April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Sporadic Case of Congenital Fibrosis of the Extraocular Muscles
Author Affiliations & Notes
  • Zahra K. Ali
    Department of Ophthalmology,
    University of Texas Southwestern Medical Center, Dallas, Texas
  • Xin Gong
    University of Texas Southwestern Medical Center, Dallas, Texas
  • Juan Pascual
    Departments of Neurology, Physiology and Pediatrics,
    University of Texas Southwestern Medical Center, Dallas, Texas
  • Vinod V. Mootha
    Department of Ophthalmology,
    University of Texas Southwestern Medical Center, Dallas, Texas
  • Footnotes
    Commercial Relationships  Zahra K. Ali, None; Xin Gong, None; Juan Pascual, None; Vinod V. Mootha, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2394. doi:
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    • Get Citation

      Zahra K. Ali, Xin Gong, Juan Pascual, Vinod V. Mootha; Sporadic Case of Congenital Fibrosis of the Extraocular Muscles. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2394.

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Abstract

Purpose: : To describe the clinical phenotype of a sporadic case of congenital fibrosis of the extraocular muscles (CFEOM) and present genotyping results.

Methods: : Pt LJ underwent thorough ophthalmologic and pediatric neurological evaluations. Karyotype analysis was undertaken. MRI with DTI (diffusion tensor imaging) analysis was performed. She underwent comparative genomic hybridization (CGH) to detect gains or losses at the TUBB3 locus on chromosome 16q24.3, known to be associated CFEOM type 3. Samples of blood were obtained for resequencing of candidate gene TUBB3 exons for detection of a de-novo variant. Samples will also be analyzed for KIF21A mutations on chromosome 12q12, known to be associated with CFEOM type 1.

Results: : LJ presented with ptosis, lagophthalmos, hypotropia, complete restrictive paralysis of all extraocular muscles, minimally reactive pupils, amblyopia, decreased lower facial nerve function, normal CN V function, minimal microcephaly, and developmental delay. MRI with DTI analysis was normal, suggesting no myelin configuration abnormalities. Karyotype analysis was normal. CGH performed showed no gains or losses at the TUBB3 locus. DNA analysis showed copy number changes of no currently known significance, including copy gains at 2q24.3, 14q32.33, and 16p12.1, and two copy losses at Xp22.33. TUBB3 exon resequencing results and KIF21A mutation analyses are to be presented once finalized.

Conclusions: : Patient LJ presents to our clinic with features of CFEOM types 1, 2, and 3, but most consistent with CFEOM3. Normal brain imaging is compatible with the CFEOM phenotype. CGH revealed no structural variation in the vicinity of the TUBB3 locus.

Keywords: extraocular muscles: development • gene mapping • gene microarray 
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