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Vision > Amblyopia > Flashcards

Amblyopia Flashcards

1
Q

What is amblyopia 2?

A

Reduced vision in one (usually) or both eyes because the brain and eye are not working together properly but there is no obvious eye pathology
Definition varies b/w paper but some say that it is when there is an interocular acuity difference of two lines or more

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2
Q

Prevalence of amblyopia 2

A
  • 2-3% of ppn

- Higher in underdeveloped and lower in developed

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3
Q

Draw the classical and current model of amblyopia aetiology by Barrett 2004

A

MD –> contrast deprivation
Aniso –> high sf astigmatism
Strab –> suppression
–> amblyopia

Monkey: 
MD > Aniso <> Strab <> 
Human:
MD> Aniso < Strab <>
- Strab>Aniso
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4
Q

Explain 5 possible amblyogenic factors

A
  1. strabismus: 4% - strabismus aims to suppress diplopia
  2. Anisometropia: anisometropic amblyopia
    - The more hyperopic eye is usually the more amblyopic eye
    - Historic theory: uncorrected anisometropia –> loss of high sf and preserved low sf –> amblyopia
    - Current theory: amblyopia –> strabismus and diplopia –> anisometropia
  3. High astigmatism: meridional amblyopia
  4. Isoametropia: high uncorrected RE in both eyes
  5. Deprivation amblyopia
    - From cataract, ptosis, occlusion
    - Evidence from Hubel and Wiesel 1965: monocular deprivation in cat studies - after 3hrs of patching, ocular dominance columns changed ie only the ipsilateral cells persist –> change in RE
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5
Q

When does stereopsis start and end?

A

Onset is 3-5months, ends at 8 years but can range from 6-11yrs depending on person

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6
Q

Relationship between CP and amblyopia

A
  • CP duration depends on different species with different visual systems
  • During CP, inadequate stimulation from both eyes leads to decreased strengthening of synapses from Hebb’s theory –> amblyopia
  • CP decreases with increasing age
  • Amblyopia treatments aim to fix this but it is more difficult post-CP
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7
Q

Prior theory about the deficit in visual pathway leading to amblyopia

A

Initially thought to be at level V1 but effect occurred across entire brain so deficit must have happened earlier on

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8
Q

Evidence for deficit at photoreceptor

A

Unimpaired across different monochromatic light

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9
Q

Evidence for deficit at retina 2

A

Tgcu 2013

  • OCT to look at RNFL, macula and fovea thickness
  • High hyperopes had thicker layers as more squished and high myopes had thinner
  • Concluded that it is not the site

Szigeti 2014

  • OCT to find outer nuclear layer thicker in amblyopes perhaps due to retrograde degeneration from higher cortical areas
  • Flawed as used fellow eye as the control
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10
Q

Evidence for deficit at ON and OT

A

Allen 2018

  • Used MRI tractography to observe connections and density of optic pathways from retina
  • ON and OT showed different densities between normal and anisometropic pxs
  • Fractional anisotropy FA: larger values indicate greater fibre density and WM integrity
  • Mean diffusivity (MD - white matter): larger values indicate greater diffusivity, perhaps due to less impedance or lower tissue density
  • Larger FA and smaller MD is typical of normal ONs
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11
Q

Evidence for deficit at LGN: method 2, result 4, significance 1

A

Hess 2019

  • high field fMRI
  • observed blood flow at LGN between amblyopic and fellow eye
  • reduced blood flow to LGN when amblyopic eye was stimulated
  • ipsilateral layers 2,3,5 had less to none cells on histological slides
  • possible that deficit is feedback rather than feedforward from the retina
  • models need to be changed with this new knowledge
  • LGN receives 6-18% of input from retina and rest is from other cortical areas meaning that deficit may be elsewhere as well
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12
Q

Evidence for deficit at primary visual cortex: result 2, significance 1

A

Changes in ocular dominance columns probably caused a decrease in activation from a decrease in WM density at V1

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13
Q

Evidence for deficit at ocular dominance columns

  • Exp 1: method 1, result 2, flaw 1
  • Exp 2: method 1, result 1
A

Hubel and Wiesel 1965

  • Sutured kitten eyes from 8-10 days after birth and looked at changes in ODC
  • Change in ODC to dominant eye increases especially during the CP
  • Tested post CP and there was no change
  • F: CP of cats may be minimal

Anderson 2006

  • Observed maps of ODC
  • Confirmed that stimulation of the dominant eye showed active activity in the amblyopic eye in adults too
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14
Q

Evidence for deficit at extra striate areas 4

A

Barnes 2001

  • Looked at scans of LGN and V1,2,3,4 to observe the connections between these areas, not activity
  • Connectivity from LGN to V1 was reduced when amblyopic eye was stimulated during both feed forward and feed backward connections –> deficit in integration –> correlation to acuity loss
  • Deficits at lower areas must have had flow on effects to higher ordered areas
  • Size of rfs were larger –> coarser and lack of detail seen by amblyopes
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15
Q

Identify the 10 functional deficits in amblyopic eyes

A
  • Despite no evident eye abnormalities, vision is impaired from reduced signals from eye to brain in amblyopic eye
    1. reduced VA
    2. spatial deficits
    3. ocular motility
    4. suppression and attention
    5. motion
    6. stereopsis
    7. accommodation
    8. colour perception
    9. eye hand coordination
    10. contour integration
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16
Q
  • Reduced VA 1
A

not just blur as amblyopes can match blurred pictures to normal

17
Q
  • Spatial deficits 4
A
  1. poor acuity:
    - grating and vernier (requires a greater offset to notice a difference)
    - Anisometropic pxs have more errors than strabismic pxs
  2. contrast sensitivity
    - quicker high sf drop off - characteristic
    - strab - usually central loss
    - aniso - across entire VF
  3. visual crowding
    - initially thought that amblyopes could see what a normal would see at the periphery as the data plot was similar but was proven wrong
  4. distortions
    - classic symptom that is often complained of
    - wavy, abrupt offsets, misperceived orientations, fragmented, scotomatous, artificial jitter
18
Q
  • Ocular motility 2
A
  • unsteady fixation - eccentric, tended to drift radially

- increased saccadic latency

19
Q
  • Suppression and attention 4
A
  • Hou 2016 measured suppression via binocular rivalry (extent to which dominant eye suppresses image created by the amblyopic eye), attention modulation (degree in increase of neural activity when attention was directed. involved suppression of previously attended object) and amblyopia
  • strabismic pxs have an eye turn –> experience diplopia –> will suppress image
  • weaker amblyopic eye corresponded to stronger suppression
  • at v1, greater degree of amblyopia was correlated with weaker attentional modulation
20
Q
  • Motion 1
A

required greater coherence of moving objects to judge motion direction

21
Q
  • Stereopsis 1
A

monocular disruption has more affect than binocular

22
Q
  • Accommodation 3
A
  • decreased amplitude
  • increased lag
  • asymmetric accommodation
23
Q
  • Colour perception
A

Deprived

24
Q
  • Eye-hand coordination 3
A
  • Suttle 2011 measured localisation and grasping accuracy
  • amblyopic children were able to do the task but took longer and made more errors than age matched controls
  • errors due to absence or presence of stereopsis (having poor stereopsis was better than having none)
25
Q
  • Contour integration
A

found difficulty

26
Q

What are the 3 neural basis hypothesis for amblyopia?

A

Undersampling, neural scrambling and neural remapping

27
Q
  • Undersampling 3, 3
A

Levi 1999

  • may be due to underdeveloped, damaged or lack of high sf cells thus requires more stimulus elements visible for amblyopic eye to recognise the stimulus
  • foveal detection: requires 45-60% of the stimulus elements
  • peripheral detection: requires 50-80% increase in elements due to less ganglion cells and PRs

Hess and Field 1994

  • believed that undersampling could not account for distortion and spatial form but neural scrambling could
  • stimulus: vernier acuity test ie middle target offset left or right between 2 flanked targets and result gathered by calculating ratio
  • if undersampling then positional errors will be made from contrast discrimination
  • if neural scrambling then positional errors will be made from distorted targets
  • neural scrambling approved
28
Q
  • Neural scrambling 2
A
  • stimulus having a topographical jitter

- due to misalignment of cortical cells leading to distortions of VFs

29
Q
  • Neural remapping
A

like scrambling but there is order to the scrambling

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