During an evaluation with a neurologist following hospitalization, the patient stated that her acute-phase CVS symptoms occurred about every two months and required hydromorphone for symptom relief. Other treatments like sumatriptan had failed for breakthrough symptom management,and gabapentin, TCAs, naproxen, oxycodone/acetaminophen, and morphine had failed forCVS symptom prophylaxis. Because a neurology assessment found a close association between the patient’s CVS and migraine headaches, OnabotulinumtoxinA injections were initiated at 155 Units IM every 12 weeks. An improvement in headaches was noted at the one-month follow-up and no acute-phase CVS symptoms returned. The patient continued to receive OnabotulinumtoxinA injections every 12 weeks and remained in remission for the next 21 months. Adverse drug events (ADRs) reported by the patient were numbness and weakness in the left shoulder after injections, with resolution a few days later.

The proposed mechanism of action for OnabotulinumtoxinA involves the inhibition of peripheral and central sensitization in the afferent neuronal pathway and is hypothesized to exert an analgesic effect via inhibition of the release of neurotransmitters and neuropeptides, leading to a reduction in the release of proinflammatory mediators suppressing peripheral and/or central sensation of pain. Because CVS is proposed to be variant of migraine, future research is necessary to identify the role of OnabotulinumtoxinA use for refractory CVS.

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