A hypothetical scheme for the brainstem control of vertical gaze

Citation
R. Bhidayasiri et al., A hypothetical scheme for the brainstem control of vertical gaze, NEUROLOGY, 54(10), 2000, pp. 1985-1993
Citations number
69
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
54
Issue
10
Year of publication
2000
Pages
1985 - 1993
Database
ISI
SICI code
0028-3878(20000523)54:10<1985:AHSFTB>2.0.ZU;2-2
Abstract
Objectives: To develop a hypothetical scheme to account for clinical disord ers of vertical gaze based on recent insights gained from experimental stud ies. Methods: The authors critically reviewed reports of anatomy, physiolog y, and effects of pharmacologic inactivation of midbrain nuclei. Results: V ertical saccades are generated by burst neurons lying in the rostral inters titial nucleus of the medial longitudinal fasciculus (riMLF). Each burst ne uron projects to motoneurons in a manner such that the eyes are tightly coo rdinated (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 con jugate saccadic palsies that are usually either complete or selectively dow nward. Each riMLF contains burst neurons for both up anti down saccades, bu t only for ipsilateral torsional saccades. Therefore, unilateral riMLF lesi ons can be detected at the bedside if torsional quick phases are absent dur ing ipsidirectional head rotations in roll. The interstitial nucleus of Caj al (INC) is important for holding the eye in eccentric gaze after a vertica l saccade and coordinating eye-head movements in roll. Bilateral INC lesion s limit the range of vertical gaze. The posterior commissure (PC) is the ro ute by which INC projects to ocular motoneurons. Inactivation of PC causes vertical gaze-evoked nystagmus, but destructive lesions cause a more profou nd defect of vertical gaze, probably due to involvement of the nucleus of t he PC. Vestibular signals originating from each of the vertical labyrinthin e canals ascend to the midbrain through several distinct pathways; normal v estibular function is best tested by rotating the patient's head in the pla nes of these canals. Conclusions: Predictions of a current scheme to accoun t for vertical gaze palsy can be tested at the bedside with systematic exam ination of each functional class of eye movements.