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Written by Erin Yeh
February 5, 2026 | Awareness of recurrent head acceleration events (RHAEs) has increased over the years, but treatment and prevention strategies remain limited. RHAE refers to repetitive external impacts that rapidly move the head, either through direct contact with the skull or through impacts on the body that cause head movement. Precipitating head events can lead to impaired cognitive performance, abnormal brain activation patterns, decreased white matter integrity, and increased neuroinflammatory biomarkers. The chronic effects are less understood, although it is estimated that between 125 and 440 head-acceleration events occur per sports-related concussion in college and professional football players, and individual players experience up to 77 head-acceleration events in a single season (Journal of NeurotraumaDigital ID: 10.1177/08977151251403554).
Current treatment focuses only on post-injury care, such as rest, symptom management, and exercise. Even with helmet improvements and game-changers, preventing RHAEs is not enough. Furthermore, current treatments do not address the microscopic damage or toxic processes that unfold over time.
To find an effective care method, researchers at University of Utah Health tested photobiomodulation (PBM), which shines near-infrared light through LEDs or lasers to specific areas of the brain. Also called red light therapy, this exposure activates mitochondrial responses that enhance energy production in cells and improve blood flow, thus delivering more oxygen and nutrients to damaged tissue.
Tested on football players
The researchers tested the PBM on 26 football players from the National Collegiate Athletic Association’s (NCAA) Division I university in the western United States. Participants were equally divided between an active or sham PBM group. Participants received the transcranial Neuro Gamma (v3) device as well as the intranasal PBM device and were given instructions on its use and maintenance. Treatments were self-administered under the supervision of research staff in the training room or at a private location when traveling to away matches. The devices were externally identical, but the fake devices did not emit any red light. Treatment duration was 20 minutes and was administered three times a week over a period of 16 weeks.
Big difference
Using correlational imaging, the research team identified significant differences in pre- and post-season changes in brain inflammation and nerve fiber damage between the active PBM and sham PBM groups. The placebo group showed widespread increases in diffusion-restricted imaging (RDI) and quantitative anisotropy (QA) — markers of brain injury. In contrast, the active group had mostly stable levels of these makers. These findings suggest that PBM helps protect the brain from changes associated with RHAEs and may reduce the effects of past accidents, although longer-term studies are needed to confirm lasting benefits.
The increases in RDI and QA in the placebo PBM group are consistent with previous research showing that RHAEs can cause neuroinflammation and nerve damage, even within a single athletic season. Higher RDI levels indicate that more immune cells are entering the brain, and higher QA levels indicate that the brain is trying to repair small structural damage in response to inflammation. Stable or lower levels of RDI and QA in the active PBM group suggest that red light therapy reduces inflammation and protects the brain from ensuing damage, including neuronal injury or loss, decreased neuroplasticity, and long-term cognitive and mood issues.
Continuous use of red light therapy may also help with the acute inflammatory effects of RHAEs during a sports season and, if applied across multiple seasons, potentially reduce the cumulative effects of brain inflammation that contribute to long-term neurodegeneration. As mentioned previously, more studies are needed to confirm this.
One key finding is that the areas of the brain most affected by PBM are the same areas known to be particularly vulnerable to repetitive head impacts, or the “cone of vulnerability.” These areas—the midbrain, brainstem, thalamus, basal ganglia, limbic association pathways of the corpus callosum, and association pathways with the terminals of the frontal and temporal lobes—are exposed to the greatest amount of physical stress during repetitive head movements. The placebo group showed the most inflammation and nerve fiber repair in these areas of the brain, while the active group saw smaller changes and decreased signs of injury, especially in parts of the back left side of the brain.
The study had a small sample size, and researchers could not report players’ locations without risking participants’ confidentiality. Recent studies have shown that player position can influence the long-term effects of repetitive head impacts, and this likely applies to RHAEs as well. In addition, the sample did not include a non-contact or limited-contact athlete group for comparison, which limited the researcher’s ability to determine whether the observed neuroinflammation and subtle structural changes could be attributed to RHAEs alone. However, the use of a permutation test, consistent results across multiple complementary analyses, and anatomical plausibility of the affected brain regions provide sufficient support for the results.