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<p>Vestibular migraine (VM) is a complex disorder that affects the vestibular system and is characterized by recurrent vestibular symptoms along with features of a migraine. Despite recent updates to the diagnostic criteria by the Barany Society and the International Headache Society, VM is often underdiagnosed. This is mainly due to its variable clinical presentation and overlap with other vestibular disorders. The pathophysiology of VM remains poorly understood. Cortical spreading depression and cortical hyperexcitability play crucial roles in VM, affecting vestibular processing and sensitivity to visual stimuli. The trigeminocervical system, influenced by calcitonin gene-related peptide (CGRP), contributes to the headache and vertigo associated with this condition. Additionally, dysregulation in the brainstem and cerebellum can worsen vestibular symptoms, while dysfunction in multisensory integration can lead to visual dependence and increased sensitivity to motion stimuli. Genetic factors, including ionic channelopathies that impact glutamate homeostasis, are also involved. This review describes the pathophysiological mechanisms underlying VM, focusing on the role of videonystagmography (VNG) in its diagnosis. With this we aim to contribute to the evolving landscape of VM research and provide new perspectives for therapeutic interventions.</p>

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The Role of Videonystagmography in Unraveling Vestibular Migraine Pathophysiology

  • 期刊论文

  • 发表日期：

    2025年6月21日

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  • Hanifa Akhtar,
  • Md Jamil,
  • Ruuzeno Kuotsu,
  • Jijitha Lakshmanan,
  • Tishya Joshi,
  • Nisha Kumari,
  • T Paramesha Patra,
  • Neizekhotuo Brian Shunyu,
  • Aswathi KV

摘要

Vestibular migraine (VM) is a complex disorder that affects the vestibular system and is characterized by recurrent vestibular symptoms along with features of a migraine. Despite recent updates to the diagnostic criteria by the Barany Society and the International Headache Society, VM is often underdiagnosed. This is mainly due to its variable clinical presentation and overlap with other vestibular disorders. The pathophysiology of VM remains poorly understood. Cortical spreading depression and cortical hyperexcitability play crucial roles in VM, affecting vestibular processing and sensitivity to visual stimuli. The trigeminocervical system, influenced by calcitonin gene-related peptide (CGRP), contributes to the headache and vertigo associated with this condition. Additionally, dysregulation in the brainstem and cerebellum can worsen vestibular symptoms, while dysfunction in multisensory integration can lead to visual dependence and increased sensitivity to motion stimuli. Genetic factors, including ionic channelopathies that impact glutamate homeostasis, are also involved. This review describes the pathophysiological mechanisms underlying VM, focusing on the role of videonystagmography (VNG) in its diagnosis. With this we aim to contribute to the evolving landscape of VM research and provide new perspectives for therapeutic interventions.