ArticleBiological psychiatry. Cognitive neuroscience and neuroimaging2026
Effect of Traumatic Brain Injury on Sensorimotor Gating.
Article in Biological psychiatry. Cognitive neuroscience and neuroimaging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTraumatic brain injury (TBI) can impair acute and long-term cognitive functions and increase risk for developing neuropsychiatric disorders, including mood disorders and posttraumatic stress disorder. Sensorimotor gating, operationalized by prepulse inhibition (PPI) of the acoustic startle response, is impaired across several neuropsychiatric disorders and can contribute to neuropsychiatric risk. Although animal models indicate TBI can robustly disrupt PPI, no well-powered studies exist in humans.
methodsWe examined associations between TBI history and sensorimotor gating in the Marine Resiliency Study, a cohort of active-duty Marines and Navy Corpsmen (N = 1725). Participants reported lifetime TBI history, injury severity, blast exposure, time since last injury, number of TBIs, and persistent self-reported TBI-related problems. Individuals completed PPI and acoustic startle habituation assessments. Analyses were adjusted for neuropsychiatric symptoms, hearing, and baseline startle.
resultsModerate to severe TBI (n = 128), but not mild TBI (n = 824), was associated with lower PPI versus no TBI (n = 773). Effects were most prominent at shorter interstimulus intervals (30-60 ms), which may reflect more alterations to automatic/preconscious processing periods. TBI-associated disruption of PPI was most strongly associated with reported loss of consciousness >30 minutes. Blast-associated TBI was uniquely associated with reduced startle habituation, but not PPI deficits. Sensorimotor gating effects were independent of self-reported problems after TBI.
conclusionsModerate-severe and blast TBIs are associated with reductions in sensorimotor gating years after injury, supporting PPI as a useful cross-species marker of TBI-associated functional disruption with translational utility. Longitudinal studies are needed to determine the contributions of TBI-associated PPI disruptions to cognitive deficits and neuropsychiatric vulnerability.
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