BPPV involves displacement of otoconia from the utricular macula into a semicircular canal. Two mechanisms are recognized: canalithiasis, where free-floating otoconia create endolymph drag that deflects the cupula during positional changes, and cupulolithiasis, where otoconia adhere directly to the cupula, making it gravity-sensitive and producing persistent positional nystagmus. The posterior canal is affected in approximately 80% of cases due to its dependent anatomical position. Horizontal canal BPPV accounts for 15-20% and presents with direction-changing horizontal nystagmus on supine roll test. Anterior canal BPPV is rare (<5%). The clinician must differentiate BPPV from central positional vertigo (cerebellar or brainstem lesions), vestibular migraine, Meniere's disease, vestibular neuritis, and posterior circulation stroke. Key differentiators include nystagmus characteristics, latency, fatigability, duration, hearing status, and associated neurological findings.