EYE MOVEMENTS IN PATIENTS WITH WALLENBERG'S SYNDROME

We studied electro-oculographic and videotape recordings of eye movements in six patients with Wallenberg's syndrome. With fixation, all patients had a spontaneous rotatory nystagmus with the fast phase directed toward the intact side. With loss of fixation, the patients' eyes deviated ton...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 1981-01, Vol.374 (1), p.600-613
Main Authors: Baloh, Robert W., Yee, Robert D., Honrubia, Vicente
Format: Article
Language:English
Subjects:
Adult
Aged
Dominance, Cerebral - physiology
Eye Movements
Female
Fixation, Ocular
Humans
Intracranial Embolism and Thrombosis - diagnosis
Kinesthesis - physiology
Lateral Medullary Syndrome - diagnosis
Lateral Medullary Syndrome - physiopathology
Male
Medulla Oblongata - physiopathology
Middle Aged
Motion Perception - physiology
Posture
Reflex - physiology
Saccades
Space life sciences
Vestibular Nuclei - physiology
Vestibule, Labyrinth - innervation
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Summary:We studied electro-oculographic and videotape recordings of eye movements in six patients with Wallenberg's syndrome. With fixation, all patients had a spontaneous rotatory nystagmus with the fast phase directed toward the intact side. With loss of fixation, the patients' eyes deviated tonically toward the side of the lesion. Voluntary and involuntary saccades had larger amplitude when directed toward the side of the lesion than away from it. The spontaneous nystagmus predictably interacted with all slow eye movements, producing asymmetric smooth-pursuit, optokinetic, and vestibular responses. In addition, smooth-pursuit and optokinetic responses were decreased significantly in both directions compared to normal subjects. Fixation suppression of vestibular nystagmus also was impaired in both directions. We concluded that two different types of oculomotor bias were present in these patients--a velocity bias and a position bias. The former resulted from damage to the caudal lateral vestibular nuclei, and the latter from interruption of cerebellopontine pathways.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.1981.tb30904.x