Bhidayasiri R, Plant G T, Leigh R J
Department of Neurology, Department of Veterans Affairs Medical Center and University Hospitals, Case Western Reserve University, Cleveland, OH 44106-5040, USA.
Neurology. 2000 May 23;54(10):1985-93. doi: 10.1212/wnl.54.10.1985.
To develop a hypothetical scheme to account for clinical disorders of vertical gaze based on recent insights gained from experimental studies.
The authors critically reviewed reports of anatomy, physiology, and effects of pharmacologic inactivation of midbrain nuclei.
Vertical saccades are generated by burst neurons lying in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). Each burst neuron projects to motoneurons in a manner such that the eyes are tightly coordinated (yoked) during vertical saccades. Saccadic innervation from riMLF is unilateral to depressor muscles but bilateral to elevator muscles, with axons crossing within the oculomotor nucleus. Thus, riMLF lesions cause conjugate saccadic palsies that are usually either complete or selectively downward. Each riMLF contains burst neurons for both up and down saccades, but only for ipsilateral torsional saccades. Therefore, unilateral riMLF lesions can be detected at the bedside if torsional quick phases are absent during ipsidirectional head rotations in roll. The interstitial nucleus of Cajal (INC) is important for holding the eye in eccentric gaze after a vertical saccade and coordinating eye-head movements in roll. Bilateral INC lesions limit the range of vertical gaze. The posterior commissure (PC) is the route by which INC projects to ocular motoneurons. Inactivation of PC causes vertical gaze-evoked nystagmus, but destructive lesions cause a more profound defect of vertical gaze, probably due to involvement of the nucleus of the PC. Vestibular signals originating from each of the vertical labyrinthine canals ascend to the midbrain through several distinct pathways; normal vestibular function is best tested by rotating the patient's head in the planes of these canals.
Predictions of a current scheme to account for vertical gaze palsy can be tested at the bedside with systematic examination of each functional class of eye movements.
基于近期实验研究获得的见解,制定一个解释垂直注视临床障碍的假说方案。
作者严格审查了中脑核团的解剖学、生理学及药理学失活效应的报告。
垂直扫视由位于内侧纵束嘴侧间质核(riMLF)的爆发神经元产生。每个爆发神经元以一种方式投射到运动神经元,使得眼睛在垂直扫视期间紧密协调(共轭)。来自riMLF的扫视神经支配对下直肌是单侧的,但对提上睑肌是双侧的,轴突在动眼神经核内交叉。因此,riMLF损伤会导致共轭性扫视麻痹,通常要么完全麻痹,要么选择性向下麻痹。每个riMLF包含用于向上和向下扫视的爆发神经元,但仅用于同侧扭转扫视。因此,如果在侧滚方向的头部旋转期间同侧没有扭转快相,则可以在床边检测到单侧riMLF损伤。 Cajal间质核(INC)对于垂直扫视后将眼睛保持在偏心注视以及协调侧滚方向的眼头运动很重要。双侧INC损伤会限制垂直注视的范围。后连合(PC)是INC投射到眼运动神经元的途径。PC失活会导致垂直注视诱发的眼球震颤,但破坏性损伤会导致更严重的垂直注视缺陷,可能是由于PC核受累。源自每个垂直半规管的前庭信号通过几条不同的途径上升到中脑;通过在这些半规管平面内旋转患者头部来最好地测试正常前庭功能。
通过对每种眼运动功能类别的系统检查,可以在床边测试当前解释垂直注视麻痹方案的预测。