Tinjauan Literatur mengenai Mekanisme Neurobiologis Vestibular Migraine

Abstract

Neurological disorders remain a major global health problem that can lead to reduced quality of life, disability, and limitations in daily activities. One of the increasingly recognized disorders is Vestibular Migraine, which is an important cause of recurrent vertigo with a prevalence of approximately 3% in the adult population and occurs more frequently in women. This condition is characterized by a combination of vertigo, balance disturbances, migraine headache, and hypersensitivity to visual and auditory stimuli. Objective: This study aims to analyze the neurobiological mechanisms of vestibular migraine based on literature studies, including the roles of the vestibular system, trigeminovascular system, neurotransmitters, neuroinflammation, and brain network connectivity disorders. Methods: This research is a literature review based on national and international scientific articles obtained from Google Scholar, PubMed, Elsevier, NCBI, and Clinical Key databases using relevant keywords. Results: The findings show that the mechanism of vestibular migraine involves activation of the trigeminovascular system, which triggers the release of neurogenic inflammatory mediators such as calcitonin gene-related peptide (CGRP), serotonin, and substance P. This activation increases the sensitivity of vestibular neurons and disrupts central neural signal transmission. In addition, increased glutamatergic activity leads to excessive neuronal excitability, contributing to vertigo and balance disturbances. Neuroimaging studies also reveal reduced connectivity in the sensorimotor network (SMN), dorsal attention network (DAN), and visual network, leading to impaired multisensory integration. Altered activity in the brainstem, cerebral cortex, and cerebellum further contributes to motion perception disturbances and sensory hypersensitivity. Conclusion: Vestibular migraine is a complex neurological disorder involving multisystem central nervous system dysfunction. Understanding its mechanisms is essential for improving diagnosis and developing more effective therapeutic strategies.