Benign paroxysmal positional vertigo (BPPV) is most often a self-limited disorder arising from the posterior semicircular canal of the undermost ear in the Hallpike position. Some individuals with this disorder have severe and protracted symptoms requiring more than expectant therapy. We describe two patients with intractable BPPV and profound sensorineural hearing loss in the affected ear treated by transmastoid posterior semicircular canal occlusion. Postoperatively, both were relieved of their BPPV and demonstrated preserved lateral semicircular canal function as measured by electronystagmography. We feel this new procedure provides a simpler and possibly safer alternative to singular neurectomy and should be given future consideration in the treatment of intractable BPPV in a normal-hearing ear.

This report outlines our experience with posterior semicircular canal occlusion, a new operative procedure for intractable benign paroxysmal positional vertigo (BPPV). We postulate that the resulting solid canal "plug" prevents endolymph movement within the posterior canal, which effectively fixes the cupula. This selectively abolishes the receptivity of the posterior canal to both angular acceleration and gravity without influencing the other inner ear receptors. We previously reported the success of this procedure in two patients with BPPV and a co-existing profound sensorineural hearing loss in the affected ear. Since that report, a slightly modified technique has been used to occlude six more posterior canals--five in normal hearing ears. While our follow-up times range from only 3 to 18 months, all eight patients continue to be relieved of their BPPV. Temporary mixed hearing losses occurred in three of the five ears with normal preoperative hearing. Hearing in all five patients ultimately returned to the preoperative state. We believe this procedure is a simpler and safer alternative to singular neurectomy for the treatment of intractable benign paroxysmal positional vertigo.

Most clinicians accept cupulolithiasis as the pathophysiological mechanism underlying benign paroxysmal positional vertigo (BPPV.) According to this theory, a cupular deposit induces a gravitational effect on the posterior canal crista. Posterior semicircular canal occlusion is a new operative procedure for treating incapacitating BPPV. It is postulated that canal occlusion abolishes endolymph movement within the canal, effectively fixing the cupula and rendering it unresponsive to both angular and linear acceleration (gravity). During two recent canal occlusions, abundant "free-floating particles" were identified within the posterior canal endolymph. When changing the position of the canal in the earth vertical plane, these free-floating particles would move under the influence of gravity. The hydrodynamic drag of the particles would induce endolymph movement with cupular displacement leading to the typical response. This finding supports an alternate explanation to cupulolithiasis as the pathophysiological mechanism underlying BPPV.

No abstract

Benign paroxysmal vertigo (BPV) is a clinical syndrome of vestibular origin although generally no evidence of vestibular dysfunction can be demonstrated with conventional tests. In a review of 1350 consecutive dizzy patients, there were 125 with BPV and of these, 33 underwent a quantitative rotational test of vestibular function. The rotational results showed reduces vestibular system gain for these BPV patients. In addition, they could be subdivided on the basis of a normal or shorter cupular time constant (Tc). Separation of patients into diagnostic categories revealed that those categorized as cupulolithiasis and viral labyrinthitis had a normal Tc range and those categorized as trauma and idiopathic had a short Tc. The reduced gain and short Tc in the latter group suggest hair cell and/or nerve damage since these same changes occur in patients with destructive peripheral vestibular disease.