Whole membranous labyrinths of bullfrogs were used in order to replicate the human vestibule. The posterior semicircular canals (PSCs) were exposed, leaving the remaining membranous labyrinth encapsulated in the otic capsule. Vibration was applied to the surface of the bony capsule using a conventional surgical drill in order to dislodge the otoconia from the utricle. The position of the preparation was controlled so that the dislodged otoconia were attached to the cupular surface. This was regarded as a cupulolithiasis model. The action potentials changed instantaneously according to the gravitational force on the cupula. When the otoconia were dislodged and held within the PSC lumen, the position of the whole preparation was changed so that the otoconia moved back and forth within the canal lumen. This is a model of canalolithiasis. The action potentials changed in combination with the otoconial movement after a latent period. Both cupulolithiasis and canalolithasis are potentially valid mechanisms of benign paroxysmal positional vertigo (BPPV). However, canalolithiasis is the most likely mechanism of BPPV, which is usually characterized by nystagmus of short duration and long latency. A vibratory stimulus was able to detach the otoconia from the utricle, suggesting that mechanical insult could be a possible etiology of BPPV.
"Cupulolithiasis may exist in the posterior canal. Compared with canalolithiasis, the cupulolithiatic type of PC-BPPV tends to have shorter latency and longer time constant (i.e., it is more persistent).43 "
[Show abstract][Hide abstract] ABSTRACT: Benign paroxysmal positional vertigo (BPPV) is characterized by brief recurrent episodes of vertigo triggered by changes in head position. BPPV is the most common etiology of recurrent vertigo and is caused by abnormal stimulation of the cupula by free-floating otoliths (canalolithiasis) or otoliths that have adhered to the cupula (cupulolithiasis) within any of the three semicircular canals. Typical symptoms and signs of BPPV are evoked when the head is positioned so that the plane of the affected semicircular canal is spatially vertical and thus aligned with gravity. Paroxysm of vertigo and nystagmus develops after a brief latency during the Dix-Hallpike maneuver in posterior-canal BPPV, and during the supine roll test in horizontal-canal BPPV. Positioning the head in the opposite direction usually reverses the direction of the nystagmus. The duration, frequency, and symptom intensity of BPPV vary depending on the involved canals and the location of otolithic debris. Spontaneous recovery may be expected even with conservative treatments. However, canalithrepositioning maneuvers usually provide an immediate resolution of symptoms by clearing the canaliths from the semicircular canal into the vestibule.
"Several experimental models of cupulolithiasis and canalithiasis have been developed. Experiments with an in vitro frog model showed that otoconia placed on the cupula or in the semicircular canal, or dislodged from the utricle in a whole labyrinth, elicited different patterns of nerve excitation   . An experiment with an in vivo model in oyster toadfish, using glass microspheres the size of otoconia, showed changes in the firing rate of the vestibular nerve consistent with canalithiasis . "
[Show abstract][Hide abstract] 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.
"Experimental investigations of BPPV models have used the vestibular systems of frogs. Otoconia were inserted into the open end of an isolated posterior semicircular canal (PSC) (Suzuki et al., 1996), or dislodged from the utricle and driven into the PSC of an intact labyrinth (Otsuka et al., 2003). Neural activity was measured following a change in PSC orientation, with free-floating otoconia ('canalithiasis') and attached otoconia ('cupulolithiasis'). "
[Show abstract][Hide abstract] ABSTRACT: Benign paroxysmal positional vertigo (BPPV) is a mechanical disorder of the vestibular system in which calcite particles called otoconia interfere with the mechanical functioning of the fluid-filled semicircular canals normally used to sense rotation. Using hydrodynamic models, we examine the two mechanisms proposed by the medical community for BPPV: cupulolithiasis, in which otoconia attach directly to the cupula (a sensory membrane), and canalithiasis, in which otoconia settle through the canals and exert a fluid pressure across the cupula. We utilize known hydrodynamic calculations and make reasonable geometric and physical approximations to derive an expression for the transcupular pressure DeltaPc exerted by a settling solid particle in canalithiasis. By tracking settling otoconia in a two-dimensional model geometry, the cupular volume displacement and associated eye response (nystagmus) can be calculated quantitatively. Several important features emerge: (1) a pressure amplification occurs as otoconia enter a narrowing duct; (2) an average-sized otoconium requires approximately 5 s to settle through the wide ampulla, where DeltaPc is not amplified, which suggests a mechanism for the observed latency of BPPV; and (3) an average-sized otoconium beginning below the center of the cupula can cause a volumetric cupular displacement on the order of 30 pL, with nystagmus of order 2 degrees/s, which is approximately the threshold for sensation. Larger cupular volume displacement and nystagmus could result from larger and/or multiple otoconia.
Journal of Biomechanics 09/2004; 37(8):1137-46. DOI:10.1016/j.jbiomech.2003.12.014 · 2.75 Impact Factor
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