Format

Send to

Choose Destination
See comment in PubMed Commons below
Exp Brain Res. 2014 Sep;232(9):2891-8. doi: 10.1007/s00221-014-3971-4. Epub 2014 May 13.

Afternystagmus in darkness after suppression of optokinetic nystagmus: an interaction of motion aftereffect and retinal afterimages.

Author information

1
Department of Neurology, University Hospital Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland.

Abstract

The afternystagmus that occurs in the dark after gaze fixation during optokinetic stimulation is directed in the opposite direction relative to the previous optokinetic stimulus. The mechanism responsible for such afternystagmus after suppression of optokinetic nystagmus (ASOKN) is unclear. Several hypotheses have been put forward to explain it, but none is conclusive. We hypothesized that ASOKN is driven by the interaction of two mechanisms: (1) motion-aftereffect (MAE)-induced eye movements and (2) retinal afterimages (RAIs) produced by fixation during the suppression of optokinetic nystagmus (OKN). We examined the correlation among ASOKN, MAE-induced eye movements, and RAIs in healthy subjects. Adapting stimuli consisted of moving random dot patterns and a fixation spot and their brightness was adjusted to induce different RAI durations. Test patterns were a stationary random dot pattern (to test for the presence of a MAE), a dim homogeneous background (to test for MAE driven eye movements), and a black background (to test for ASOKN and RAIs). MAEs were reported by 16 out of 17 subjects, but only 7 out of 17 subjects demonstrated MAE-induced eye movements. Importantly, ASOKN was only found when these seven subjects reported a RAI after suppression of OKN. Moreover, the duration of ASOKN was longer for high-brightness stimuli compared with low-brightness stimuli, just as RAIs persist longer with increasing brightness. We conclude that ASOKN results from the interaction of MAE-induced eye movements and RAIs.

PMID:
24820290
DOI:
10.1007/s00221-014-3971-4
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center