Incomitant Strabismus

Kushner, Burton J.

doi:10.1001/archophthalmol.2010.301

Cited by 17 publications

(12 citation statements)

References 42 publications

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“…Insulin-like growth factor 1 is a major factor that regulates EOM contractile strength, as demonstrated by effects of endogenous IGF1 49 and of exogenous IGF1, 50 as well as the fact that exogenous IGF1 can induce strabismus. 51 Variability in expression levels of IGF1 in strabismic muscles likely reflects variability in causes and/or phases of strabismus, 12 or a mismatch between gene expression and protein levels. 31,52 …”

Section: Discussionmentioning

confidence: 99%

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Altered Protein Composition and Gene Expression in Strabismic Human Extraocular Muscles and Tendons

Agarwal

Feng

Altick

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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PurposeTo determine whether structural protein composition and expression of key regulatory genes are altered in strabismic human extraocular muscles.MethodsSamples from strabismic horizontal extraocular muscles were obtained during strabismus surgery and compared with normal muscles from organ donors. We used proteomics, standard and customized PCR arrays, and microarrays to identify changes in major structural proteins and changes in gene expression. We focused on muscle and connective tissue and its control by enzymes, growth factors, and cytokines.ResultsStrabismic muscles showed downregulation of myosins, tropomyosins, troponins, and titin. Expression of collagens and regulators of collagen synthesis and degradation, the collagenase matrix metalloproteinase (MMP)2 and its inhibitors, tissue inhibitor of metalloproteinase (TIMP)1 and TIMP2, was upregulated, along with tumor necrosis factor (TNF), TNF receptors, and connective tissue growth factor (CTGF), as well as proteoglycans. Growth factors controlling extracellular matrix (ECM) were also upregulated. Among 410 signaling genes examined by PCR arrays, molecules with downregulation in the strabismic phenotype included GDNF, NRG1, and PAX7; CTGF, CXCR4, NPY1R, TNF, NTRK1, and NTRK2 were upregulated. Signaling molecules known to control extraocular muscle plasticity were predominantly expressed in the tendon rather than the muscle component. The two horizontal muscles, medial and lateral rectus, displayed similar changes in protein and gene expression, and no obvious effect of age.ConclusionsQuantification of proteins and gene expression showed significant differences in the composition of extraocular muscles of strabismic patients with respect to important motor proteins, elements of the ECM, and connective tissue. Therefore, our study supports the emerging view that the molecular composition of strabismic muscles is substantially altered.

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Section: Discussionmentioning

confidence: 99%

“…Numerous attempts have been made to identify structural differences between normal and strabismic EOMs, at the level of histology 8–13 and at the ultrastructural level. 8,9,14–20 Unless specific molecules were probed, most abnormalities were subtle and to some extent also present in normal control tissues, or they could not be identified at all.…”

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confidence: 99%

Altered Protein Composition and Gene Expression in Strabismic Human Extraocular Muscles and Tendons

Agarwal

Feng

Altick

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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“…Magnetic resonance imaging (MRI), however, may be used to measure human extraocular muscle contractility, because, in part, a very close correlation exists between ocular duction angle and quantitative aspects of extraocular muscle morphology. 6,7 Although functional MRI cannot directly indicate extraocular muscle force, 8 the same criticism applies to recordings of extraocular muscle motor neurons, where a discrepancy between horizontal rectus muscle force and motor neuron firing during convergence has been reported. 9,10 The purpose of the present study was to obtain functional MRI data on the size and contractility of human horizontal rectus muscles in concomitant esotropia.…”

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confidence: 99%

Functional magnetic resonance imaging of horizontal rectus muscles in esotropia

Schoeff

Zia

Demer

2013

Journal of American Association for Pediatric Ophthalmology and

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PURPOSE Monkey neurophysiology suggests that changes in neural drive rather than extraocular muscle structure underlie sensory-induced strabismus. If this is true, then extraocular muscle structure should be normal. We used magnetic resonance imaging to measure horizontal rectus muscle size and contractility to determine whether muscle structure is a factor in human concomitant esotropia. METHODS High-resolution, quasicoronal plane magnetic resonance imaging was performed in target-controlled central gaze, abduction, and adduction in 13 orthotropic controls (mean age, 38 ± 19 years) and 12 adults (mean age, 52 ± 16 years) who had concomitant esotropia averaging 28Δ ± 18Δ at distance. Thyroid ophthalmopathy was excluded. Horizontal rectus muscle cross sections were determined in 6 contiguous, 2-mm-thick midorbital image planes. Contractility was computed in each plane as the difference in cross section from contraction to relaxation. RESULTS Medial rectus muscle cross sections in multiple planes averaged up to 39% larger in esotropic patients than in controls (P <0.005), whereas lateral rectus muscle cross sections in esotropia were up to 28% larger but only significantly larger in one plane (P <0.02). Medial rectus contractility was increased by up to 60% in esotropic patients (P <0.005), whereas lateral rectus contractility in esotropia was slightly but not significantly supernormal. CONCLUSIONS Medial rectus muscle size is supernormal and lateral rectus muscle size is not subnormal in concomitant esotropia. This finding indicates that human concomitant esotropia is associated with peripheral muscular abnormality.

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“…The term inferior oblique overaction to describe all cases of over elevation in adduction is in some cases misleading because it suggests that hypertrophy or hypercontractility causes the muscle to “overact.” However, superior oblique weakness, co-contraction of the horizontal rectus muscles (Duane syndrome), restriction of rectus muscles, aberrant innervation of the extraocular muscles, or anomalies in the insertion of other extraocular muscles may all result in overelevation in adduction. 3 27 In patients with craniosynostosis, excyclorotation of the globes and orbits alone may cause apparent overaction of the inferior oblique muscles because the medial rectus muscles elevate as well as adduct the globes. For these reasons, the term “overelevation in adduction” may be preferred.…”

Section: Indicationsmentioning

confidence: 99%