ArticleThe Journal of physiology2017
Gaze-evoked nystagmus induced by alcohol intoxication.
Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Acute Vertigo, Dizziness and Imbalance in the Emergency Department-Beyond Stroke and Acute Unilateral Vestibulopathy-A Narrative Review.Brain sciences · 2025Review
- The eyes have it: Alcohol-induced eye movement impairment and perceived impairment in older adults with and without alcohol use disorder.Alcohol, clinical & experimental research · 2025Article
- Downbeat Nystagmus Is Abolished by Alcohol in Nonalcoholic Wernicke Encephalopathy.Neurology. Clinical practice · 2022Article
- Stochastic Physiological Gaze-Evoked Nystagmus With Slow Centripetal Drift During Fixational Eye Movements at Small Gaze Eccentricities.Frontiers in human neuroscience · 2022Article
- Asymmetry in Gaze-Holding Impairment in Acute Unilateral Ischemic Cerebellar Lesions Critically Depends on the Involvement of the Caudal Vermis and the Dentate Nucleus.Cerebellum (London, England) · 2021Article
- Cerebellar Rebound Nystagmus Explained as Gaze-Evoked Nystagmus Relative to an Eccentric Set Point: Implications for the Clinical Examination.Cerebellum (London, England) · 2021Article
- Bruns' nystagmus revisited: A sign of stroke in patients with the acute vestibular syndrome.European journal of neurology · 2021Article
- Dose-dependent sensorimotor impairment in human ocular tracking after acute low-dose alcohol administration.The Journal of physiology · 2021Article
- Nystagmus characteristics of healthy controls.Journal of vestibular research : equilibrium & orientation · 2020Article
- Prevalence and Characteristics of Physiological Gaze-Evoked and Rebound Nystagmus: Implications for Testing Their Pathological Counterparts.Frontiers in neurology · 2020Article
- Negative optokinetic afternystagmus in larval zebrafish demonstrates set-point adaptation.Scientific reports · 2019Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
key pointsThe cerebellum is the core structure controlling gaze stability. Chronic cerebellar diseases and acute alcohol intoxication affect cerebellar function, inducing, among others, gaze instability as gaze-evoked nystagmus. Gaze-evoked nystagmus is characterized by increased centripetal eye-drift. It is used as an important diagnostic sign for patients with cerebellar degeneration and to assess the 'driving while intoxicated' condition. We quantified the effect of alcohol on gaze-holding using an approach allowing, for the first time, the comparison of deficits induced by alcohol intoxication and cerebellar degeneration. Our results showed that alcohol intoxication induces a two-fold increase of centripetal eye-drift. We establish analysis techniques for using controlled alcohol intake as a model to support the study of cerebellar deficits. The observed similarity between the effect of alcohol and the clinical signs observed in cerebellar patients suggests a possible pathomechanism for gaze-holding deficits. 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 behaviour were quantified measuring eye-drift velocity as a continuous function of gaze eccentricity over a large range (±40 deg) of horizontal gaze angles and characterized using a two-parameter tangent model. The effect of alcohol on gaze stability was assessed analysing: (1) overall effects on the gaze-holding system, (2) specific effects on each eye and (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); P = 0.002] of eye-drift velocity at all eccentricities. Results were confirmed analysing each eye and hemifield independently. 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 behaviour observed here suffered from diffuse deficits in the gaze-holding system as well.
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