumulative damage? That question does not have a definitive answer yet, but the fact that DTI can detect them at all means it has potential as a monitoring tool.
Beyond Structure: Functional and Chemical MRI Techniques
MRI is not limited to taking pictures of anatomy. Functional MRI measures blood flow changes associated with brain activity, and it has been used to study how subconcussive head trauma alters the brain’s network connectivity. In one study, football players underwent resting-state functional MRI before and after games. Even without a diagnosed concussion, post-game scans showed altered connectivity in the default mode network, with some connections strengthening and others weakening. Players with a history of prior concussions appeared to respond differently than those without one, hinting at a cumulative vulnerability.7PubMed Central. Effects of subconcussive head trauma on the default mode network of the brain
Magnetic resonance spectroscopy takes yet another angle: instead of imaging the brain’s structure or activity, it measures the concentration of specific chemicals in brain tissue. In athletes with a history of repetitive brain trauma, spectroscopy showed substantially higher levels of several markers compared to controls. Glutamine and glutamate, neurotransmitters involved in excitatory signaling, were about 31% higher. Choline, a marker often associated with membrane turnover and inflammation, was roughly 65% higher. Phenylalanine, an amino acid, was 46% higher.8PubMed Central. Changes in the neurochemistry of athletes with repetitive brain trauma: preliminary results using localized correlated spectroscopy These chemical shifts suggest ongoing neuroinflammation and metabolic disruption, processes that could be feeding into the progression of CTE-related damage.
Another advanced technique, dynamic contrast-enhanced MRI, evaluates the integrity of the blood-brain barrier by tracking how a contrast agent leaks from blood vessels into brain tissue. A 2025 study found that retired combat and collision sports athletes showed detectable blood-brain barrier disruption years after leaving their sport. Among those with the most extensive barrier breakdown, cognitive decline was worse compared to those with less disruption.9PubMed. Blood-brain barrier disruption, traumatic encephalopathy, and cognitive decline in retired athletes The blood-brain barrier finding is particularly interesting because it offers a potential mechanism, not just a correlate, for how repetitive head impacts might cause ongoing damage long after the impacts stop.
How PET Scans Differ from MRI
PET, or positron emission tomography, works on a completely different principle from MRI. Instead of using magnetic fields, it injects a radioactive tracer that binds to a specific molecule in the brain and then detects the radiation that tracer emits. For CTE research, the molecule of interest is tau, the same protein whose deposits define the disease at autopsy. Tau PET tracers like flortaucipir can reveal where tau is accumulating in a living brain, and in some at-risk patients, the binding patterns look strikingly different from what you would see in Alzheimer’s disease. One patient studied with both PET and MRI showed extremely high tau tracer uptake across the cortex, reaching over 20 standard deviations above age-matched controls, with relative sparing of the sensorimotor and occipital areas. Other patients showed a frontotemporal pattern of uptake.10PubMed Central. Tau PET and multimodal brain imaging in patients at risk for chronic traumatic encephalopathy
PET can see things MRI simply cannot, because it is detecting molecular pathology rather than structural anatomy. But PET has its own significant limitations: it is expensive, involves radiation exposure, and the current tracers were originally designed to detect Alzheimer’s-pattern tau. Whether they reliably distinguish CTE tau from Alzheimer’s tau in the general population remains an open question. PET also lacks the spatial resolution to pinpoint tau at sulcal depths the way a neuropathologist can under a microscope. For now, PET and MRI serve complementary roles in research, with neither one sufficient on its own to confirm CTE in a living person.
The Overlap Problem with Other Brain Diseases
One of the biggest obstacles to using any imaging technique for CTE diagnosis is that the brain changes associated with CTE overlap substantially with those seen in Alzheimer’s disease, frontotemporal dementia, and even normal aging. Brain atrophy, white matter lesions, tau deposits, and neurochemical shifts are features of multiple neurodegenerative conditions. A review of imaging and fluid biomarkers concluded that none of the currently studied biomarkers have the discriminatory power to reliably differentiate CTE from other tauopathies.11PubMed. The diagnostic potential of fluid and imaging biomarkers in chronic traumatic encephalopathy (CTE) It is unlikely that a single test will be sufficient to properly diagnose and distinguish CTE from other neurodegenerative diseases.12PubMed Central. Emerging advances of in vivo detection of chronic traumatic encephalopathy and traumatic brain injury
This is why the research community is increasingly focused on multimodal approaches, combining structural MRI, diffusion imaging, PET, blood biomarkers, clinical symptoms, and exposure history into a composite picture. The DIAGNOSE CTE Research Project, a major multicenter effort, was designed specifically to develop and validate in vivo biomarkers for CTE, refine clinical diagnostic criteria, and examine how factors like genetics and head impact exposure interact.13PubMed. Developing methods to detect and diagnose chronic traumatic encephalopathy during life: rationale, design, and methodology for the DIAGNOSE CTE Research Project The working clinical label for what researchers believe may be CTE during life is traumatic encephalopathy syndrome, or TES. It is a research framework, not a confirmed diagnosis, and it relies heavily on exposure history and symptom profile alongside imaging findings.
Machine Learning as a Potential Shortcut
If no single MRI measure can reliably flag CTE, perhaps a computer analyzing dozens of measures simultaneously could do better than a human radiologist. That is the premise behind machine learning approaches to CTE detection. In one study, researchers fed diffusion MRI data from individuals with and without a history of chronic traumatic brain injury into classification algorithms. Standard T1-weighted imaging, the kind of structural scan you would get clinically, achieved classification accuracy of only about 52 to 57%, barely better than flipping a coin. Diffusion-based models performed better, reaching up to 73% accuracy.14Frontiers in Neuroscience. Machine learning-based classification of chronic traumatic brain injury using hybrid diffusion imaging
A replication study found similar or improved results, with classification accuracy reaching about 82.5% when combining different diffusion metrics, and sensitivity as high as 85% for certain measures.15PubMed Central. Machine learning classification of chronic traumatic brain injury using diffusion tensor imaging and NODDI: A replication and extension study Those numbers are encouraging for research, but they are far from what you would want for clinical diagnosis. An 85% sensitivity rate means roughly one in seven affected people would be missed. And these studies classified individuals based on self-reported history of traumatic brain injury, not autopsy-confirmed CTE, so what the algorithms are actually detecting remains uncertain. Still, the trajectory is promising. As datasets grow and MRI acquisition protocols improve, machine learning could become part of a diagnostic toolkit, especially when combined with clinical data and other biomarkers.
What Athletes and Families Can Realistically Expect Today
If you or someone you care about has a history of contact sports and is experiencing memory problems, mood changes, or cognitive difficulties, getting an MRI is still a useful step. It can rule out other conditions, including tumors, strokes, hydrocephalus, and large areas of atrophy that might point toward Alzheimer’s or frontotemporal dementia. What it will not do is give you a CTE diagnosis. No radiologist will read a scan and write “CTE” in the report, because the imaging features are not specific enough to support that conclusion in an individual case.
The research techniques described here, DTI, spectroscopy, functional MRI, and dynamic contrast-enhanced imaging, are almost entirely confined to academic medical centers and research studies. They require specialized equipment, analysis pipelines, and expertise that are not available in community hospitals or outpatient imaging centers. A few clinical research programs, such as the DIAGNOSE CTE project, are enrolling participants and providing advanced imaging as part of their protocols. For most people, though, the practical reality is that clinical evaluation for cognitive and behavioral symptoms will rely on neuropsychological testing, symptom history, and standard imaging to exclude other diagnoses.
This gap between research findings and clinical availability is one of the more frustrating aspects of CTE science. There is genuine progress being made, from the discovery of distinctive white matter lesion patterns to machine learning classifiers trained on diffusion data. But translating those advances into a test your doctor can order remains years away. The field’s honest consensus is that CTE cannot currently be diagnosed during life,16PubMed Central. Structural MRI profiles and tau correlates of atrophy in autopsy-confirmed CTE and anyone claiming otherwise is ahead of the evidence.
Emerging Blood-Brain Barrier Research
One of the more intriguing recent developments is the finding that blood-brain barrier disruption can be detected with MRI long after an athlete has retired. The barrier is a tightly sealed layer of cells lining the brain’s blood vessels, and when it breaks down, molecules that normally stay in the bloodstream leak into brain tissue and trigger inflammation. The 2025 study of 47 retired combat and collision sports athletes found that a subgroup of 17 individuals with the most extensive barrier disruption also showed worse cognitive decline over time.9PubMed. Blood-brain barrier disruption, traumatic encephalopathy, and cognitive decline in retired athletes This matters because it points toward a vascular mechanism for ongoing brain damage, one that persists even after the hits have stopped. If barrier disruption can be reliably measured with contrast-enhanced MRI and correlates with clinical outcomes, it could eventually become both a prognostic marker and a treatment target. Drugs that stabilize the blood-brain barrier or reduce the inflammation caused by its breakdown are an active area of pharmacological research, though none have been validated specifically for CTE-related pathology.