ReviewDocumenta ophthalmologica. Advances in ophthalmology2026
Review of the clinical electrooculogram - Part 1: Mechanism of the Light-Rise.
Review in Documenta ophthalmologica. Advances in ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical electrooculogram (EOG) is the sole clinical electrophysiological test for assessing the function of the retinal pigment epithelium (RPE). However, despite several lines of investigation, the complete mechanism of the response has evaded a comprehensive description. The standard model implicates the rod photoreceptors and a signaling molecule termed the 'light-rise substance' that binds to an apical membrane 'light-rise receptor' or is transported across the membrane to elevate intracellular calcium concentration. The identity of the calcium activated chloride channel in the basolateral membrane was thought to be bestrophin, given the association of mutations in the hbest1 gene with Best Vitelliform Macular Dystrophy. However, recent findings have implicated a member of the anoctamin family as the calcium activated chloride channel with bestrophin regulating intracellular calcium in conjunction with the L-type calcium channel. How the changes in intracellular calcium are manifested as well as how the interaction with light in the dark-adapted state gives rise to the slow-dark and -light damped oscillations are yet to be described fully. This review summarizes the cellular mechanisms of the RPE that have been implicated in the generation of the light-rise and describes the likely candidates for the light-rise substance. A companion paper provides a summary of the bestrophinopathies and possible clinical modifications to enhance the EOG's clinical utility.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.