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Psychophysics H > abnormal visual development - Amblyopia > Flashcards

abnormal visual development - Amblyopia Flashcards

1
Q

when do post-natal/experiential causes to abnormal visual development such as amblyopia occur in life

A

during the critical period of early life

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2
Q

what does post-natal/experiential causes to abnormal visual development such as amblyopia disrupt

A

the promotional (stabilising) and refinement process

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3
Q

what type of visual development does someone with amblyopia have

A

arrested or altered/sub-optimal development

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4
Q

what is the likeliness of someone with amblyopia to have recovery from it

A

there is potential for partial recovery

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5
Q

what is the treatment for someone with amblyopia

A

visual stimulation-based cures e.g. patching

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6
Q

what is amblyopia a developmental disorder of

A

spatial vision

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7
Q

how many children are affected by amblyopia

A

common 2-3%

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8
Q

name three risk factors of having abnormal vision in one eye and state the only time that this can occur

A
  • strabismus/squint (eye misalignment)
  • form deprivation e.g. cataract (or any anterior eye disease)
  • anisometropia (refractive imbalance between the 2 eyes, usually ± 2D)

which only occurs during the critical period if the px is to get blunted vision, if these things occur after the critical period, then the px will have no blunted vision

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9
Q

at what age is the risk factors of having normal visual development (amblyopia) most susceptible and at which age does this start to decline

A

birth to 3 years of age = most susceptible

then declines until 7-8 years of age

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10
Q

what three things does the affected/amblyopic eye experience during blunted vision

A
  • reduced visual acuity and contrast sensitivity
  • (always) poor object and (sometimes) motion perception
  • (always) parvo and (sometimes) magno system deficits
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11
Q

where does the pathology of amblyopia occur and what does it result in with a person who has amblyopia

A

there is no pathology seen in the retina ,so is suppression in the visual cortex

  • reduced/loss of amblyopic eye activity in cortical visual system
  • the other good/fellow fixing eye dominates the person’s vision
  • so this causes binocular vision and depth perception to also be absent and reduced (i.e. no stereo acuity)
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12
Q

what is the probability of getting amblyopia if a 3 years old child has a risk factor

A

100% chance of getting amblyopia

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13
Q

what is the probability of getting amblyopia if someone has a risk factor later in life

A

they will not develop amblyopia if its past the critical period

and have a less likely chance than a 3 year old of developing amblyopia if they developed the risk factors later on in the critical period

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14
Q

what are the chances of someone developing amblyopia if they had VA deficits between 0-3 years old

A

100% chance of getting amblyopia

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15
Q

what are the chances of someone developing amblyopia if they had VA deficits at 8 years old

A

1% chance of getting amblyopia

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16
Q

what is the amblyopia ‘definition’ in terms of visual acuity

A

2 line difference in inter-ocular acuity affected verses good/fellow fixing eye (not absolute acuity deficit)

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17
Q

what is the difference in visual acuity between the amblyopic and fellow fixing eye in low spatial frequencies

A

no difference

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18
Q

what is the difference in visual acuity between the amblyopic and fellow fixing eye in high spatial frequencies (>6 cpd)

A

there is a loss of contrast sensitivity in the affected eye

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19
Q

which system has a deficit if there is only a difference in visual acuity between the amblyopic and fellow eye in high spatial frequencies only and no difference in low spatial frequencies

A

the parvo cellular system has a deficit only

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20
Q

what impact on contrast sensitivity will there be on the amblyopic eye if there was a deficit in BOTH the parvo and magno cellular systems

A

the contrast sensitivity will be affected/lower in the amblyopic eye compared to the fixing eye at ALL spatial frequencies

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21
Q

as well as a loss of visual acuity at higher spatial frequencies in an amblyopic patient, what else is less a loss of

A

loss of form/contour perception = defective form perception

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22
Q

what happens to an amblyopic patient as a result of them having defective form perception

A

they have a misperception of the spatial frequency of gratings when they are at higher spatial frequencies beyond 1-2 cpd, whereby there vision becomes impaired

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23
Q

what does an fMRI scan show in the primary visual cortex, of someone with an amblyopic eye due to a squint

A

in the fixing eye: v1 and v2 has lots of stimulation

in the amblyopic eye: v1 and v2 has no stimulation i.e. reduced activity

24
Q

what does a VEP recording show when you stimulate the good eye, with someone who has amblyopia

A

you get a good response from both sides of the brain (contralateral and ipsilateral channels)

25
Q

what does a VEP recording show especially with the p100 wave, when you stimulate the amblyopic eye and what does this implicate

A

you get a bad response from both sides of the brain (contralateral and ipsilateral channels), showing a reduced amplitude and longer latency responses of the p100 wave, even in the largest 80’ (>1 deg visual angle) check size

meaning the weak eye doesn’t stimulate the visual cortex, but the good eye does

26
Q

what is the aim or treating someone with amblyopia

A

to improve vision in the affected eye

27
Q

what is the first method of treating a child with amblyopia, and how is it done and what is it’s disadvantage

A

refractive adaptation

  • spectacle correction
  • can lead to very good improvement of visual acuity over a period of time
  • but doesn’t cure amblyopia, so must move onto stage two which is occlusion therapy
28
Q

describe how occlusion therapy works and what the outcome is on an amblyopic child

A
  • patch the good eye to make the lazy eye work
  • patching for 4-6 hours a day and often done for >1 years to get marked improvement in the affected eye
  • this stimulates the affected eye to relieve cortical suppression
  • the mean va recovery is 1 line for every 80-120 hours of patching (e.g. a month to get 1 snellen line)
29
Q

how can the amount of time that the patch has been used by the child be monitored

A

can be monitored via skin sensors on the patch/occluder

30
Q

what is a disadvantage to occlusion therapy used on children with amblyopia

A

compliance can be a big problem - as children dont like to wear the patch because they’re unable to see anything with the lazy eye, it can be uncomfortable and can experience bullying etc.
vision may also not fully recover i.e. binocularity and depth perception almost never fully recover. therefore patching doesn’t fully recover the co-operation between the two eyes

31
Q

when is treatment such as refractive adaptation and occlusion therapy most effective

A

during the critical period

32
Q

what visual problems can occlusion therapy ‘clinically cure’ i.e. is very successful with, on a child with severe strabismic amblyopia va ~ 6/60 in the amblyopic eye

A

contrast sensitivity and visual acuity with patching by 1 year later both eyes were equalised (this is quick because it was done in the critical period)

33
Q

up to what age can occlusion therapy cure contrast sensitivity and vision in the amblyopic eye

A

can extend well into adult life

34
Q

list the 4 things that improved when a 30 y/o amblyopic adult did the patching therapy for 16 weeks

A
  • crowded letter acuity
  • orientation discrimination
  • single letter acuity
  • vernier acuity
35
Q

what still did not improve after a 30 y/o amblyopic adult did the patching therapy for 16 weeks

A

binocular stereo vision, still did not change

36
Q

in an animal with normal visual development, how many v1 cells are present at birth that show orientation selectivity, and to which orientations are these preferences

A

33% OS cells at birth
90 % of these cells show preferences to horizontal or vertical lines, edges and contours, with very low preference to obliques
10% of these cells respond to contours of any orientation i.e. non-selective

they are hard wired to become orientation-selective due to innate process

37
Q

what does an animal who is given rich vision during their critical period acquire more of during this time

A

acquire more orientation selectivity with all possible orientation, represented equally by different cells

38
Q

what prevents the increase in orientation selective cells and preferences for obliques, in an animal during their critical period

A

total deprivation e.g. dark rearing
this prevents the cells from developing further so there are still 33% of OS cells, but the remaining 67% of OS cells never acquire orientation selectivity as they don’t see anything

39
Q

what alters the development of OS cells in an animal during their critical period and how is this done

A

restricted vision e.g. by stripe rearing
development is altered and cells do acquire orientation selectivity, but with most of the cells having a bias towards the line orientation that they have seen

40
Q

which two methods of restricted vision are there that can be carried out on an animal in their critical period

A
  • goggles: so only allow the animals to see vertical orientations in the world
  • kept in a bin with stripes for 3-4 hours a day and then kept in the dark for the rest of the day, so only allowing to see vertical lines
41
Q

what does exposure to a restricted environment restrict in an animal during their critical period

A

restricts the number of responses to which the cells are interested in

42
Q

at birth, how many v1 cells outside layer 4c are excited by both eyes in animals

A

33% i.e. are binocularly driven

other cells respond only to one eye i.e. monocularly driven

43
Q

how many cells acquire binocularity during the critical period in animals

A

80% (so more cells that at time of birth)

44
Q

what prevents the normal increase in the percentage of binocular cells in an animal

A

total deprivation e.g. dark-rearing ‘arrests’ the normal increase in percentage of binocular cells (so never get those extra binocular cells)

45
Q

what implications does altered vision e.g. by monocular deprivation or a squint have in the percentage of binocular cells in an animal

A

this devastates binocularity and ~90% of cells are instead driven by the open (seeing) eye in monocular deprivation or only by the fixing eye or squinting eye
depth perception is also permanently disrupted

46
Q

how many % of cells are activated by stimuli presented to both eyes

A

80%

47
Q

how many cells are activated by stimuli only presented to the L eye alone or R eye alone i.e. monocularly driven

A

10%

48
Q

what happens if both eyes are not being used together during the critical period and what consequences does this have

A

binocularly-driven cells are not generated and if that does happen then you lose binocularity and the fixing eye takes over the vision in the cortex

49
Q

how many % of cells are driven and from which eye, by a stimulus when the L eye is monocularly deprived e.g. stitched together

A

80-90% (most) of the cells in adult cat v1 cortex are driven by stimulus presented exclusively to the right eye and only a small % to the left eye and also a small % are activated by both eyes together

50
Q

how many cells are driven and from which eye, by a stimulus when the left eye has a squint and the right eye is the fixating eye

A

only a small % of cells is driven by both eyes and majority is activated by the fixing R eye and also a small % by the deviating L eye

51
Q

describe how a reverse suture procedure is done and what the outcome of this procedure is

A
  • monocular deprivation i.e. one eye is sutured close from birth up till 4 weeks after birth (still within the critical period)
  • open the originally deprived ‘amblyopic’ eye and close the originally open ‘fixing’ eye (similar to amblyopia treatment)

results after as little as 3-7 days:

  • the amblyopic and better eyes now activate equal number of v1 cells (equalisation, must patch good eye and make bad eye work to get the switch)
  • although binocularity still fails to improve
  • if you simply open the deprived/amblyopic eye without also closing i.e. patching the open/better eye, nothing will happen/there is no effect, the better eye will still be the dominating eye
52
Q

what is the outcome with a reverse suture procedure, if you open the deprived/amblyopic eye without patching the open/better eye

A

nothing will happen/there is no effect, the better eye will still be the dominating eye

53
Q

how is perceptual learning in children and adults with amblyopia done

A

it is done during patching therapy whereby the patients are asked to do near work/tasks in order to make the lazy eye work.
a patch is put over the good eye and the lazy eye is made to work hard by doing forced choice preferential looking tests
the stimulus can be manipulated to different spatial frequency gratings to get a staircase, and to improve the va’s

54
Q

how does perceptual learning in amblyopic patients carry out positive reinforcement in their tasks

A

the patient will get a tone when they get the preferential looking task right and nothing when they get it wrong, this gives them motivation and feedback which proves to show changes

55
Q

how is perceptual learning a better method of treating amblyopia than simply patching the good amblyopic eye alone

A

the results shows that va’s can become as good as 6/6 oe 0 LogMar by the end of the treatment, and the treatment is much quicker where by full improvements can be achieved in a matter of weeks, compared to patching with can take months/> 1 year

56
Q

what is the disadvantage to perceptual learning techniques in curing amblyopia

A

the neural correlations of visual recovery after perceptual learning in amblyopia shows that the neural activities aren’t really showing much change in before and after therapy in fMRI, therefore it is a useless study

Psychophysics H (11 decks)

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