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Early Autonomic Dysfunction Following TBI and Possible Interventions: A Narrative Review
Mohamed-Yahia Monawar1, Monica Vavilala2, Zeljka Minic3
1Duke University School of Medicine.
Journal of Neurosurgical Anesthesiology
|June 18, 2026
Summary
Traumatic brain injury (TBI) causes a catecholamine surge, initially adaptive but harmful if prolonged. This adrenergic dysregulation worsens outcomes and requires targeted therapeutic interventions for better neurological recovery.
Area of Science:
- Neuroscience
- Endocrinology
- Critical Care Medicine
Background:
- Traumatic brain injury (TBI) initiates an acute neuroendocrine stress response.
- This involves a surge in catecholamines (epinephrine, norepinephrine, dopamine) and hypothalamic-pituitary-adrenal axis activation.
- Prolonged early autonomic dysfunction can lead to secondary brain injury and systemic complications.
Purpose of the Study:
- To review the current understanding of adrenergic dysregulation following TBI.
- To explore its multisystem sequelae and impact on patient outcomes.
- To discuss potential therapeutic interventions and future research directions.
Main Methods:
- This study is a narrative review of existing literature.
- It synthesizes current knowledge on catecholamine surge and autonomic dysfunction post-TBI.
- It examines the downstream effects of dysregulated catecholaminergic signaling.
Main Results:
- Elevated catecholamine levels post-TBI correlate with increased mortality and worse outcomes.
- Adrenergic dysregulation disrupts neurotransmitter pathways, immune function, and cerebrovascular homeostasis.
- Prolonged sympathetic hyperactivity is linked to extended hospitalization and poor neurological recovery.
Conclusions:
- Adrenergic dysregulation is a critical factor in TBI pathophysiology and outcomes.
- Targeted modulation of adrenergic and related neurotransmitter systems shows therapeutic potential.
- Further controlled studies are needed to validate interventions for managing TBI-induced autonomic dysfunction.
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