December 2012
Volume 12, Issue 14
Free
OSA Fall Vision Meeting Abstract  |   December 2012
Mechanisms underlying the etiology and treatment of Convergence Insufficiency
Author Affiliations
  • William Bobier
    School of Optometry, University of Waterloo, Waterloo, ON, Canada
  • Vidhyapriya Sreenivasan
    School of Optometry, Indiana University, Bloomington, Indiana, USA
Journal of Vision December 2012, Vol.12, 35. doi:10.1167/12.14.35
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to Subscribers Only
      Sign In or Create an Account ×
    • Get Citation

      William Bobier, Vidhyapriya Sreenivasan; Mechanisms underlying the etiology and treatment of Convergence Insufficiency. Journal of Vision 2012;12(14):35. doi: 10.1167/12.14.35.

      Download citation file:


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

      ×
  • Supplements
Abstract

Introduction: Developmental anomalies that arise within the cross-linkages between ocular vergence and accommodation such as convergence insufficiency (CI) are associated with complaints of blur and diplopia. We hypothesize that reduced vergence adaptation (VAdapt) found in CI[1,2,3] leads to an excess of convergence driven accommodation (CA). Further, the observed improvement in (VAdapt) following "vision training" (VT)[4,5] leads to an improved control of CA output. Method: Nine participants (X=17.4±2.3 yrs ) recruited from an eye clinic, met CI criteria (reduced prism acceptance based on established norms and/or Sheard's criterion). The asymptotic reduction in phoria (while viewing through 12? base out at 40cm taken in 3 min intervals over 15 minutes) defined VAdapt. Concurrent measures of CA were obtained using the MCS PowerRefractor, while the subject viewed a 0.2-cpd DOG target. VT was prescribed for a 12 week period with weekly clinical checks . CA and VAdapt measures were repeated at 5 and 12 weeks. Six CI participants completed. Six controls were recruited. Results: CI's showed a significantly less VAdapt and higher CA output (P=0.014 and 0.017 respectively) compared with controls. After 12 weeks of VT (but not 5 weeks) this difference disappeared (P>0.05). Clinical findings normalized after 5 weeks but symptoms were not ameliorated until 12 weeks. Conclusion: Both hypotheses were retained. Reduced VAdapt in CI leads to excessive levels of CA. When VAdapt is enhanced with VT, excessive CA is normalized. Symptom relief was linked more with VAdapt and CA correction than with normalized clinical findings.

Meeting abstract presented at OSA Fall Vision 2012

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×