Demer J L, Zee D S
Invest Ophthalmol Vis Sci. 1984 Jun;25(6):739-45.
Vestibular and optokinetic responses were recorded in three albino subjects with congenital nystagmus. Although an ice-water caloric stimulus did not elicit nystagmus, all patients showed a response to rotational stimuli containing high frequency components. Vestibular responses to a constant velocity rotation decremented with abnormally short time constants of 1-2 sec (normal 15-20 sec). For sinusoidal oscillation, in one subject, the cut-off frequency (where the amplitude of the response was 70% of maximum) was increased to 0.8 Hz (normal about 0.01 Hz). Full-field optokinetic stimulation generated no nystagmus response. These abnormalities may be due to defects in networks that act as mathematical integrators : either the final common neural gaze-holding network that converts velocity into position information for the ocular motor neurons or the "velocity-storage" mechanism that normally combines sensory inputs from both the labyrinths and visual system to generate appropriate (per-rotatory) nystagmus during rotation and to suppress inappropriate (post-rotatory) nystagmus after rotation.
记录了三名患有先天性眼球震颤的白化病受试者的前庭和视动反应。尽管冰水热量刺激未引发眼球震颤,但所有患者对包含高频成分的旋转刺激均有反应。对匀速旋转的前庭反应以异常短的1 - 2秒时间常数衰减(正常为15 - 20秒)。对于正弦振荡,在一名受试者中,截止频率(响应幅度为最大值的70%处)增加到0.8赫兹(正常约为0.01赫兹)。全视野视动刺激未产生眼球震颤反应。这些异常可能是由于作为数学积分器的网络存在缺陷:要么是将速度转换为眼动神经元位置信息的最终共同神经凝视保持网络,要么是通常结合来自迷路和视觉系统的感觉输入以在旋转期间产生适当的(旋转性)眼球震颤并在旋转后抑制不适当的(旋转后)眼球震颤的“速度存储”机制。