Fixing amblyopia before six
The final result after 6 months to 2 years Patching is
certainly an improved function in the majority of cases. However, when the
patch is removed, the two eyes often do not work as they should, 3D vision is
often not achieved and the other eye suppresses the amblyopic eye, eventually
leading to a reduction in visual acuity.
More importantly, there is only a limited time window in
which patching therapy works. Children are only patched up to the age of 12
years. Adults with amblyopia are not offered treatment.
The current treatment approach is based on the assumption
that amblyopia is the major problem and the loss of binocular function is the
secondary consequence.
The fact that reducing patch amblyopia does not automatically
result in improved use of the two eyes raises a question of validity.
There is reason to believe that the logic must be reversed,
namely that the main problem is that the two eyes either stop cooperating due
to an ocular misalignment or an out-of-focus eye, the secondary consequence
being amblyopia. The link between interrupted binocular vision and amblyopia is
oppression.
The outdated belief that lazy eyes need to be treated at a
very young age, or not at all, still exists today due to the following theories
and practices:
First, amblyopia develops only in childhood, usually before
the age of eight. Since amblyopia occurs in childhood, it has been assumed that
the disorder can only be treated in early childhood.
Second, laboratory studies in the 1960s on animals such as
cats and monkeys indicated that at the beginning of life there was a
"critical phase" in which the visual system developed. In the
studies, when one eye of an animal was occluded (covered) shortly after birth,
the two-eye visual system did not develop normally. That is, it was seen that
fewer neurons in the visual cortex of the animal's brain reacted to the eye,
which was occluded after removal of the cover. This lack of response in the
brain of the animal could be reversed in the study, but only if the subject's
occluded eye was uncovered or opened during the critically considered short
developmental period in infancy. These experimental results on animals were
then transferred to humans and it was assumed that amblyopia can only be reversed
if the patient was treated very early in life.
However, most children with amblyopia were not exposed to
the severe degree of visual impairment produced by these famous laboratory
experiments with cats and monkeys. The experimental animals were often freed on
the first days of life on an eye of vision. In contrast, most children with
sluggish eyes receive enough visual stimuli through their affected eye. In
these laboratory experiments, the most dramatic negative effects on normal
brain and visual development were observed when one eye of the animal was
occluded in the first weeks after birth. Animals that were later blinded in one
eye of vision showed fewer changes in "brain wiring" or neural
pathways. These laboratory tests are a good model for Deprivationsamblyopie as
z. B. occurs when a congenital cataract is present, which blocks the sight in
one or both eyes at birth. In these cases, early cataract removal surgery is
important to restore as much function as possible to the affected eye. However,
deprivation amblyopia occurs in only one in eighty (1 in 80) amblyopes. The
vast majority of amblyopes have strabismic or anisometropic amblyopia. These
conditions develop months or even years after birth. Therefore, the effects of
these conditions on the brain wiring may be much lower than those observed in
animal experiments. While early intervention is always best, numerous studies
have shown that visual improvement can still occur in older adults.
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