May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Inflection in the Inactive Lateral Rectus Muscle: Evidence for Pulleys Rather Than Fat as Determinants of Extraocular Muscle Paths
Author Affiliations & Notes
  • J. L. Demer
    David Geffen Sch of Medicine, Ophthalmology Dept., Jules Stein Eye Institute, UCLA, Los Angeles, California
  • Footnotes
    Commercial Relationships J.L. Demer, None.
  • Footnotes
    Support NIH Grant EY08313
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5625. doi:
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      J. L. Demer; Inflection in the Inactive Lateral Rectus Muscle: Evidence for Pulleys Rather Than Fat as Determinants of Extraocular Muscle Paths. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5625.

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

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We studied paths of paralyzed, atrophic lateral rectus (LR) muscles to investigate putative roles of orbital fat and intrinsic muscle stiffness suggested (Schutte et al, Vis Res 36:1724, 2006) to be alternatives to connective tissue pulleys as determinants of pulling direction.


7adults with chronic, unilateral LR paralysis, and 15 normal controls, underwent surface coil orbital magnetic resonance imaging in 2 mm thick axial planes. Fixation was controlled using targets, and ranged among subjects from 36º ad- to 29º abduction, with some subjects imaged in multiple gazes after vertical rectus transposition surgery. Images were analyzed quantitatively.


Paralyzed LRs exhibited marked atrophy in comparison with functional contralateral LRs and those of normal subjects. The normal LR exhibited a gradual 18.8±4.5º (mean±SD) lateral inflection 14.4±2.6 mm posterior to globe center, representing bowing of the LR away from the orbital center in a region of abundant orbital fat. The paralyzed LR exhibited a significantly (p<0.002) larger and more discrete 29.2±8.8º lateral inflection; this inflection was 13.2±4.0 mm posterior to globe center, similar to normal (p<0.3). While location of the normal lateral LR inflection was uncorrelated with horizontal gaze, the paralyzed LR inflection's location was 0.17 mm further posterior per degree abduction (linear fit R=0.85).


While not corresponding spatially to the more anterior inflection that occurs in secondary and tertiary gazes and underlies Listing's Law, the lateral inflection in the atrophic, paralyzed LR cannot be due to intrinsic muscle stiffness. Sharper and more discrete lateral inflection in the flaccid than tense LR suggests that the lateral inflection is due to discrete connective tissues. Connective tissue pulleys, 8 mm posterior to globe center, are located in a region focally dense with collagen and elastin, tissue but sparser in fat than the region of the lateral inflection. These observations are incompatible with diffuse pressure of orbital fat as the major determinant of rectus muscle paths or ocular kinematics.  

Keywords: extraocular muscles: structure • strabismus • eye movements 

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