Abstract:Vestibular Migraine (VM)? presents a core clinical challenge in the co-occurrence of headache and vestibular symptoms. Current research has clarified that the anatomical basis for this co-occurrence lies in the neural convergence of the trigeminovascular system and the vestibular system within the brainstem, thalamus, and other regions. At the molecular level, Calcitonin Gene-Related Peptide (CGRP), through its bidirectional synergistic amplification effect with central sensitization, is considered the core mechanism of this co-occurrence, with downstream processes like neurogenic inflammation, serotonin dysregulation, and the emerging role of autophagy dysfunction? also involved. Consequently, therapies targeting CGRP represent a significant breakthrough.However, key questions remain unresolved: the specific role of autophagy in clearing inflammatory mediators is unclear; the precise function of the cerebellum is not well-defined; and the temporal dissociation of clinical symptoms suggests the potential existence of unknown novel mechanisms. Therefore, future research should utilize multimodal technologies to analyze the pain-vestibular integration network, delve deeper into the interaction between the CGRP-central sensitization axis and pathways like autophagy at the molecular level, and explore cerebellar circuits and new therapeutic targets. This will provide a theoretical foundation for developing precise diagnostic and treatment strategies for VM.