Citation

Romano F, Tarnutzer AA, Straumann D, Ramat S, Bertolini G. J. Physiol. 2016; 595(6): 2161-2173.

Affiliation

Department of Neurology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.

Copyright

(Copyright © 2016, The Physiological Society, Publisher John Wiley and Sons)

DOI

10.1113/JP273204

PMID

27981586

Abstract

Gaze-evoked nystagmus (GEN) is an ocular-motor finding commonly observed in cerebellar disease, characterized by increased centripetal eye-drift with centrifugal correcting saccades at eccentric gaze. With cerebellar degeneration being a rare and clinically heterogeneous disease, data from patients are limited. We hypothesized that a transient inhibition of cerebellar function by defined amounts of alcohol may provide a suitable model to study gaze-holding deficits in cerebellar disease. We recorded gaze-holding at varying horizontal eye positions in 15 healthy participants before and 30 min after alcohol intake required to reach 0.6‰ blood alcohol content (BAC). Changes in ocular-motor behavior were quantified measuring eye-drift velocity as a continuous function of gaze eccentricity over a large range (±40°) of horizontal gaze angles and characterized using a 2-parameters tangent model. The effect of alcohol on gaze stability was assessed analyzing: 1) overall effects on the gaze-holding system, 2) specific effects on each eye, 3) differences between gaze angles in the temporal and nasal hemifields. For all subjects, alcohol consumption induced gaze instability, causing a two-fold increase (2.21 [0.55], median [median absolute deviation, MAD]; P = 0.002) of eye-drift velocity at all eccentricities.

RESULTS were confirmed analyzing independently each eye and hemifield. The alcohol-induced transient global deficit in gaze-holding matched the pattern previously described in patients with late-onset cerebellar degeneration. Controlled intake of alcohol seems a suitable disease model to study cerebellar GEN. With alcohol resulting in global cerebellar hypofunction, we hypothesize that patients matching the gaze-holding behavior observed here suffered from diffuse deficits in the gaze-holding system as well. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

Language: en