A hypothetical scheme for the brainstem control of vertical gaze

被引:87
作者
Bhidayasiri, R
Plant, GT
Leigh, RJ
机构
[1] Case Western Reserve Univ Hosp, Cleveland, OH 44106 USA
[2] Dept Vet Affairs Med Ctr, Dept Neurol, Cleveland, OH 44106 USA
[3] Dept Vet Affairs Med Ctr, Dept Biomed Engn, Cleveland, OH 44106 USA
[4] Dept Vet Affairs Med Ctr, Dept Neurosci, Cleveland, OH 44106 USA
[5] Guys & St Thomas Hosp, Dept Neurol, London SE1 9RT, England
关键词
saccades; vestibulo-ocular reflex; interstitial nucleus of Cajal;
D O I
10.1212/WNL.54.10.1985
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objectives: To develop a hypothetical scheme to account for clinical disorders of vertical gaze based on recent insights gained from experimental studies. Methods: The authors critically reviewed reports of anatomy, physiology, and effects of pharmacologic inactivation of midbrain nuclei. Results: 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 anti 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. Conclusions: 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.
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页码:1985 / 1993
页数:9
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