Brandt T, Steddin S
Department of Neurology, University of Munich, Germany.
J Vestib Res. 1993 Winter;3(4):373-82.
Theoretical evidence is presented that all the typical features of BPPV (benign paroxysmal positioning vertigo) cannot be explained by cupulolithiasis in that otoconial debris become settled on the cupula of the posterior semicircular canal. A free floating clot of inorganic particles (heavier than endolymph) in the ampullofugal branch of the posterior semicircular canal is more likely to cause the syndrome. The clot always gravitates to the most dependent part of the canal as soon as the patient's head is moved in a way that alters the angle between the canal's plane and the gravity vector. As compared to a plunger (depending on the direction it moves) the clot produces push or pull forces on the cupula, thereby eliciting the BPPV attack. This clot-induced endolymph flow mechanism is compatible with all features of BPPV such as latency, limited duration, fatigability, change in direction of the induced nystagmus, and the efficacy of physical therapy in both posterior and horizontal semicircular canal BPPV. The floating clot is only activated by changes in position of the head relative to the gravitational vector (positioning vertigo) but not by prolonged static positions of the head (positional vertigo), which fits clinical experience. Therefore, canalolithiasis rather than cupulolithiasis provides a better definition of the underlying mechanism in BPPV.
有理论证据表明，良性阵发性位置性眩晕（BPPV）的所有典型特征无法用嵴帽结石症来解释，因为耳石碎片沉积在后半规管的嵴帽上。后半规管离壶腹较远一侧分支内的无机颗粒（比内淋巴重）形成的自由漂浮凝块更有可能引发该综合征。一旦患者头部移动，改变了半规管平面与重力矢量之间的夹角，凝块就会始终下沉到半规管最下垂的部位。与活塞类似（取决于其移动方向），凝块会对嵴帽产生推力或拉力，从而引发BPPV发作。这种由凝块引起的内淋巴流动机制与BPPV的所有特征相符，如潜伏期、持续时间有限、易疲劳性、诱发性眼球震颤方向的改变，以及后半规管和水平半规管BPPV的物理治疗效果。漂浮的凝块仅在头部相对于重力矢量的位置发生变化时（位置性眩晕）被激活，而不是在头部长时间保持静止时（位置性眩晕）被激活，这与临床经验相符。因此，半规管结石症而非嵴帽结石症能更好地解释BPPV的潜在机制。
