September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Slow Changes in Strabismus: Clinical Observations and Theoretic Mechanisms
Author Affiliations & Notes
  • David L Guyton
    Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Footnotes
    Commercial Relationships   David Guyton, None
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Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      David L Guyton; Slow Changes in Strabismus: Clinical Observations and Theoretic Mechanisms. Invest. Ophthalmol. Vis. Sci. 2016;57(12):No Pagination Specified.

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      © ARVO (1962-2015); The Authors (2016-present)

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Presentation Description : Increased stimulation of skeletal muscle leads to the loss of sarcomeres, shortening the muscle, and decreased stimulation leads to a gain of sarcomeres if the muscle is under stretch, lengthening the muscle. The level of muscle stimulation thus plays a key role in the normal process of muscle length adaptation throughout life, adapting the muscle length for optimal function over its range of action. But for the exraocular muscles, which type of stimulation is involved - version stimulation, vergence stimulation, or both?
Fast fusional vergence (binocular fusion) leads to vergence adaptation which regulates the level of vergence tonus. Accumulating observations suggest that it is specifically the level of vergence tonus that normally provides the feedback stimulus for the regulation of extraocular muscle length. But if binocular fusion is faulty or absent, vergence tonus is unguided and if non-zero can drive the eyes into inceasing misalignment over time.
Patients with long-standing unilateral strabismus, such as esotropia with unilateral amblyopia, or "sensory" exotropia with a poorly seeing eye, typically show bilateral deviations under anesthesia, usually symmetric. Forced ductions show symmetric muscle tightness. Abnormal extraocular muscle lengths thus appear to develop bilaterally, driven by unguided vergence tonus.
The convergence occurring with uncorrected refractive esotropia typically leads to an increasing element of "basic" esotropia no longer correctable by glasses. In presbyopes, uncompensated accommodative demand can lead to increased activation of the near triad, with the increased convergence tonus leading to recurrence of previous esotropia or to the development of divergence insufficiency from shortened medial rectus muscles.
In theory, excess cyclovertical vergence tonus can lead to the clinical picture of "congenital superior oblique palsy,” which in many cases is probably nothing more than a primary cyclovertical deviation of the eyes, representing a true fourth cranial nerve palsy no more frequently than esotropia represents a true sixth cranial nerve palsy.
Better knowledge of the normal control mechanisms involving disparity feedback, vergence tonus, and muscle length adaptation will be critical in our understanding of the causes of strabismus and its evolution over time.

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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