188
E. Gao et al.
It is well known that there are two sources of blood supply to the neurosensory
retina; the central retinal artery and the choroidal blood vessels, which supply the
inner and outer retina, respectively. There are two layers of capillary networks originating from the branches of the central retinal artery. The inner capillary network
lies within the GCL. The outer capillary network runs from the IPL to the OPL
through the INL [39]. The results showed that the optical intensities increased from
the GCL to the OPL in CRAO patients. This finding shows a local correspondence of
image intensity increases with layers supplied by the central retinal artery. On histology of a CRAO mouse model, pyknotic nuclei, vacuolated spaces, and degenerative
changes were noted in the GCL and INL [40]. In this study, the maximum increases
of optical intensity or optical intensity ratio were detected in the INL. Furthermore,
discriminant analysis found that the optical intensity of INL is the best indicator of
CRAO. Recently, it was reported that deep capillary ischemia frequently manifests
itself by increased optical intensities in the middle retinal layers, especially the INL
[41]. There is a large number of metabolically active cells in the INL and the INL
is surrounded by a deep capillary network branched from the central retinal artery
system and is therefore subject to ischemia.
Most impressively, the optical intensity of RNFL was not different between the
CRAO and control groups. The blood supply of RNFL is also provided from the
central retinal artery system. In a pathological study of human autopsy eyes with
CRAO, severe edema of the RNFL was frequently noted [42]. It is conceivable that
edema of RNFL does not affect its OCT optical intensity. The exact cellular and
molecular mechanism of change of optical intensity in CRAO remains unknown and
deserves further investigation. The ONL, photoreceptor, RPE and choroidal layers are
not supplied by the retinal artery and its branches. Animal and human autopsy studies
previously showed that the outer retina does not change in CRAO [40, 42]. Our results
found that the optical intensities in the outer retina from the photoreceptor layer to
the choroid were reduced in the acute CRAO phase, especially in the photoreceptor
and RPE layers. However, the optical intensities of the photoreceptor and RPE layers
are still high at the foveal region, where no layered inner retinal structure is present
(Fig. 7.9c–f.) On ophthalmoscopic examination, the whitish opacification of the
CRAO retina is caused by reduced transparence of the inner retina, and the cherry
red spot at the fovea is due to a relative transparency of the fovea devoid of the inner
retina layer tissue [43]. This evidence suggests that the reduction of optical intensities
in outer layers may be associated with a shadowing effect caused by increased optical
density in the inner retina as observed on CRAO patients.
In conclusion, the OCT optical intensity of inner retina increases in patients with
CRAO compared to normal controls, possibly due to layer-specific ischemia, while
the optical intensities of the outer retina and the choroid decrease, possibly due to a
shadowing effect associated with the inner retinal density increases.
E. Gao et al.
It is well known that there are two sources of blood supply to the neurosensory
retina; the central retinal artery and the choroidal blood vessels, which supply the
inner and outer retina, respectively. There are two layers of capillary networks originating from the branches of the central retinal artery. The inner capillary network
lies within the GCL. The outer capillary network runs from the IPL to the OPL
through the INL [39]. The results showed that the optical intensities increased from
the GCL to the OPL in CRAO patients. This finding shows a local correspondence of
image intensity increases with layers supplied by the central retinal artery. On histology of a CRAO mouse model, pyknotic nuclei, vacuolated spaces, and degenerative
changes were noted in the GCL and INL [40]. In this study, the maximum increases
of optical intensity or optical intensity ratio were detected in the INL. Furthermore,
discriminant analysis found that the optical intensity of INL is the best indicator of
CRAO. Recently, it was reported that deep capillary ischemia frequently manifests
itself by increased optical intensities in the middle retinal layers, especially the INL
[41]. There is a large number of metabolically active cells in the INL and the INL
is surrounded by a deep capillary network branched from the central retinal artery
system and is therefore subject to ischemia.
Most impressively, the optical intensity of RNFL was not different between the
CRAO and control groups. The blood supply of RNFL is also provided from the
central retinal artery system. In a pathological study of human autopsy eyes with
CRAO, severe edema of the RNFL was frequently noted [42]. It is conceivable that
edema of RNFL does not affect its OCT optical intensity. The exact cellular and
molecular mechanism of change of optical intensity in CRAO remains unknown and
deserves further investigation. The ONL, photoreceptor, RPE and choroidal layers are
not supplied by the retinal artery and its branches. Animal and human autopsy studies
previously showed that the outer retina does not change in CRAO [40, 42]. Our results
found that the optical intensities in the outer retina from the photoreceptor layer to
the choroid were reduced in the acute CRAO phase, especially in the photoreceptor
and RPE layers. However, the optical intensities of the photoreceptor and RPE layers
are still high at the foveal region, where no layered inner retinal structure is present
(Fig. 7.9c–f.) On ophthalmoscopic examination, the whitish opacification of the
CRAO retina is caused by reduced transparence of the inner retina, and the cherry
red spot at the fovea is due to a relative transparency of the fovea devoid of the inner
retina layer tissue [43]. This evidence suggests that the reduction of optical intensities
in outer layers may be associated with a shadowing effect caused by increased optical
density in the inner retina as observed on CRAO patients.
In conclusion, the OCT optical intensity of inner retina increases in patients with
CRAO compared to normal controls, possibly due to layer-specific ischemia, while
the optical intensities of the outer retina and the choroid decrease, possibly due to a
shadowing effect associated with the inner retinal density increases.