Search

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]

The bilateral lateral medullary lesions disrupt both the inhibitory Purkinje outflow to bilateral vestibular nuclei and the climbing fibers participating in the cerebellar VOR adaptation, resulting in phenotypically identical HIS compared to the global cerebellar lesions. During vertical HITs for left or bilateral anterior canal semicircular canals, the VOR gain was slightly increased and small corrective saccades were followed in the anti-compensatory direction (Fig. Normally, vertical eye movements derived from each vertical canal are offset but not when the anterior canal gain is increased due to the vestibulocerebellar lesions [[9]]. [Extracted from the article]