April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
A New Clinical Sign in Parafoveal Telangiectasia
Author Affiliations & Notes
  • Avinash Pathengay
    Retina and Uveitis Services, L. V. Prasad Eye Institute, Vishakhapatnam, India
  • Animesh Jindal
    Retina and Uveitis Services, L. V. Prasad Eye Institute, Vishakhapatnam, India
  • Himadri Choudhury
    Retina and Uveitis Services, L. V. Prasad Eye Institute, Vishakhapatnam, India
  • Footnotes
    Commercial Relationships Avinash Pathengay, None; Animesh Jindal, None; Himadri Choudhury, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5949. doi:
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      Avinash Pathengay, Animesh Jindal, Himadri Choudhury; A New Clinical Sign in Parafoveal Telangiectasia. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5949.

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

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Abstract
 
Purpose
 

To describe a new clinical sign in parafoveal telangiectasia

 
Methods
 

Four patients with clinical features of parafoveal telangiectasia including parafoveal graying were examined and serial fundus photographs were taken at baseline and then every 5 seconds. After 30 - 40 seconds, dark adaptation was done for 15 mins and repeat fundus photograph was taken after dark adaptation.

 
Results
 

The intensity of parafoveal graying gradually decreased with continuous exposure to light and was evident on serial photographs. After 15 minutes of dark adaptation, the intensity of parafoveal graying returned to baseline intensity.

 
Conclusions
 

This phenomenon of change in the intensity of parafoveal graying with light has not been described before and points towards a possible photochemical reaction in the region of parafoveal graying. We hypothesize that because of disrupted Muller cells in parafoveal telangiectasia, this 11-cis retinoid chromophore, which are synthesized and stored in cone Muller cells, may be released into the surrounding tissue, causing graying and upon exposure to light, isomerize to all-trans form (which is not a chromophore) with resultant decrease in the intensity of graying. Further, during dark adaptation, the chromophores are regenerated and released again into the surrounding tissue, causing reappearance of parafoveal graying. Since only the cone Muller cells (concentrated in parafoveal area) are involved in visual pigment regeneration, this may also explain the typical parafoveal location of retinal graying observed in cases of PFT. This phenomenon of progressive decrease in the intensity of parafoveal graying on exposure to light and reappearance of graying after dark adaptation may be a new sign in PFT and may help in the better understanding of the disease pathophysiology.

 
 
Macular photographs of parafoveal graying of first patient taken at (a) baseline, (b) 15 seconds and (c) 30 seconds of light exposure. The progressive decrease in the intensity of parafoveal graying is evident. (d) Photograph taken after 15 minutes of dark adaptation documenting return of parafoveal graying. The difference is most marked between photograph (c) and (d) that is before and after dark adaptation.
 
Macular photographs of parafoveal graying of first patient taken at (a) baseline, (b) 15 seconds and (c) 30 seconds of light exposure. The progressive decrease in the intensity of parafoveal graying is evident. (d) Photograph taken after 15 minutes of dark adaptation documenting return of parafoveal graying. The difference is most marked between photograph (c) and (d) that is before and after dark adaptation.
 
 
Macular photographs of parafoveal graying of second patient taken at (a) baseline, (b) 15 seconds and (c) 30 seconds of light exposure. (d) Photograph taken after 15 minutes of dark adaptation.
 
Macular photographs of parafoveal graying of second patient taken at (a) baseline, (b) 15 seconds and (c) 30 seconds of light exposure. (d) Photograph taken after 15 minutes of dark adaptation.
 
Keywords: 585 macula/fovea • 603 Muller cells  
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