Related Experiment Video
Updated: Apr 7, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
Published on: June 2, 2014
Exercise suppresses COX-2 pro-inflammatory pathway in vestibular migraine
Yi-Yen Lee1, Yi-Ping Yang2, Pin-I Huang3
1Institute of Clinical Medicine, National Yang-Ming University, No. 155, Sec. 2, Linong Street, Taipei 11221, Taiwan; Division of Pediatric Neurosurgery, Neurological Institute, Taipei Veterans General Hospital, No. 201, Sec. 2, Shih-Pai Road, Taipei 11217, Taiwan; Faculty of Medicine, National Yang-Ming University, No. 155, Sec. 2, Linong Street, Taipei 11221, Taiwan.
Abstract:
Migraine and dizziness are relatively common disorders. Patients with dizziness have a higher incidence of migraines than the general population. The discomfort experienced by these patients is often poorly controlled by medication. However, the pathophysiology of vestibular migraine (VM) remains unclear. We hypothesized that patients with VM would experience remission from symptoms after exercise training and that this effect may be mediated through the suppression of cyclooxygenase-2 (COX-2)-mediated inflammation. Thus, the aim of the present study was to investigate the efficacy and possible anti-inflammatory benefits of exercise in patients with VM. We assessed the level of soluble inflammatory mediators in plasma from VM patients and control subjects. Our analysis of cytokine expression in the patients with VM undergoing exercise treatment revealed a significant reduction in pro-inflammatory cytokines and/or cytotoxic factors, such as tumor necrosis factor-α, interleukins, nitric oxide (NO), inducible NO synthase, and reactive oxygen species. In contrast, we found an increase in the level of anti-inflammatory cytokines after exercise. Moreover, the group undergoing exercise training showed significant symptomatic improvement and demonstrated suppressed antioxidant enzyme activity. To summarize, our data suggest that exercise significantly inhibits COX-2 activity, leading to the suppression of pro-inflammatory cytokines and changes in redox status. These results suggest that there is a molecular link between the central nervous system and the immune system. Furthermore, elucidation of the neurobiological mechanisms underlying VM could potentially lead to the development of novel therapeutic interventions for these patients.
Related Concept Videos
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids
Two synthetic agonists of THC,...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists
Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists
Antiasthma Drugs: Muscarinic Receptor Antagonists
Antimuscarinic agents compete with ACh for the same binding site on the muscarinic receptors. By binding to these receptors, they inhibit the downstream effects of ACh and block the parasympathetic...

