Purpose of Review: Migraine is increasingly recognized as a multisensory neurologic disorder whose manifestations extend beyond headache to include tinnitus, aural fullness, dizziness, vertigo, and motion sensitivity. This review synthesizes current clinical and mechanistic evidence and proposes a framework linking low-amplitude or fluctuating vestibulocochlear perturbations with intracranial-inner ear coupling, altered sensory gain, impaired habituation, and prolonged temporal persistence. Recent Findings: Recent clinical and epidemiologic studies support an association between migraine and auditory and vestibular symptoms, although causality and specific mechanisms remain uncertain. Peripheral contributors may include dynamic changes in inner-ear perfusion, vascular pulsatility, autonomic regulation, fluid homeostasis, or pressure transmission. Central migraine mechanisms may determine whether these marginal signals remain clinically silent or become amplified and persistent. The model does not imply that all patients with migraine have an occult structural peripheral vestibular disorder or that peripheral perturbations are the primary origin of migraine. Summary: Migraine-associated tinnitus and vestibular symptoms may represent related expressions of abnormal sensory regulation rather than unrelated comorbidities. The proposed framework emphasizes the interaction between low-amplitude or fluctuating input and a susceptible central sensory network and may help explain substantial symptoms despite normal or near-normal routine testing. No validated biomarker currently exists, but the framework suggests testable candidate physiologic signatures based on response threshold, gain, habituation, and temporal decay. The model remains hypothesis-generating and requires prospective validation.