Revisiting benign paroxysmal positional vertigo pathophysiology

Department of Otolaryngology-Head and Neck Surgery, Edith Wolfson Medical Center, Tel-Aviv University Sackler School of Medicine, Holon, Israel.
American journal of otolaryngology (Impact Factor: 0.98). 07/2009; 30(4):250-5. DOI: 10.1016/j.amjoto.2008.06.009
Source: PubMed


Benign paroxysmal positional vertigo is the most common peripheral cause of vertigo. Although its pathophysiologic mechanisms remain unclear, different locations have been attributed throughout the last century, from the days of Bárány. Disease was initially located by Dix and Hallpike in the utricle, but later, Schuknecht's works elicited the cupulolithiasis and canalolithiasis theories, localizing the pathology to the semicircular canal system and mainly to the posterior one. However, conflicting evidences from temporal bone studies accumulated against this theory, which suggest other explanations. Although this clinical entity is well defined, and can usually be effectively treated with certain physical maneuvers, its pathophysiology is still obscure and is being critically discussed in this article, which reviews the milestones of benign paroxysmal positional vertigo understanding.

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    • "The considerable variation in the vertical and torsional contributions to the nystagmus induced by the Dix Hallpike maneuver, especially when considering the anterior and posterior canals, constitutes another pathophysiologic and diagnostic question which cannot be explained solely by the canalolithiasis and cupulolithiasis theories [20]. The role of the interactions between the semicircular canals and the otolith organs in the clinical signs and symptoms, as well as the recovery from BPPV, is still under investigation [21] [22]. "

    International Journal of Otolaryngology 10/2011; 2011(4):353865. DOI:10.1155/2011/353865
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    • "The history of ideas about benign paroxysmal positional vertigo (BPPV) dates back to at least 1921, possibly earlier [1] [2]. Briefly, two possible mechanisms or subtypes have been proposed: 1) the presence of otoconial material on the cupula of the semicircular canal, or cupulolithiasis, and 2) the presence of otoconia material in the semicircular canal, or canalithiasis . "
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    ABSTRACT: Although computational models suggest the existence of canalithiasis and cupulolithiasis subtypes of benign paroxysmal positional vertigo (BPPV), these subtypes cannot be distinguished from each other based on characteristics of nystagmus. Therefore, although the subtypes probably exist more information is needed from each patient than is available without invasive procedures. Also, some patients may have clinical syndromes that include both canalithiasis and cupulolithiasis subtypes. To determine if the parameters of nystagmus provide sufficient information to determine the subtype of nystagmus in a patient with BPPV. Patients (n = 118) had unilateral BPPV of the posterior canal; 15 patients also had BPPV of the lateral canal. The main outcome measures were parameters of nystagmus in response to the Dix-Hallpike maneuver: latency to onset of nystagmus, maximum slow phase velocity, and maximum duration. Correlations between pairs of variables showed minimal or no relationships. Also, cluster analyses showed no significant subtypes. The contralateral eye moved significantly faster than the ipsilateral eye.
    Acta oto-laryngologica 03/2010; 130(9):1019-23. DOI:10.3109/00016481003664777 · 1.10 Impact Factor
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    ABSTRACT: Otopetrin 1 (OTOP1) is a multitransmembrane domain protein, which is essential for mineralization of otoconia, the calcium carbonate biominerals required for vestibular function, and the normal sensation of gravity. The mechanism driving mineralization of otoconia is poorly understood, but it has been proposed that supporting cells and a mechanism to maintain high concentrations of calcium are critical. Using Otop1 knockout mice and a utricular epithelial organ culture system, we show that OTOP1 is expressed at the apex of supporting cells and functions to increase cytosolic calcium in response to purinergic agonists, such as adenosine 5'-triphosphate (ATP). This is achieved by blocking mobilization of calcium from intracellular stores in an extracellular calcium-dependent manner and by mediating influx of extracellular calcium. These data support a model in which OTOP1 acts as a sensor of the extracellular calcium concentration near supporting cells and responds to ATP in the endolymph to increase intracellular calcium levels during otoconia mineralization.
    Journal of Neurophysiology 12/2010; 104(6):3439-50. DOI:10.1152/jn.00525.2010 · 2.89 Impact Factor
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