Here we characterize persistent apogeotropic type of central positional nystagmus, and compare it with the apogeotropic nystagmus of benign paroxysmal positional vertigo involving the lateral canal. Nystagmus was recorded in 27 patients with apogeotropic type of central positional nystagmus (22 with unilateral and five with diffuse cerebellar lesions) and 20 patients with apogeotropic nystagmus of benign paroxysmal positional vertigo. They were tested while sitting, while supine with the head straight back, and in the right and left ear-down positions. The intensity of spontaneous nystagmus was similar while sitting and supine in apogeotropic type of central positional nystagmus, but greater when supine in apogeotropic nystagmus of benign paroxysmal positional vertigo. In central positional nystagmus, when due to a focal pathology, the lesions mostly overlapped in the vestibulocerebellum (nodulus, uvula, and tonsil). We suggest a mechanism for apogeotropic type of central positional nystagmus based on the location of lesions and a model that uses the velocity-storage mechanism. During both tilt and translation, the otolith organs can relay the same gravito-inertial acceleration signal. This inherent ambiguity can be resolved by a ‘tilt-estimator circuit’ in which information from the semicircular canals about head rotation is combined with otolith information about linear acceleration through the velocity-storage mechanism. An example of how this mechanism works in normal subjects is the sustained horizontal nystagmus that is produced when a normal subject is rotated at a constant speed around an axis that is tilted away from the true vertical (off-vertical axis rotation). We propose that when the tilt-estimator circuit malfunctions, for example, with lesions in the vestibulocerebellum, the estimate of the direction of gravity is erroneously biased away from true vertical. If the bias is toward the nose, when the head is turned to the side while supine, there will be sustained, unwanted, horizontal positional nystagmus (apogeotropic type of central positional nystagmus) because of an inappropriate feedback signal indicating that the head is rotating when it is not.

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地磁中心位置性眼球震颤的特征和机制

在这里，我们描述了中央位置性眼球震颤的持久型，并将其与良性阵发性位置性眩晕累及侧管的中性肌力性眼球震颤进行了比较。眼球震颤记录在27例患有多发性类型的中央位置性眼球震颤（22例单侧和5例有小脑弥散性病变）和20例良性阵发性位置性眩晕的中性多发性眼球震颤。他们在坐着的同时进行了测试，头部仰卧，仰卧，左右耳垂。自坐性眼球震颤的强度在坐位和仰卧位均质性类型的中央位置性眼球震颤时相似，但在仰卧性良性阵发性位置性眩晕性眼球震颤中更强。在中枢性眼球震颤中，由于局灶性病理，病变大部分重叠在前庭小脑（结节，小舌和扁桃体）中。我们基于病变的位置和使用速度存储机制的模型，提出了一种均质型中央位置眼球震颤的机制。在倾斜和平移期间，耳石器官可以传递相同的重力惯性加速度信号。这种固有的歧义性可以通过“倾斜估算器电路”解决，其中通过速度存储机制将来自半圆形通道的有关头部旋转的信息与有关线性加速度的耳石信息相结合。这种机制在正常对象中如何工作的一个例子是持续的水平眼球震颤，当正常对象绕恒定角度的轴旋转时会产生该持续水平眼震，该轴偏离真正的垂直方向（离垂直轴旋转）。我们建议，当倾斜估算器电路发生故障时，例如前庭小脑中有病变时，重力方向的估算值会错误地偏离真实的垂直方向。如果偏向鼻子，则在仰卧时将头部转向侧面时，由于不适当的反馈信号表明头部在旋转时会持续出现不必要的水平位置眼球震颤（中心型眼球震颤型）。它不是。