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These corrective saccades were only noticeable during the bedside HITs and had been interpreted as back-up saccades. Herein, we describe overt back-up saccades during HITs due to hypermetric covert saccades in a patient with an acute circumscribed lesion involving the cerebellum, which were misinterpreted as reversed corrective saccades due to the hyperactive VOR during bedside examination. When these corrective saccades are hypermetric due to cerebellar dysfunction, the eyes would overshoot the target with corrective saccades in the opposite direction. (MP4 15487 KB) Graph: Supplementary file3 Video-head impulse tests show hypermetric covert corrective (red arrowhead) and overt back-up saccades (red arrow) during stimulation of the left horizontal semicircular canal and covert corrective saccades (blue arrowhead) during stimulation of the right horizontal canal. [Extracted from the article]

Fixation nystagmus refers to the nystagmus that appears or markedly increases with fixation. While relatively common in infantile (congenital) nystagmus, acquired fixation nystagmus is unusual and has been ascribed to lesions involving the cerebellar nuclei or the fibers projecting from the cerebellum to the brainstem. We aimed to report the clinical features of patients with acquired fixation nystagmus and discuss possible mechanisms using a model simulation and diagnostic significance. We describe four patients with acquired fixation nystagmus that appears or markedly increases with visual fixation. All patients had lesions involving the cerebellum or dorsal medulla. All patients showed direction-changing gaze-evoked nystagmus, impaired smooth pursuit, and decreased vestibular responses on head-impulse tests. The clinical implication of fixation nystagmus is that it may occur in central lesions that impair both smooth pursuit and the vestibulo-ocular reflex (VOR) but without creating a spontaneous nystagmus in the dark. We develop a mathematical model that hypothesizes that fixation nystagmus reflects a central tone imbalance due to abnormal function in cerebellar circuits that normally optimize the interaction between visual following (pursuit) and VOR during attempted fixation. Patients with fixation nystagmus have central lesions involving the cerebellar circuits that are involved in visual–vestibular interactions and normally eliminate biases that cause a spontaneous nystagmus. [ABSTRACT FROM AUTHOR]