Ординатура / Офтальмология / Английские материалы / Atlas of Fundus Autofluorescence Imaging_Holz, Schmitz-Valckenberg, Spaide, Bird_2007

192 Samantha S. Dandekar, Alan C. Bird

Fig. 14.4  Colour, fluorescein angiogram, and fundus autofluorescence (FAF) images of two eyes with classic choroidal neovascularization (CNV). Left column: Predominantly classic CNV lesion with near “normal” or background FAF signal, implying preserved retinal pigment epithelium (RPE) function. This lesion does not show a surrounding area of increased FAF. Right column: Classic lesion with some increased FAF signal towards the edge of the lesion. This may also represent proliferation of RPE cells. Images courtesy of V. Vaclavik

194 Samantha S. Dandekar, Alan C. Bird

Fig. 14.5  Colour, fluorescein angiogram, and fundus autofluorescence (FAF) images of two eyes with occult choroidal neovascularization (CNV). Left column: Occult CNV lesion with a heterogeneous appearance on the FAF image. Right column: Occult lesion with areas of decreased signal corresponding to blood and possibly to areas of retinal pigment epithelium loss (temporal part)

196 Samantha S. Dandekar, Alan C. Bird

Fig. 14.6  Retinal pigment epithelium tear following development of choroidal neovascularization secondary to age-related macular degeneration, illustrated by fundus photograph, fundus autofluorescence image, and fluorescein angiogram (early and late phases)

200 Peter Charbel Issa et al.

matic capillary changes are accompanied by a cystic macular edema with exudation (Fig. 15.1a, b). FAF imaging may show an increased signal that may be explained by a reduced MPOD due to retinal tissue defects in the area with cystoid changes (Fig. 15.1c,d,f). However, overall the distribution is normal, with the highest MPOD in the fovea and attenuation towards the periphery.

15.3

FAF in Type 2 Idiopathic Macular Telangiectasia

Type 2 IMT is the most common form of IMT and occurs without obvious gender predilection. It typically becomes symptomatic in the 5th or 6th decade of life. Be­ cause of a cumulated occurrence within families and monozygotic twins, a genetic background has been suggested [1].

The major vascular abnormality appears to mainly affect the deep parafoveal cap­ illary network. Early-phase fluorescein angiography reveals ectatic-appearing para­ foveal capillaries (Fig. 15.2a). A diffuse parafoveal hyperfluorescence is seen in latephase fluorescein angiography, predominantly located in the deep neurosensory retina and/or subretinal space (Fig. 15.2b). There is no accompanying cystoid edema but rather an atrophic neurosensory retina. Ophthalmoscopically, superficial crystalline deposits and, in later stages, intraretinal pigment clumping may occur (Fig. 15.2c). Funduscopically, a characteristic parafoveal loss of retinal transparency (“retinal greying”) may be observed (Fig. 15.2c). Moreover, there is an increased reflectance in confocal blue reflectance imaging within the area of retinal greying (Fig. 15.2d).

MPOD is typically reduced in the macular area (Fig. 15.2f), and the area of deple­ tion largely corresponds to angiographic late-phase hyperfluorescence (Fig. 15.2b) and increased confocal blue reflectance (Fig. 15.2d). Possibly, the latter is a secondary phe­ nomenon to the decreased macular pigment. FAF may be only minimally altered in very early disease stages (Fig. 15.3b). However, in later disease stages the FAF signal is typically grossly abnormal. (Fig. 15.3d, f). When intraretinal pigment clumping has oc­ curred, FAF may show a reduced signal due to a blockade phenomenon (Fig. 15.2e).

References

1.Charbel Issa P, Scholl HPN, Helb HM, et al. (2007) Macular telangiectasia. In: Holz FG, Spaide RF (eds). Medical retina. Springer, Heidelberg, 183–197

2.Gass JD, Blodi BA (1993) Idiopathic juxtafoveolar retinal telangiectasis. Update of classifica­ tion and follow-up study. Ophthalmology 100:1536–1546

3.Helb HM, Charbel Issa P, Pauleikhoff D, Scholl HPN, Holz FG (2006) Macular pigment density and distribution in patients with macular telangiectasia. Invest Ophthalmol Vis Sci:#5701/B795 [ARVO abstract]

4.Yannuzzi LA, Bardal AM, Freund KB, et al. (2006) Idiopathic macular telangiectasia. Arch Ophthalmol 124:450-460

202 Peter Charbel Issa et al.

Fig. 15.1  a,b Earlyand late-phase fluorescein angiogram of an eye with type 1 idiopathic macular telangiectasia (IMT). The funduscopically visible aneurysms show a marked leakage. Late-phase leakage fills a large foveal cyst. c,d Fundus autofluorescence image at excitation wavelengths of 488 nm (c) and 514 nm (d). The increased signal in the area of the cystoid foveal changes might be explained by the lack of macular pigment (f). e,f Macular pigment optical density distribu­ tion in the healthy right eye (e) and in the left eye with type 1 IMT (f)

Fig. 15.2  Earlyand late-phase fluorescein angiography, colour fundus photo­ graph, confocal blue reflectance image, fundus autofluorescence (FAF) image, and macular pigment optical density in an eye with a late disease stage of type 2 idiopathic macular telangiectasia. There is an increased signal in FAF imaging in proximity to the intraretinal pigment clumping temporal to the fovea (e). The lack of macular pigment (f) is topographically related to the diffuse hyper­ fluorescence in late-phase fluorescein angiography (b), to the parafoveal loss of transparency (c), and to the increased parafoveal confocal blue reflectance (d)