Asymmetric motion visually evoked potentials in infantile strabismus are not an artifact of latent nystagmus

Irene Anteby, Hui Fang Zhai, Lawrence Tychsen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Background: Patients who have infantile strabismus exhibit a directional asymmetry of motion visually evoked potentials (MVEPs) recorded under conditions of monocular viewing. The majority of these patients also have latent nystagmus, raising the possibility that the MVEP asymmetry is an artifact of the nystagmus. To explore this issue, we correlated MVEPs and eye movements under conditions that eliminated or increased latent nystagmus. Methods: MVEPs and eye movements were recorded under conditions of monocular viewing in three adults who had combined infantile-onset strabismus and latent nystagmus. The subjects viewed vertically oriented grating stimuli that oscillated horizontally at temporal frequencies of 6.6 to 11.0 Hz by use of spatial frequencies of 1 to 3 cycles/degree. Quantitative eye movement recordings of latent nystagmus and horizontal pursuit/optokinetic nystagmus were also obtained. Results: Eye movement recordings showed that the latent nystagmus was absent or markedly diminished when the viewing eye was in a 45-degree adducted position, whereas nystagmus velocity increased 10 to 40 times (to 2.2 to 4.5 degrees/second) when the viewing eye was in an abducted position (p < 0.05). MVEPs were abnormal (asymmetry indices >0.40) when the viewing eye was in an adducted or abducted position of gaze. No correlation was found between the MVEP asymmetry index and the velocity of latent nystagmus. Conclusions: MVEP asymmetries in infantile strabismus remain robust under conditions that eliminate or greatly reduce the oscillations of latent nystagmus. MVEP asymmetries and ocular motor abnormalities both characterize infantile strabismus, but the ocular motor defects do not cause the MVEP asymmetries. The nasotemporal asymmetry of MVEPs and the nasotemporal asymmetry of pursuit and latent nystagmus are likely caused by deficits in related but separate binocular visual cortical circuits.

Original languageAmerican English
Pages (from-to)153-158
Number of pages6
JournalJournal of AAPOS
Issue number3
StatePublished - 1998
Externally publishedYes

Bibliographical note

Funding Information:
From the Departmem of Ophthalmology and Visual Seience~, St. Louis Children's Hospital at Washiugton University School of Medicine, St. Louis, Missouri. Supported by National Instiz~tes of Health Program Project grant No. PO1 NS 17763-12 (L.T.), National Institutes of Health grant No. RO1 EY 10214-01A3 (L.T.), McDonnell Center for Higher Brain Function research grant (LA.), Knights Templar Eye Foundation research grant (I.A.), and in part by National Institutes of Health grant No. EY02687 and an unrestricted grant to the Department of Ophthalmology and Visual Sciences from Research to Prevent Blindness, Inc. Submitted September 19, 1997. Revision acceptedJ anual 7 24, 1998. Reprint requests: L. Tychsen, MD, St. Louis Children's Hospital at ~/~ashington University School of Medicine, One Children's Place, Room 2 South 89, St. Louis, 3/10 63110. Copyright © 1998 by the American Associationf or Pediatric Ophthalmology and Strabismus. 1091-8%31/98 $Y.O0 + 0 7%/1/90038


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