Feldon S E, Hoyt W F, Stark L
Brain. 1980 Mar;103(1):113-37. doi: 10.1093/brain/103.1.113.
High resolution infra-red oculographic recordings were obtained in 19 patients with clinically evident internuclear ophthalmoplegia. The major findings were attenuated phasic and tonic components of adducting saccades, fractionated phasic components of abducting saccades, equally long durations for phasic components of adducting and abducting saccades with refixation, and nasal drift of the abducting eye which initiated abducting nystagmus. Ipsilateral gaze paresis and abduction lag were occasionally associated with primarily unilateral cases of internuclear ophthalmoplegia. These findings were interpreted using available anatomical, electromyographic and oculographic data as well as computer simulations of internuclear ophthalmoplegia. We concluded that deficient excitation of the ipsilateral medial rectus was due to interruption of burst-tonic neurons within the medial longitudinal fasciculus which mediate horizontal eye movements. This resulted in a decreased pulse height and step of the agonist neural controller signal. We were also able to determine that variably slowed fractionated abducting saccades were caused by deficient intrasaccadic inhibition of the antagonist medial rectus. When medial rectus excitation was more deficient than medial rectus inhibition of the opposite eye, then a typical internuclear ophthalmoplegia resulted; when the amount of medial rectus excitation was equal to the amount of medial rectus inhibition of the opposite eye, then a gaze paresis occurred; and when medial rectus excitation was less deficiennt than medial rectus inhibition of the opposite eye, abduction lag resulted in the oculographic appearance of internuclear ophthalmoplegia of abduction. Abducting nystagmus appeared to be initiated by a tendency for the abducted eye to drift nasally from the increased level of tonic inhibition of the antagonist medial rectus. Some oculographic patterns were attributed to higher level adaptive changes in innervation. These changes were a consequence of disordered excitatory and inhibitory controller signals at the lower, internuclear level. Possible anatomical pathways which might carry these inhibitory controller signals were discussed. High resolution eye movement recordings of patients with internuclear ophthalmoplegia were interpreted directly and by computer simulations as being most consistent with disordered inhibitory and excitatory control of the medial rectus motor pool during rapid eye movements and eccentric gaze.
对19例临床上有明显核间性眼肌麻痹的患者进行了高分辨率红外眼动图记录。主要发现包括：内收扫视的相位和张力成分减弱，外展扫视的相位成分分离，内收和外展扫视伴重新注视时的相位成分持续时间相等，以及引发外展性眼球震颤的外展眼鼻侧漂移。同侧凝视麻痹和外展滞后偶尔与原发性单侧核间性眼肌麻痹病例相关。利用现有的解剖学、肌电图和眼动图数据以及核间性眼肌麻痹的计算机模拟对这些发现进行了解释。我们得出结论，同侧内直肌兴奋不足是由于介导水平眼球运动的内侧纵束内爆发 - 张力神经元中断所致。这导致激动剂神经控制信号的脉冲高度和阶跃降低。我们还能够确定，外展扫视的可变减慢分离是由拮抗肌内直肌的扫视内抑制不足引起的。当内直肌兴奋比另一只眼的内直肌抑制更不足时，则导致典型的核间性眼肌麻痹；当内直肌兴奋量等于另一只眼的内直肌抑制量时，则发生凝视麻痹；当内直肌兴奋比另一只眼的内直肌抑制不足程度较小时，则外展滞后导致外展性核间性眼肌麻痹的眼动图表现。外展性眼球震颤似乎是由外展眼因拮抗肌内直肌张力抑制增加而向鼻侧漂移的趋势引发的。一些眼动图模式归因于神经支配的更高水平适应性变化。这些变化是核内较低水平兴奋和抑制控制信号紊乱的结果。讨论了可能携带这些抑制控制信号的解剖学途径。核间性眼肌麻痹患者的高分辨率眼球运动记录经直接解释和计算机模拟，最符合快速眼球运动和偏心注视期间内直肌运动池抑制和兴奋控制紊乱的情况。
