The Epley Maneuver and Osteopathy
The Science Behind Benign Paroxysmal Positional Vertigo
An Abbreviated Diagnostic Maneuver for Posterior Benign Positional Paroxysmal Vertigo – Pia Michael, Carolina Estibaliz Oliva, Marcia Nuñez, Cristian Barraza, Juan Pablo Faúndez, and Hayo A. Breinbauer. Front Neurol. 2016; 7: 115.
Benign paroxysmal positional vertigo represents a common clinical entity that is encountered not only by specialists in neuro-otology and balance disorders but also by non-specialized otolaryngologists, neurologists, or geriatricians and general practitioners in primary care or emergency departments, among many other settings, in routine clinical practice (10–12). It is widely accepted that BPPV is caused by the dislodgement of otoconia from the otolith macula (8, 12). These particles then float until they become trapped within a semicircular canal (canalolithiasis) or attached to its cupula (cupulolithiasis). Then, after a change in head position in the plane of the affected canal, gravity induces the trapped otoconia to move, resulting in abnormal endolymph flow and the subsequent deflection of the cupula in cases of canalolithiasis or direct cupular deflection in cases of cupulolithiasis. In both scenarios, the vestibular afferents from the affected canal are modulated (stimulated or inhibited) in an abnormal and augmented fashion, particularly in comparison to the “paired canal” in the contralateral ear, which lacks the “extra weight” of the dislodged otoconia required to react normally to head movements. The computation of this asymmetry at the vestibular nuclei triggers not only vertigo or dizziness but also a specific type of nystagmus that depends on the canal that is affected by the disease. All three semicircular canals can be afflicted by this condition (11–13).