ArticleExpert review of ophthalmology2017
Basic and translational neuro-ophthalmology of visually guided saccades: disorders of velocity.
Article in Expert review of ophthalmology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Advanced Eye Movement Features Measured by Quantitative Oculography as Candidate Biomarkers for Progressive Supranuclear Palsy.Diagnostics (Basel, Switzerland) · 2026Review
- Response times for reflexive saccades correlate with cognition in parkinson's disease, not disease severity or duration.Frontiers in neurology · 2022Article
- New Cerebello-Cortical Pathway Involved in Higher-Order Oculomotor Control.Cerebellum (London, England) · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
introductionSaccades are rapid, yoked eye movements in an effort to direct a target over fovea. The complex circuitry of saccadic eye movements has been exhaustively described. As a result clinicians can elegantly localize the pathology if it falls on the neuraxis responsible for saccades. Traditionally saccades are studied with their quantitative characteristics such as amplitude, velocity, duration, direction, latency and accuracy. AREAS COVERED: Amongst all subtypes, the physiology of the visually guided saccades is most extensively studied. Here we will review the basic and pertinent neuro-anatomy and physiology of visually guided saccade and then discuss common or classic disorders affecting the velocity of visually guided saccades. We will then discuss the basic mechanism for saccade slowing in these disorders. EXPERT COMMENTARY: Prompt appreciation of disorders of saccade velocity is critical to reach appropriate diagnosis. Disorders of midbrain, cerebellum, or basal ganglia can lead to prolonged transition time during gaze shift and decreased saccade velocity.
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