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Clinic Director, Pittsford Performance Care
Pittsford, New York, USA
Web Version. Clinical Case Review. 2025.
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Download PDFCyclic vomiting syndrome is a debilitating functional gastrointestinal disorder characterized by recurrent episodes of severe nausea and vomiting separated by periods of relative symptom stability. In adults, the condition is frequently underdiagnosed and often resistant to conventional medical management, leading to prolonged patient suffering and repeated hospital utilization.
Emerging evidence suggests that cyclic vomiting syndrome may involve dysregulation of cortical, brainstem, and autonomic pathways governing visceral function and stress response. This case review describes an adult patient with long-standing, refractory cyclic vomiting syndrome and explores how functional neurological assessment and targeted neuro-autonomic rehabilitation informed clinical decision making in the absence of structural pathology.
A 57-year-old female presented with a 13-year history of cyclic vomiting syndrome marked by recurrent episodes of intense nausea followed by forceful vomiting occurring three to eight times per hour. Individual episodes lasted between 12 and 30 hours and were associated with profound dehydration, acute malnutrition, and persistent hiccups.
Episodes occurred every two to four weeks and were largely unpredictable, resulting in significant functional impairment and reduced quality of life. The patient had undergone extensive gastrointestinal evaluation, including advanced imaging and metabolic screening, without identification of a structural cause. She was under the care of a cyclic vomiting syndrome specialist and previously completed a comprehensive diagnostic evaluation at a tertiary referral center.
Relevant medical history included a high-impact motor vehicle accident in 2006 resulting in traumatic brain injury and left-sided hemothorax. Although acute injuries resolved, post-concussive symptoms persisted for several months following the event.
Given the absence of structural gastrointestinal pathology, evaluation focused on functional neurological and autonomic domains. A comprehensive examination assessed oculomotor control, vestibular integration, gait under cognitive load, autonomic regulation, and cervical spine contribution.
Findings included asymmetric smooth pursuit, delayed optokinetic responses, dysmetric saccades, gait instability during dual-task challenge, inter-arm blood pressure asymmetry, peripheral signs of autonomic instability, and reduced parasympathetic tone on heart rate variability assessment. Cervical spine examination revealed segmental fixation with reduced motion.
The constellation of findings suggested impaired cortical and subcortical integration influencing autonomic and visceral regulation rather than isolated gastrointestinal pathology.
The patient was assessed as having refractory cyclic vomiting syndrome with contributing neuro-autonomic dysregulation, likely influenced by prior traumatic brain injury and persistent imbalance between sympathetic and parasympathetic control. This framework provided a unifying explanation for symptom persistence and resistance to conventional treatment approaches.
A three-week, individualized neuro-rehabilitation program was implemented, designed to influence cortical, cerebellar, and autonomic pathways through multimodal sensory and motor input. Care emphasized adaptability and frequent reassessment rather than rigid protocol application.
Intervention principles included vestibulo-ocular rehabilitation, autonomic retraining with biofeedback, targeted manual therapy to support vagal outflow, neuroplasticity-based cognitive-motor integration tasks, and lifestyle strategies addressing hydration, nutrition, and environmental stress modulation. Nutraceutical support was incorporated to support mitochondrial and autonomic function.
Following completion of care, the patient reported absence of vomiting episodes for a 12-week observation period. When prodromal symptoms occurred, their intensity was reduced and recovery time following episodes shortened from several days to less than 24 hours.
Objective findings demonstrated improvement in autonomic balance, with reduced inter-arm blood pressure asymmetry and improved heart rate variability markers consistent with enhanced parasympathetic tone. The patient also reported improvements in sleep quality, emotional resilience, and overall quality of life.
This case illustrates the potential role of neuro-autonomic dysregulation in refractory cyclic vomiting syndrome, particularly in patients with a history of traumatic brain injury. Functional neurological findings may persist long after structural healing and contribute to visceral symptom expression through altered brain–gut communication.
Assessment and rehabilitation strategies that address cortical, brainstem, and autonomic integration may offer clinically meaningful insight in complex functional syndromes where standard diagnostic pathways fail to explain symptom persistence.
This publication describes a single observational case and does not establish causality or generalizable treatment efficacy. Outcomes reflect an individual response to care and should not be interpreted as predictive for all patients with cyclic vomiting syndrome or related conditions.
This case aligns with the clinical philosophy of Pittsford Performance Care, which emphasizes individualized neurological assessment, integration of autonomic and cortical function, and outcome-guided clinical reasoning. It reinforces the value of functional evaluation in complex visceral syndromes resistant to conventional care pathways.
The patient reported that the structured, neurologically informed approach provided clarity after years of uncertainty and ineffective treatment. She emphasized improved predictability of symptoms, faster recovery following episodes, and a meaningful improvement in daily functioning and quality of life.
This case review is provided for educational purposes only. It does not constitute medical advice, clinical guidelines, or treatment recommendations. Content reflects a de-identified retrospective observation from clinical practice and is not intended to establish generalizable clinical evidence.
No external funding was received for the development of this material.