Amblyopia Flashcards
what is Strabismic amblomyopia?
Eye misalignment. when you’ve got the
two eyes out of alignment.
This causes some issues from the brain perspective because our
eyes share a common visual direction.
So our eyes, when they’re both pointing straight ahead when
we’re actually looking at something, we’re fixating on something.
The image images for each eye will fall on the
phobia of each eye.
And as far as the brain is concerned, the phobia
represents straight ahead. Causes double vision
Mono-ocular deprivation
Strabismic = Eye misalignment
Anisometropic = Image aneisokonia
stimulus deprivaiton
Anisometropic
Image aneisokonia. you have a difference in
the glasses prescription between the two eyes.
So you’ve got one eye that may be relatively more
plus or minus than the other.
And so you know, there’s obviously asymmetrical levels of image
blur between the two eyes.
stimulus deprivation amblyopia.
So you can have as a child, you can have
like, a droopy lid, or you can have, um, a
cataract in one eye and not the other.
Um, anything that stops the light from getting to the
back of the eye can also cause amblyopia.
Um, so you know those are examples of what
we call monocular amblyopia.
OK, so it only affects one eye and not the
other well,
bin-ocular types of amblyopia?
So another big angiogenic risk factor is refractive error.
So any kind of glasses prescription, if it’s big enough,
can actually cause that underdevelopment of the connections between the eye and the brain.
So if you have binocular image blur, then you can
actually get a form of amblyopia that affects both eyes.
The connect between the eye and the brain are just
not that well developed because you don’t have a very
good quality visual image.
Spatial frequency
visual acuity
Vernier acuity
Vernier acuity, which is where you
show somebody a line in relation to another line, and
you ask them to figure out whether the line is
in alignment or not.
Is it in line, or is it out of line
and if so, which direction?
How is contrast sensitivity affected?
For strabismic amblyopia, there is a drop off in contrast sensitivity deficit. There is a higher spatial frequency deficit. But for Ansiometropic amblyopia
and stimulus deprivation
amblyopia, it’s actually any spatial frequency that you get that
change.
there is that drop off for any spatial frequency.
How are vernier and grating acuities affected?
Both are impacted and decrease.
what is the main aspect of ablomyopia?
binocular vision is one of the primary mechanisms of
amblyopia
what do characterisitcs of different types of amblyopia show as evidence?
Limited differences within groups of amblyopia.
Early evidence for the role of decorrelated Binoocular vision.
Diff btw strasbic amblomyopia and Anisometropic amblomyopia?
But the actual main difference between these two groups is
that the strasbics , the ones with the eye misalignment, don’t
have as much impaired contrast sensitivity Ihowever impaired visual acuity) compared to the asinometropes and other non strasbics that aren’t associated with that eye misalignment.
So that’s pretty interesting. So you’ve got a bit of a dichotomy here.
Treatment affects what aspects of amblomyopia? What things does it not treat soemtimes?
when we treat amblyopia, we address the
local deficits, the primary contrast sensitivity and visual acuity deficit.
OK, those things get better when you treat amblyopia.
But actually we have deficits in other areas (global) in amblyopia
as well. Such as
Motion processing
Form processing
Veridical perception
Stereopsis
How do global defects result?
Local’ deficits cascade to affect processing in
extrastriate visual cortex, but improving high contrast visual acuity does not always translate into complete resolution of ‘global’ deficits in motion processing, Form processing, Veridical perception, Stereopsis
What are the cortical changes in response to amblomyopia?
we get cortical changes **( V2 AND V3) **in relation to
the areas that are responsible for disparity detection.
And disparity is one of our crucial, um, mechanisms for
stereopsis. lOSS OF STRIPES IN VISUAL CORTEX
What is the relationship between behavioural and
Behavioural losses exceeds that explained by physiological changes in numbers of visual cortical cells driven by the deprived eye, i.e. cortical neurons driven by amblyopic eye responded to Contrast Sensitivity and Spatial Frequencies not detected psychophysically.
In severe amblomyopia what changes occur to eye dominance?
Number of cortical cells driven by one eye.
There is profound bias btw the two eyes. But in less severe amblomyopia there may be less significant skews. So the cases that had the most significant loss of input of amblyomyopic eye to cortex.
Strasbics skew wasn’t so significant.
how do underactivation of straite cortex impact extrastriatal cortices?
Underactivation of striate cortex seems to be correlated with underactivation in extra-striatal cortices as well.
Can contrast senstivity deficits predict whats happening?
We’ve got this V 1 activation deficit, which then correlates
quite nicely with the extra striate deficits.
But actually, the contrast sensitivity deficit alone is not enough
to actually predict what’s going on with that
2 theories that explain amblomyopia?
Neural disarray
-Mislabelled cortical projections
-Cell responding to stimulation in one area of visual space -> retinotopic representation of different, nearby area of space
-Fundamental distortion positional
**Undersampling **
- receptive field size/spacing in central field = normal peripheral retina
- Increased positional uncertainty/distortion, temporal instabilities
What is a limitation of Levi’s theory?
because under sampling
is only really effective at explaining like a limited number
of types of amblyopia.
Um, because it doesn’t, it doesn’t really account for detection.
Um, deficits.
It’s literally only about that discrimination side of things.
How did Levi change his theory?
So later on, he was like, Oh, maybe instead of
it just being fundamental under sampling, maybe it’s more like
irregular sampling.
So you’ve still got this loss of cortical cells.
But it’s just that you’ve also got a little bit
of this, this disarray going on as well.
Which theories work?
- you can get both types of anomalous
processing in the same Amblyope - Neither theory completely explains the behavioural deficits
- May depend on Amblyopia type
What is the updated theory of these two ideas?
- demonstrated that both of these theories can come off
the same sampling framework. - Neural disarray= spatial disorder without a loss of samples = irregular sampling
- Main contributer but still only at high Spatial frequencies
- Undersampling = fewer samples within regular or irregular array
- *Limited contributor *and only at high SFs