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Journal of Ophthalmology
Volume 2013, Article ID 301256, 6 pages
Review Article

Pattern Strabismus: Where Does the Brain's Role End and the Muscle's Begin?

1Cole Eye Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
2Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA

Received 15 March 2013; Accepted 6 June 2013

Academic Editor: Hazel I. Blythe

Copyright © 2013 Fatema F. Ghasia and Aasef G. Shaikh. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Vertically incomitant pattern strabismus comprises 50% of infantile horizontal strabismus. The oblique muscle dysfunction has been associated with pattern strabismus. High-resolution orbit imaging and contemporary neurophysiology studies in non-human primate models of strabismus have shed light into the mechanisms of pattern strabismus. In this review, we will examine our current understanding of etiologies of pattern strabismus. Speculated pathophysiology includes oblique muscle dysfunction, loss of fusion with altered recti muscle pull, displacements and instability in connective tissue pulleys of the recti muscles, vestibular hypofunction, and abnormal neural connections. Orbital mechanical factors, such as abnormal pulleys, were reported as a cause of pattern strabismus in patients with craniofacial anomalies, connective tissue disorders, and late-onset strabismus. In contrast, abnormal neural connections could be responsible for the development of a pattern in infantile-onset strabismus. Pattern strabismus is likely multifactorial. Understanding the mechanisms of pattern strabismus is pivotal to determine an appropriate surgical treatment strategy for these patients.