1022 - Utility of Sympathetic Nervous System Modulation for the Treatment of Traumatic Brain Injury (TBI): An Immune, Mitochondrial, Oxidative Stress, Apoptotic, and Genetic Perspective

Thursday, February 19, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

JP

Jordan Patierno, BS

OMS-III
Chicago College of Osteopathic Medicine
Chicago, Illinois, United States

Co-Author(s)

EL

Eugene Lipov, MD

Chief Medical Officer
Stella Center
Westmont, Illinois, United States

Submitter(s)

JP

Jordan Patierno, BS

Chicago College of Osteopathic Medicine
Downers Grove, Illinois, United States

Objectives: Traumatic brain injury (TBI) has a biphasic clinical course. While the primary insult is often mechanical, secondary injury mechanisms drive progressive neurological decline. Those mechanisms include neuroinflammation, mitochondrial dysfunction, oxidative stress, apoptosis, and maladaptive gene regulation. Stellate ganglion block (SGB) and cervical sympathetic block (CSB) have been shown to reduce TBI symptomatology, likely by mitigating these processes. By anesthetizing cervical sympathetic ganglia, SGB/CSB influences end-organ targets, including thymus, bone marrow, and spleen. Traditionally used for pain syndromes, its relevance to TBI is increasingly recognized. This study summarizes preclinical and clinical evidence of SGB/CSB’s impact on mechanisms central to secondary injury in TBI.

Design: We conducted an extensive review and synthesis of experimental and observational studies evaluating clinical and mechanistic effects of SGB/CSB related to TBI. Key endpoints included changes in clinical outcomes, symptom burden, and validated biomarkers, as well as mechanistic effects on inflammatory cytokines, mitochondrial dysfunction, oxidative stress, gene expression, and neuronal apoptosis.

Results: Retrospective cohorts of patients with chronic TBI symptoms reported significant reductions in Neurobehavioral Symptom Inventory (NSI) scores at one to three months after CSB, indicating improvement in symptom burden. A case series combining subanesthetic ketamine with SGB showed greater NSI reductions at two weeks, suggesting a synergistic benefit. Mechanistically, SGB/CSB downregulates NF-κB expression and lowers IL-6, TNF-α, and IL-1β. S100b levels also decrease, reflecting reduced astroglial activation and blood–brain barrier disruption. SGB/CSB treatment attenuated oxidative stress through genetic suppression of Reactive Oxygen Species Modulator 1 and enhanced superoxide dismutase activity. Preclinical studies further demonstrated that SGB/CSB shifts apoptotic signaling by increasing Bcl-2 protein synthesis and reducing Bax protein synthesis, thereby promoting neuronal survival.

Conclusions: SGB/CSB exerts durable immunomodulatory, antioxidant, genetic, and anti-apoptotic effects that extend beyond the anesthetic’s half-life. These mechanisms position SGB/CSB as a promising therapeutic strategy to limit secondary injury and improve TBI management.