September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Congenital and Acquired Exotropia: Underlying Mechanisms
Author Affiliations & Notes
  • Avery H Weiss
    Seattle Children's Hosp/W-7729, Seattle, Washington, United States
    Ophthalmology, university of Washington, Seattle, Washington, United States
  • John P Kelly
    Seattle Children's Hosp/W-7729, Seattle, Washington, United States
    Ophthalmology, university of Washington, Seattle, Washington, United States
  • James O. Phillips
    Seattle Children's Hosp/W-7729, Seattle, Washington, United States
    Ophthalmology, university of Washington, Seattle, Washington, United States
  • Footnotes
    Commercial Relationships   Avery Weiss, None; John Kelly, None; James Phillips, None
  • Footnotes
    Support  Supported by an unrestricted grant from grant from the Barbara Anderson, Peter LeHaye, and William O. Rogers Endowment Funds
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Avery H Weiss, John P Kelly, James O. Phillips; Congenital and Acquired Exotropia: Underlying Mechanisms
      . Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © 2017 Association for Research in Vision and Ophthalmology.

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Abstract

Purpose : Binocular eye alignment is maintained under static and dynamic viewing by the interactive relationship between interocular positional disparity and 2 vergence systems, one mediated by fine stereo-disparities (≤12D) and one mediated by gross disparities >12D. We postulated that the inability to establish or maintain binocular alignment during targeted eye movements could underlie congenital and acquired XT.

Methods : Twenty–six children (mean age 5.6y) with congenital or acquired exotropia had assessments of eye alignment, visual acuity, stereopsis (Titmus test), measurement of disparity-driven convergence (DDC). Targeted smooth pursuit and saccades were quantified by binocular video-oculography (VOG).

Results : Six children with congenital XT (35-75D) had no demonstrable DDC on VOG; 4 had developmental abnormalities of the brainstem or cerebellum. Eleven of 13 children with intermittent XT (10 to 45D) had stereo-acuities of 40-60 arcsec. During targeted EOM recordings children with X(T) displayed variable interocular disparities, both horizontal and vertical due to inferior oblique overaction (IOOA) or breakdown of DDC. The loss of eye alignment due to limited vergence reserve is further demonstrated by 3 subjects with acquired loss of DDC due to antecedent brainstem compression or trauma. Two children acquired convergence insufficiency type XT related to a tectal plate glioma or hydrocephalus. One child with distal arthrogryposis presented with an XT related to hypoplastic rectus EOMs.

Conclusions : We found that children with congenital XT uniformly failed to generate DDC, likely due to a developmental abnormality of vergence neurons in the cerebellum and brain stem. Most children with intermittent XT had stereopsis of 40-60 arcsec indicating normal co-development of binocular vision and fine DDC. The delayed onset of XT ranging from 10-45D is consistent with loss of fine or gross DDC due to accumulation of vergence errors resulting from IOOA or loss of binocular alignment during conjugate eye movements. We postulate that the slow temporal dynamics of vergence eye movements relative to the faster dynamics of conjugate eye movements underlies the loss of alignment during targeted eye movements. Exotropia is the final outcome for numerous congenital and acquired abnormalities of the extended vergence pathway.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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