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Lee Schwamm’s recent editorial in the New England Journal of Medicine lamented the failure of the PROTECT III and SYNAPSE clinical trials after recruitment of more than 2000 brain injured patients, despite their being ‘exceptionally well designed and conducted’ [1]. Both of these trials selected and stratified patients on the basis of Glasgow Coma Scale (GCS) score and assessed outcome with extended Glasgow Outcome Scale Scores and secondary measures. Schwamm cited the lack of biomarkers for brain injury as one of the many causes of failure, and noted that “the investigators appropriately call for a comprehensive review of the TBI translational research strategy,” particularly in light of the fact that these represent only the most recent of a long string of failed clinical trials for the treatment of brain injury [1]. Even before the failure of these most recent trials, recognition of the brain’s complexity and propensity for astonishing heterogeneity of injury has spurred a 22 country, 80 center effort in Europe. The Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury trial is a prospective longitudinal observational study with one of its goals listed as improving ‘characterization and classification of TBI’ [2,3]. At a fundamental level, the mild/moderate/severe paradigm for brain injury most frequently based on GCS, loss of consciousness and post-traumatic amnesia has utility for triage and rapid communication during the acute phase of injury, but it is neither sufficiently sensitive to assess cognitive and neuropsychiatric deficits of TBI nor predictive of outcome [3]. Recently, I cared for a 44-year-old woman who had bumped her head at home, without any loss of consciousness or other symptoms whatsoever. She did not seek medical care. Two weeks later she had a headache and took aspirin. She developed a mild expressive aphasia and reported to her local ED, where a head CT revealed a subdural hemorrhage. This woman had a GCS that never slipped from 15. She never met the criteria for mild, moderate or severe TBI, yet could potentially have died without neurosurgical intervention and would likely have residual deficit requiring therapy. Dogmatically, physicians will admit to the hospital or observe in the ED, any acute brain injury we can see on a CT scan, with the idea that these patients are at the highest risk for requiring surgical intervention. Equally dogmatically, we dismiss any patient without a visible structural brain injury on CT. And therein lies the problem. This subconscious allowance that the CT scan defines acute brain injury belittles the cryptic nature of concussive injury. The idea that something should be called ‘mild’ TBI, when it can potentially lead to a spiral of disabling and potentially lifelong symptoms, needs to be discarded. “...eye tracking might ultimately be used to classify – or even define concussion – and limit its scope to traumatic neurologic injury not apparent on CT scanning and resulting in intracranial mass effect, elevated intracranial pressure or disruption of neurologic pathways.” Editorial

Will eye tracking change the way we diagnose and classify concussion and structural brain injury?