6 Diagnostic Capability of Optical Coherence Tomography …
149
6.3.3 Amblyopia
Amblyopia remains an important cause of low visual acuity, affecting 2–6% of
the general population [154–157]. Unilateral amblyopia is defined as reduced bestcorrected visual acuity (BCVA) secondary to an abnormal visual experience during
the critical period of visual development. Classic causes include strabismus, anisometropia, form deprivation or a combination of these factors [158].
The neural sites that are influenced by visual deprivation are still under investigation. Nevertheless, it has been reported by several studies in humans [159, 160]
and also in animal species [160–164] that visual deprivation has an effect on the cell
growth in the lateral geniculate body that receives input from the amblyopic eye and
on the shift in the dominance pattern in the visual cortex [165], Banko et al. revealed
that latencies of the event-related potential components increased and were more
variable in the amblyopic eye compared to the fellow eye, although the initial neural
site of the visual deficit in this condition is still under investigation [166].
Evidences for direct retinal changes in amblyopic eyes are still inconclusive and
controversial [167–169], although electroretinograms elicited by patterned stimuli in
humans with various types of amblyopia were found to be significantly reduced [170,
171]. Studies using OCT imaging of the retina have produced discordant results, some
investigators have found an increased circumpapillary RNFL(cpRNFL) [172–174]
or/and macular thickness [172, 174–178] in amblyopic eyes, whereas others have
found no significant differences between amblyopic and healthy eyes [179–184].
Amblyopia occurs during the period when the neuronal network between the retina
and the cerebral cortex is developing and maturing. The neural sites that are influenced
by visual deprivation are still under investigation. However, some animal studies
demonstrated abnormal findings in retinal microstructures, including degeneration
of retinal ganglion cells [158, 185], decreased nucleolar volume and cytoplasmic
cross-sectional area of retinal ganglion cells [168], an increased number of amacrine
synapses in the IPL [186, 187], a reduction in the number of bipolar synapses in the
IPL [186], thinning of the IPL [168, 188], and a decrease in the density of Müller
fibres [188].
Evidence for direct retinal changes in amblyopic eyes remain inconclusive and
controversial. Yen et al. hypothesized that amblyopia may affect the postnatal maturation of the retina, including the postnatal reduction of retinal ganglion cells, which
would lead to a measurable increase in the thickness of the RNFL in amblyopic eyes
[173]. If this indeed occur, it is likely that the arrest of normal postnatal changes would
result not only in increased RNFL thickness but also would affect the normal maturation of the macula, including movement of Henle’s fibers away from the foveola and
a decrease in foveal cone diameter, and would result in increased foveal thickness
[173]. According to this assumption and the above-mentioned animal studies we
could reasonably hypothesize that some anatomic rearrangement could be present in
the retina.
A small number of previous studies that aimed the assessment of retinal structural
changes in amblyopia has been reported. Enoch were the first of many authors to sug-
149
6.3.3 Amblyopia
Amblyopia remains an important cause of low visual acuity, affecting 2–6% of
the general population [154–157]. Unilateral amblyopia is defined as reduced bestcorrected visual acuity (BCVA) secondary to an abnormal visual experience during
the critical period of visual development. Classic causes include strabismus, anisometropia, form deprivation or a combination of these factors [158].
The neural sites that are influenced by visual deprivation are still under investigation. Nevertheless, it has been reported by several studies in humans [159, 160]
and also in animal species [160–164] that visual deprivation has an effect on the cell
growth in the lateral geniculate body that receives input from the amblyopic eye and
on the shift in the dominance pattern in the visual cortex [165], Banko et al. revealed
that latencies of the event-related potential components increased and were more
variable in the amblyopic eye compared to the fellow eye, although the initial neural
site of the visual deficit in this condition is still under investigation [166].
Evidences for direct retinal changes in amblyopic eyes are still inconclusive and
controversial [167–169], although electroretinograms elicited by patterned stimuli in
humans with various types of amblyopia were found to be significantly reduced [170,
171]. Studies using OCT imaging of the retina have produced discordant results, some
investigators have found an increased circumpapillary RNFL(cpRNFL) [172–174]
or/and macular thickness [172, 174–178] in amblyopic eyes, whereas others have
found no significant differences between amblyopic and healthy eyes [179–184].
Amblyopia occurs during the period when the neuronal network between the retina
and the cerebral cortex is developing and maturing. The neural sites that are influenced
by visual deprivation are still under investigation. However, some animal studies
demonstrated abnormal findings in retinal microstructures, including degeneration
of retinal ganglion cells [158, 185], decreased nucleolar volume and cytoplasmic
cross-sectional area of retinal ganglion cells [168], an increased number of amacrine
synapses in the IPL [186, 187], a reduction in the number of bipolar synapses in the
IPL [186], thinning of the IPL [168, 188], and a decrease in the density of Müller
fibres [188].
Evidence for direct retinal changes in amblyopic eyes remain inconclusive and
controversial. Yen et al. hypothesized that amblyopia may affect the postnatal maturation of the retina, including the postnatal reduction of retinal ganglion cells, which
would lead to a measurable increase in the thickness of the RNFL in amblyopic eyes
[173]. If this indeed occur, it is likely that the arrest of normal postnatal changes would
result not only in increased RNFL thickness but also would affect the normal maturation of the macula, including movement of Henle’s fibers away from the foveola and
a decrease in foveal cone diameter, and would result in increased foveal thickness
[173]. According to this assumption and the above-mentioned animal studies we
could reasonably hypothesize that some anatomic rearrangement could be present in
the retina.
A small number of previous studies that aimed the assessment of retinal structural
changes in amblyopia has been reported. Enoch were the first of many authors to sug-