Semicircular canal dehiscence: a possible direct cause of benign paroxysmal positional vertigo?

Abstract

Sir, It is commonly accepted that benign paroxysmal positional vertigo (BPPV) accounts for the majority of peripheral vestibular disorders, although it results largely underdiagnosed [1]. Despite its diffusion, and its ascertained link with traumas, the underlying causes often remain unknown. On the other hand, semicircular canal dehiscence (SCD), even if it was initially considered as a non-frequent entity [2], has been ever more largely reported in the last years, thus acquiring a not negligible role among the causes of peripheral vertigo. Even considering the number of interconnections among different vestibular disorders [3], and the actual possibility of misleading clinical pictures [4], it seems of some interest to speculate about the possibility of a direct causal interconnection between these two affections. It is well-known that both BPPV and SCD can lead to similar manifestations linked to different mechanisms: the former is linked to the abnormal canal stimulation due to labyrinth lithiasis, whereas the latter can cause the same abnormal stimulation by an increase of fluid pressure due to the ‘third window effect’; this can represent a confounding factor and must be kept in mind. Moreover, a concrete risk of developing a BPPV following surgery for SCD has been widely reported, and can easily be explained by the inner ear pressure changes caused by the surgical manoeuvres [5]: in this case, obviously, the surgical trauma by itself acts as a causal factor as habitually known. A more immediate relationship between these disorders can be postulated considering the shared abnormality of the endolymph displacement, often resulting in an alteration of the physiologic stimulation of the vestibular receptors, on the basis of mechanical alterations derived from the substrate that underlie both disorders. A recent interesting analysis on the physiologic and pathologic biomechanics of semicircular canals [6] well explains how dehiscence is able to create a difference in fluid displacement and velocity that can influence the labyrinthine structures. Despite the principal stimulation does not seem to involve the vestibule, a prolonged traumatic effect is reasonably expected also on the maculae. Hence, the fluid displacement derived from the ‘third window’, usually quantitatively linked to the width of the dehiscence, and even as extended as possibly resulting in a tympanic membrane displacement [7], may have a sub-continuous action on the macular structures; this could in turn result in an action possibly able to threaten the otolith integrity: in presence of a condition deteriorated by aging and eventual alterations of calcium metabolism, they can be weaker and therefore more exposed to repeated mechanical sub-clinical solicitations [8,9]. It must be underlined that both dehiscence and labyrinth lithiasis more typically present in adult/elderly subjects, in which the calcium metabolism usually undergoes some changes that affect bone reabsorption and replacement, possibly responsible for the clinical manifestation of dehiscence [10]. Briefly, an overall more fragile condition of both the bony labyrinthine capsule and the sensorial inner ear structures could reasonably concur to the development of a labyrinthine imbalance of mechanical origin. As the vascular impairment is usually considered among the possible risk factors for labyrinth lithiasis, it must be outlined that the hypothesized mechanism could be more or less dependent on circulation abnormalities as described by our group concerning the anterior partition of the inner ear [11,12]. An investigation about this hypothesis might be complicated by the above reported possibility of similar signs and symptoms linked to different mechanisms; however, an accurate analysis based not only on the clinical presentation, but also on the anamnesis, could help clarify this aspect. Should our hypothesis be confirmed, due to the definitely ascertained reliability of high resolution temporal bone CT in the diagnosis of inner ear affections [13], this exam could be considered in the routinary diagnostic workup of BPPV.