May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Infrared Autofluorescence Imaging in Inherited Macular Dystrophies
Author Affiliations & Notes
  • C.N. Keilhauer
    Department of Ophthalmology, University Würzburg, Würzburg, Germany
  • F.C. Delori
    Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA
  • Footnotes
    Commercial Relationships  C.N. Keilhauer, None; F.C. Delori, None.
  • Footnotes
    Support  NIH Grant EY08511 (FCD)
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 4045. doi:
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    • Get Citation

      C.N. Keilhauer, F.C. Delori; Infrared Autofluorescence Imaging in Inherited Macular Dystrophies . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4045.

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

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Purpose: : To determine the distribution of fundus infrared autofluorescence (AF) in patients with inherited macular dystrophies and compare it to the pattern of lipofuscin AF and color imaging.

Methods: : Twenty–five patients with inherited macular dystrophies were included in the study. These were Stargardt disease (n=10), Best disease (n= 8), and central areolar choroidal dystrophy (n=7; CACD). Infra–red AF–images, AF[Exc.: 787],were obtained with a standard HRA (Heidelberg Retinal Angiograph) using the same excitation wavelength (787 nm) and detection filter (>800 nm) as used for ICG angiography. For all subjects we also recorded lipofuscin AF images, AF[Exc.: 488], and digital color images.

Results: : The distribution of AF[787] does not generally correspond with the distribution of AF[488]. In early Stargardt disease, flecks that exhibited high AF[488] revealed high AF[787] particularly for isolated flecks at the periphery of the lesion. In more advanced disease, these flecks exhibited low AF[787] over an area that was typically larger than the focus of high AF[488]. Areas of atrophy exhibited low AF[787] and AF[488], but islands of brownish pigment often had high AF[787]. In Best disease, the lack of correspondence of AF[787] and AF[488]–distributions is particularly evident for the vitelliform lesion. AF[787] is low in areas of accumulations of yellow lipofuscin–like material (high AF[488]). However, high AF[787] corresponds with areas of brownish material in the color image. Early stages of CACD were characterized by diffusely increased AF[488] within a well delineated central area (oval–shaped) that is not seen by color imaging. AF[787] did not reveal the periphery of this lesion but showed areas of incipient atrophy (low AF) and foci of hyperpigmentation (high AF in both AF–modes).

Conclusions: : Different AF distributions observed in AF[787] suggest that a fluorophore different than lipofuscin is responsible for the AF under infra–red excitation. The fluorescence of RPE melanin and/or melanolipofuscin may account for the high AF[787] in early Stargardt flecks and in areas of brownish rather than yellow material in Best disease and CACD. Low AF[787] at high AF[488] flecks in Stargardt disease or yellow lesion in Best disease may point to loss of melanin in areas of high concentration of lipofuscin, as reported by histopathologic studies. Long time observations will be necessary to determine whether the change in AF distributions provides information about the turnover of specific fluorophores during progression of these conditions.

Keywords: imaging/image analysis: clinical • clinical research methodology • degenerations/dystrophies 

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