Dysregulated Cardiovascular Autonomic Responses to Orthostatic Challenge in Mild Traumatic Brain Injury

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Mild traumatic brain injury (mTBI) often presents with symptoms of dizziness, headache, and brain fog. Prior work has linked these symptoms to impaired autonomic nervous system function and associated changes in cerebral blood flow after mTBI. Arterial baroreflex function is central to the regulation of cerebral perfusion—modulating heart rate (HR) and blood pressure (BP) in response to postural changes and daily activity—and thus, of particular interest in understanding symptoms resulting from head trauma. This study sought to characterize sympathetic and parasympathetic baroreflex function in individuals with mTBI (≤14 days post injury) using standardized autonomic testing, and to assess the relationship between autonomic impairment and symptom severity. Seventy participants (35 mTBI, 35 age- and sex-matched controls) completed symptom questionnaires and a standardized autonomic battery that included heart rate variability during deep breathing, Valsalva maneuver, and 10-min head-up tilt (HUT) testing with beat-to-beat HR and BP monitoring. Outcome measures included HR/BP variability (SD), along with low frequency (LF) and high frequency power during supine and HUT phases. LF power during HUT was designated as the primary outcome of interest. Correlation and regression analyses assessed the relationship between autonomic outcome measures and postconcussion related symptom severity scores (Rivermead Post-Concussion Symptom Questionnaire-13), while controlling for potential confounders. Group-wise comparisons revealed significantly lower HR and BP variability, as well as reduced LF power of mean BP during HUT in the mTBI cohort compared to controls ( p = 0.002); LF power of HR was also significantly lower in mTBI compared to controls ( p = 0.011). Associations between autonomic metrics and symptom severity scores were weak. Individuals with mTBI (≤14 days since injury) exhibited blunted sympathetic baroreflex responses to orthostatic challenge as well as reduced HR/BP variability. These findings suggest physiological impairment in sympathetic activation post-mTBI, which may contribute to stressor-response based clinical symptomatology, but does not fully explain global symptom burden. Future studies should employ domain-specific symptom assessments (e.g., differentiating orthostatic from vertiginous or proprioceptive dizziness) and targeted physiological testing to further elucidate these relationships.

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