Case Report: Relief of long-standing severe motion sickness following stellate ganglion block.

Background: Motion sickness is a common and often debilitating condition arising from sensory conflict within the vestibular-visual-proprioceptive system, with downstream activation of autonomic and emetic pathways. Despite its prevalence in travel, maritime operations, aviation, spaceflight, and virtual environments, effective prophylaxis remains limited by adverse side effects. Experimental and clinical evidence implicates autonomic imbalance and sympathetic nervous system (SNS) hyperactivity in motion sickness susceptibility and symptom severity. Case presentation: We report the incidental resolution of long-standing, severe motion sickness in a 68-year-old man undergoing treatment with stellate ganglion block (SGB) for complex regional pain syndrome (CRPS) of the left upper extremity. The patient had experienced incapacitating motion sickness triggered by air and sea travel for approximately 28 years, substantially limiting occupational and recreational activities. He underwent a series of left-sided SGBs over several months as part of CRPS management. Following several rounds of treatment, he unexpectedly reported complete and sustained remission of motion sickness. Over 12 months of follow-up, he remained symptom-free during repeated boating activities without pharmacologic prophylaxis. Discussion: Motion sickness is associated with increased sympathetic activity, reduced parasympathetic tone during symptom provocation, and hemodynamic changes including reduced cerebral blood flow. The stellate ganglion is a major sympathetic relay to the head, neck, and thorax, and SGB is known to transiently reduce sympathetic outflow and alter cerebral perfusion. Although local anesthetic effects are short-lived, some clinical benefits of SGB appear durable, suggesting longer-term modulation of autonomic reflexes. Genetic and physiological studies further support a role for exaggerated vestibulosympathetic reflex activity in motion sickness susceptibility. Additionally, both the stellate ganglia and the central autonomic network exhibit functional lateralization, and neuroimaging data suggest a left-hemisphere contribution to motion sickness susceptibility, raising the possibility of side-specific effects. Conclusion: This case represents, to our knowledge, the first report of durable remission of chronic motion sickness following SGB. While causality cannot be established from a single observation, the finding supports further systematic investigation of SGB as a non-pharmacologic and potentially durable prophylactic treatment for motion sickness.