Cupulolithiasis: A Critical Reappraisal

Abstract

AbstractObjectiveTo review the history and pathophysiologic theories for cupulolithiasis and canalith jam in benign paroxysmal positional vertigo.Data SourcesPubMed, Google Scholar.Review MethodsThree PubMed and Google Scholar searches were performed, keywords: “cupulolithiasis,” “apogeotropic [and] benign,” and “canalith jam,” resulting in 187 unique full‐text articles in English or with English translation. Figures—Labyrinthine photographs were obtained of fresh utricles, ampullae, and cupulae of a 37‐day‐old mouse.ConclusionsFreely moving otoconial masses explain most cases (>98%) of benign paroxysmal positional vertigo. Evidence that otoconia adhere strongly or persistently to the cupula is lacking. Apogeotropic nystagmus in the horizontal canal form is often attributed to cupulolithiasis; however, periampullary canalithiasis explains self‐limited nystagmus, and reversible canalith jam explains prolonged apogeotropic nystagmus. Treatment‐resistant cases can be explained by entrapment of particles in the canals or ampullae, but persistent adherence to the cupula remains theoretical.Implications for PracticeApogeotropic nystagmus is usually due to freely moving particles and should not be used in studies of horizontal canal benign paroxysmal positional vertigo as the sole method to define entrapment or cupulolithiasis. Caloric testing and imaging may help differentiate jam from cupulolithiasis. Treatment for apogeotropic benign paroxysmal positional vertigo should include maneuvers that rotate the head through 270° to fully clear the canal of mobile particles, using mastoid vibration or head shaking if entrapment is suspected. Canal plugging can be used for treatment failures.