House Mattew G, Honrubia Vicente
Victor Goodhill Ear Center, UCLA School of Medicine, Division of Head and Neck Surgery, Los Angeles, Calif. 90095-1624, USA.
Audiol Neurootol. 2003 Mar-Apr;8(2):91-9. doi: 10.1159/000068998.
Benign paroxysmal positional vertigo (BPPV) is a common vestibular disorder resulting from a malfunction of the semicircular canal. Prior studies attempting to elucidate the mechanics of BPPV have focused on clinical and laboratory findings, and have discussed theoretical aspects only in qualitative terms. The goal of this study is to create a mathematical description of BPPV mechanics based on biophysical principles, in order to improve the physiopathological understanding of the most common varieties of the disorder, canalithiasis and cupulolithiasis. First, the abnormal stimulus being applied to the vestibular system during BPPV episodes is estimated by an analysis of the vestibulo-ocular reflex (VOR) response of clinical BPPV patients. The magnitude and time course of the head motion stimulus that would, in a normal test subject, produce a VOR response similar to that observed during BPPV nystagmus are inferred from eye motion data using an inverse transfer function approach. Next, physicomathematical models to describe the mechanics of the abnormal stimulations of the crista are created: the cupulolithiasis model is based on the principle that dense particulate matter becomes attached to the cupula of affected patients and effectively changes the specific gravity of the cupula; the canalithiasis model is based on the hydrodynamic effects from a cluster of particles falling within the canal endolymph. The stimuli predicted by these two models are compared to the stimuli estimated from physiological and clinical studies. The model predictions are found to be consistent with the empirical evidence for a reasonable set of model parameters. The cupulolithiasis model predicts a value of 0.69 micro g as the mass of particles contributing to the disorder. The canalithiasis model predicts a value of 0.087 micro g. These results support and expand our understanding of the mechanisms underlying the production of the cupulolithiasis and canalithiasis varieties of vertigo in humans. On the basis of these models, several predictions that can help the clinician improve the evaluation of BPPV patients are discussed.
良性阵发性位置性眩晕(BPPV)是一种常见的前庭疾病,由半规管功能故障引起。先前试图阐明BPPV机制的研究主要集中在临床和实验室结果上,仅从定性角度讨论了理论方面。本研究的目的是基于生物物理原理创建BPPV机制的数学描述,以增进对该疾病最常见类型——管结石症和嵴顶结石症的病理生理学理解。首先,通过分析临床BPPV患者的前庭眼反射(VOR)反应,估计BPPV发作期间施加于前庭系统的异常刺激。使用逆传递函数方法,从眼动数据推断出在正常测试对象中会产生与BPPV眼震期间观察到的VOR反应相似的头部运动刺激的大小和时间过程。接下来,创建描述嵴异常刺激机制的物理数学模型:嵴顶结石症模型基于致密颗粒物附着于受影响患者的壶腹并有效改变壶腹比重的原理;管结石症模型基于管内淋巴液中一群颗粒下落产生的流体动力学效应。将这两个模型预测的刺激与从生理和临床研究估计的刺激进行比较。发现对于一组合理的模型参数,模型预测与经验证据一致。嵴顶结石症模型预测导致该疾病的颗粒质量值为0.69微克。管结石症模型预测值为0.087微克。这些结果支持并扩展了我们对人类嵴顶结石症和管结石症性眩晕产生机制的理解。基于这些模型,讨论了一些有助于临床医生改进BPPV患者评估的预测。