Velocity Storage Integrator (VSI): Mechanisms, circuits, and clinical implications A narrative review

agonist baclofen shortens VSI time constants and reduces motion-sickness susceptibility while sparing high-frequency VOR gain. Human data extend VSI to vertical rotational VOR, link sustained Off-vertical axis rotation (OVAR) bias to the indirect pathway, and demonstrate a shared storage for reflexes and self-motion perception. Altered-gravity experiments show immediate dependence of VSI persistence and Coriolis cross-coupling on g-level and reveal that gravity/contact cues gate dumping. Afferent-class mapping reconciles divergent behaviors across stimuli: irregular, Type I-origin afferents preferentially feed the direct pathway (vibration can evoke nystagmus without afternystagmus), whereas regular, Type II-origin afferents preferentially load the VSI during low-frequency canal/otolith paradigms (rotation, calorics, head-shaking, OVAR), producing robust after-responses. This unified framework yields testable biomarkers and mechanism-based targets for diagnosis, phenotyping, and therapy in vestibular disorders. This narrative review synthesizes anatomical, physiological, computational, and clinical evidence on velocity storage, with particular emphasis on its gravity dependence and multisensory updating. Throughout, velocity storage is treated explicitly as two separable levels: the Velocity Storage Integrator (VSI) as the neural substrate (circuits and state variables), and the Velocity Storage Mechanism (VSM) as the emergent behavioral/perceptual phenotype expressed by that substrate under specific sensory and contextual conditions.