BVP Flashcards

1
Q

Heterophoria definition, tests and Fusional reserve compensation

A

1) Eyes misaligned when one is covered or viewing different objects.
if decompensated then becomes a tropia.

2) CT, Maddox rod (Distance), Maddox wing (near)
3) How much fusion we have in reserve to compensate a heterophoria

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2
Q

Symptoms decompensated heterophoria,

vision problems, binocular problems, asthenopia problems

A

Sx - symptoms when using for prolonged time period

VISION PROBLEMS
Diplopia (after long periods) , blurred vision

BINOCULAR PROBLEMS
accom difficulties, stereopsis problems, monoc comfort

ASTHENOPIA
headaches -(x heterophoria frontal headaches, y heterophoria occipital headaches)
eye ache -(intense eye use)
soreness,
general irritation -(difficulty in maintaining BSV)

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3
Q

Order of correcting decompensated heterophoria

A

Sx, CT, Rx, FD, FR, Stereopsis, suppression

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4
Q

Fusional Reserves for heterophoria (Percivals and Sheards)

A

EXOP - investigate convergence with Base Out
ESOP - investigate convergence with Base In

Percival’s - convergent and divergent should have balanced FR.
Sheards’s - opposing fusional reserve should be twice the degree of phoria. Works well at distance aswel

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5
Q

Fixation Disparity (what is it?)

A

Both eyes correspond to the same points on the retina. (Panums). This allows eyes to deviate a small amount with BSV. FD is this small deviation.
Too small to detect with CT.

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6
Q

Mallett Unit disparity test for Fixation Disparity

A

corrected
1) unit held at reading distance and measure
2) px fixate on OXO
3) ask if strips in straight line
4) visor on and ask if strips still seen
5) if no, suppression, stop and record
if flashing, intermittent suppression.
both seen, proceed
6) px read 2-3 lines of text surrounding
7) ask if strips aligned. top strip LE, bottom strip RE. FLASHCARD 4
8) add min prism to realign markers (associated phoria).

Greater prism, worse sx
FD suggests decom heterophoria
if no sx, no need for treatment,
For others, can have prism in specs

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7
Q

Suppression Test - Mallett Unit

A

if BV understress, small parts of central field of one eye is inhibited by mismatched images. Compensatory mechanism to keep BSV.

Visor on and corrected, unit at 35cm

1) read letters from top to lowest line, record
2) occlude LE, some letters may change, record polarised letters seen by RE
3) swap eyes
4) abnormal if read one line further monocularly

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8
Q

Vertical heterophoria

A

VFR small, as little as 1D can be decomp

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9
Q

Order of correction for phoria

A
Remove cause of decompensation
Refractive correction
Orthoptic exercises
Prescribe prism relief
Refer to another practitioner
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10
Q

Removing cause of phoria

A

Less near screen work

Better illumination and contrast

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11
Q

EXOP, ESOP, -ve, +ve, Quantity of refractive correction?

Review time?

A

ESOP
+ve) Full plus, relax accom
-ve) Avoid over correction

EXOP
+ve) least plus (partial)
-ve) Min overcorrection which compensates

Review every 3- 4 months

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12
Q

Orthoptic exercises, who for?, what is it for? what information to give when prescribing

A

If rx doesnt fix sx, 12-35, px motivated

1) Develop FR and relative accom
2) train accom and convergence
3) develop appreciation of physiological diplopia
4) treatment of suppression

written instruction, 15 mins everyday, px must relax eyes after by looking far for 10 mins, monitored 3/4 weeks, sx may worsen initially

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13
Q

Prism relief for heterophoria and adaptation

A

EXOP - BASE IN
ESOP - BASE OUT

May adapt 2-3 mins and heterophoria return to normal

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14
Q

Where does the weakness lie for EXO and ESO Phoria?, how to manage?

A

EXOP -
Convergence weakness -
(Convergence FR development, increase BOUT, maintain BSV at near,
Develop negative relative accom, +ve sph, maintain BSV
Appreciation, jump and negative fixation)

Divergence XS -
Same as convergence weakness

ESOP -
Convergence XS -
(Divergence FR development, inc BIN maintain BSV at Near,
Development of positive relative accom, -ve spheres while BSV)

Divergence weakness - (when + corrected, compensation, appreciative exercises)

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15
Q

Exercises to develop FR and relative accom.

A

1) Dissociated methods - polarized vectogram and anaglyph techniques
2) free space non dissociated methods
3) prisms in free space
4) lenses in free space
5) pencil to nose
6) near/far jump exercises

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16
Q

Dissociated method - Polarized vectogram and anaglyph techniques
TECHNIQUE

A

1)cross polarized/anaglyph filters
2)2 identical slides given, except 1 red, 1 green
3)

CONVERGENCE TRAINING - move green to left and red to right

DIVERGENCE TRAINING - move green to right and red slide to left

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17
Q

Free space non dissociated methods

A

3 cats -card with 2 similar cats but differing characteristics, 33cm

EXO

1) card near, px holds pencil in between and fixates on it, px must fuse images together
2) exercises relative negative accom

ESO

1) card near and transparent, px fixates distance and above, must fuse images together
2) exercises positive relative accom

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18
Q

Prisms in free space

A

C AND D FR

1) practitioner increases BOUT prism, px maintain BSV at N. For decompensated exophoria
2) if fusion breaks, px regain BSV
3) if unable to, prism reduced until able to

BIN for eso

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19
Q

Lenses in free space

A

+ve relative accom: ESO
1-px view small letters 40cm away
2-lenses added in -0.25 increments until blurry
3-encourage px to make single again, 1try to increase -

-ve relative accom: EXO
1-same but +ve lenses

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20
Q

Pencil to nose

A

pencil 50cm away, maintain BSV as brought close.

Repeat to bring convergence closer

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21
Q

Jump exercises

A

Ensure px can see targets clear

Fixation jumps between D and N

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22
Q

Physiological diplopia appreciation

A

pencil(N) in front of picture(D).
When px focussed N, picture is double
When px focussed D, pencil is double

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23
Q

Exercises to develop NPC

and other benefit

A

DOT CARD
BROCK STRING

can develop physiological diplopia

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24
Q

Treatment of suppression - exercises

A

Usually when correcting heterophoria, suppression is treated

If not:
Bar reading
1)pencil between eyes and book, used to occlude part of the text
2)if suppression, they have to move head to be able to read
3)px should be encouraged to use suppressing eye.

Vertical septims, vertical prisms and anaglyphs

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25
Q

What is vision screening? and why do it?

A

Identifiying healthy people that may be at risk to a disease or condition.
Information given from tests, how we can act to reduce risks.

Reduce risks of?
Amblyopia - one of leading causes
high rx - high myopia may indicate associated or systemic disorder
strabismus - infantile/accommodative SOT
stereopsis - usually conjunction with amblyopia
CV - ishihara test

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26
Q

Community screening, what ages

A
  • Screening of all infants in 1st yr of life. After 6-8 weeks (neonatal, red reflex)
  • <4yrs, unreliable
  • Between 4 and 5 yrs is the best time (sure start programme)
  • school entry - some form of assessment
  • 8 to teens - diversity
  • children with special needs
  • Health of all children - hall report
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27
Q

Community screening tests

A
  • new born and 6-8 months- red reflex, corneal light reflex, inspection of eyes
  • VA - Power refractor
  • City Vision screener for school
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28
Q

City vision screener

A

245 children, 5-8yrs
Defect found in 19.6% - not including colour def
2/3 unaware of problem
47.3% never had an eye test

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29
Q

Impacts and Consequences of vision screening

A
  • Q of disability caused by RX unknown
  • Blurred vision affects child’s progress
  • affects academic and sporting ability
  • CV issues may cause difficulty with colour coded materials
  • some defects prevent individuals entering certain professions
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30
Q

What is convergence?

A
  • Coordination and simultaneous inward movement of the eyes.
  • Does not happen in isolation.
  • Accom essential for Binocular Visual acuity
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31
Q

What is accommodation?

A
  • Ability of eye to focus dioptric power to obtain a clear image.
  • Does not happen in full isolation
  • essential for BV at near
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32
Q

Convergence insufficiency and cause and sx. order of correction

A
  • Inability to produce comfortable NBVA
  • Can result from another BV anomaly

–>cause
primary - illness, fatigue, drugs, antidepressants, pregnancy
secondary - heterophoria, presbyopia, uncorrected rx, accommodative insufficiency.

–>sx - headaches, eyestrain, sore eyes

treat pathology, rx, cyclopleg, exercies,

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33
Q

Test for convergence insufficiency, and exercises

A

NPC - target positioned medially from 50cm, RAF rule. cm until double vision

  • ideally 5 to 10cm
  • assess 3 times, to make sure its not for fatigue

tO IMPROVE
Jump 50 to 15cm, repeat 4 to 5x
Pencil to nose
to train accom use a target w fine detail

CT, FR, VA, STEREOACUITY, OCULAR MOTILITY

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34
Q

Convergence insufficiency vs convergence weakness/exophoria

A
  • decompensated exophoria does not deduce convergence
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35
Q

Convergence paralysis, cause, sx, signs

A
  • Ability to converge to infinity lost
  • cause - closed head injury, viral illness, MS, encephalitis
  • sx - diplopia, blurred vision at distance closer than infinity
  • signs - XOT closer than infinity, reduced accom, absence of pupillary response.
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36
Q

Accommodative insufficiency, cause, sx

A

-Inability to maintain adequate accommodation for comfortable NBVA
-half of cases with AI have CI
sx - blurred vision at near, asthenopia, micropsia

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37
Q

Accommodative Fatigue, what is it, cause, sx

A

-Inability to sustain adequate accom over time. Due to repeated to sustained visual effort.

  • causes - poor general health, fatigue, drugs
  • sx - near vision normal then reduces over time.
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38
Q

Accommodative Infacility, what is it, cause, sx

A

Inability to adequately change accom
Difficulty in relaxing and exerting accom

cause - accommodative spasm, uncorrected hyperopia, presbyopia, excessive close work

sx - blurred vision, when changing fixation from Near to D. reduced visions.

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39
Q

Accommodative paralysis

A

The ability to accom, to near objects is entirely gone. No accom can be exerted
may be assoc with convergence paralysis

causes - convergence paralysis, neurological 3CN palsy, trauma

Sx - blurred vision for distance closer than infinity

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40
Q

Convergence/Accommodation spasm, what is it, the muscles affected, causes, sx

A

convergence spasm usually causes accommodative spasm

Convergence spasm - MR becomes contracted
Accommodation spasm - CM becomes contracted

causes - uncorrected hyperopia, intermittent XOT, drugs/alcohol and inflam

sx - blurred vision, intermittent diplopia, headahe, asthenopia

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41
Q

Test for diagnosis of accom anomalies

A

Near point of Accommodation
- amp of accom - midpoint between blur and clear, repeat 3 times (to diff if it fatigue) . monoc an binoc.
compare to the norm for the age

-accom facility (rate of accom)
+-2.00D flippers at 40cm. ask px to keep word clear and keep flipping when clear. repeat for 1 min binoc and monoc.
measure cycles per min, one cycle is plus and negative/
average is 7.7cpm

  • accommodative lag - objective test. Useful in young patients. 2 methods.

1)accommodative lag: MEM.
px focus on detail placed on ret and kept clear.
ret carried out on x with hand held lenses. held for less than 0.5 secs, avoids distrupting accom.
typical lag +0.75.
more plus - under accom, excessing accom lag.
plano or negative - accom excess. reduced lag.

2)accommodative lag: Nott.
distance rx in place, focus on near target 20cm. next to ret.
reflex if accommodating accurately
under accom - a with   move ret closer
over accom - an against    move ret away
0.75 each way is normal
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42
Q

Dyslexia, cause, diagnosis, signs and sx, perception

A

unknown cause
diagnosis by psych
signs - closing and covering 1 eye, excessive blinking
sx - headache, eye ache
perception - move n float, blur, wobbly print

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43
Q

Visual factors which correlate with dyslexia, testing, improving, pattern glare

A

converg, accom anomalies
assoc and decomp heterophoria

binoc instability, - despite heterophoria correction (percivals and sheards), they still have poor binoc coordination.

Due to low FR, Mwing or Mrod used to test

Use vectogram and anaglyph, 3 cats, prism in free space to improve

pattern glare - sx when experiencing repetitive patterns, colours can reduce it. If so, Maeres-irlen syndrome

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44
Q

Visual stress in dyslexia and colorimetry

A

distortions, washed out colour, visual discomfort, sensitive to light

dyslexic people more likely to suffer from it. Not all do.

PTL and intuitive colorimetry
-Hue, saturation and brightness changed independently
-start with 0- S, increase from 0 to 30 then wait and drop to 0.
-repeat with another hue
when best hue found, use attenuators to check best brightness
-can combine tints for best colour
-lenses tried out under different lighting and refined
-then spec tint

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45
Q

What is amblyopia? Types, when does it develop

A

1) one eye
Decrease in best VA, not due to any pathology or structural abnormality. Refractive correction does not overcome.
Impediment/disturbance in vision

2)
- Anisometropic - refractive error - one eye receives better input

  • Meridonal - astigmatic - blurred on one axis. Monoc - anisometropic. Binoc - ametropic
  • Deprivation - Disease - not enough adequate light entering eye (eg, ptosis/cataract). If binoc, congenital
  • Strabismic - strabismus, monoc, likely to have ESOT
    3) Neural circuitry malleable in critical period due to visual input. At this point in time treatment is more effective. 2- 3 yrs and decreases until 8 yrs
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46
Q

Treating Amblyopia, pros and cons,

A

Pros

  • Better VA in this eye
  • if good eye damaged, then backup available

Cons

  • BVA already good
  • may develop abnormal BV
  • may not work
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47
Q

Investigation of amblyopia and explained. how to test

A

1) HS, VA, CT, stereopsis, refraction, amp of accom, ophthalmoscopy and suppression

2) Crowded Keeler logMAR designed for amblyopia.
Amblyopic eye measured first. If single letters, present in box to induce crowding.

4-5 yrs -
Crowded 0.087 - 6/7.5
Uncrowded -0.010 - 6/6

3) If strabismus - note whether alternating/unilateral. constant/intermittent
4) stereopsis - normal 50 degrees, children w amblyopia >70deg
5) reduced amplitude of accom and amblyopia assoc w abnormal accom

6) in ophthalmoscopy, eccentric fixation should be tested
EF - another point on retina used for fixation. Usually like this if strabismic amblyopia. EF reduces VA

7)Suppression
Sbiza bar.
- graded red filter w increasing density held over normal eye. patient asked what colour light is seen.
- continued until two lights or white light reported
- measures likelihood of diplopia, greater density then lower chance.
- useful after occlusion treatment

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48
Q

Eccentric Fixation, process

A

1)project ophthalmoscope target on normal retina
2) eye not being tested is occluded
3) px look at centre of target
4) look at centre of the part of the fundus shown
5) swap eyes and see if the same location is shown
if diff part, eccentric fixation occurring.
severity - further from centre, worse it is

Carry out on all strabismics, can be used to measure progression over time

Dilated and cycloplegia to make easier.

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49
Q

Amblyopia, steps for management, factors to consider

A

1) cycloplegic RX, no hidden RX
2) fundus exam to reveal pathology
3) confirm presence of amblyogenic factors (strabis, anisometropia)

type - worse prognosis for strabismus, mixed
age - older less likely
age of onset - if recent, likely to be able to restore more
acuity - if worse than 6/36, unlikely to respond to treatment
how motivated they are

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50
Q

Refractive correction for amblyopia, occlusion therapy, MOTAS

A
  • 18 weeks to adjust to specs before occlusion therapy and allow VA to plateau
  • good eye occluded: frosted lenses, adhesive patches, opaque CL
    2 hrs patching (6/9-6/12) -
    6 hrs patching (6/24) -
    6- 12week monitoring, more reg in children
    stop when no VA improvement in 2 weeks
    follow up for a yr to prevent relapse

Dose monitors, measure how long patch has been worn for. 120 hrs, 0.1 improv on LOGMAR

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51
Q

Penalization, what is it, types and fogging method

A
  • Blurs good eye enough to make the other work.
  • alternative method for those who cant tolerate
  • done w specs and enhanced by cycloplegic

Near penalization

  • 0.5-1% atropine or cyclopentolate in normal eye
  • improvement best with +3.00 over correction.
  • Non-amblyopic eye will be used at distance
  • Amblyopic eye wilt +3.00D will be used at near

Distance penalization

  • blur normal eye with +3.00
  • amblyopic eye needs full correction
  • clear distance vision in amblyopic eye
  • clear near vision in normal eye

Total penalization

  • amblyopic eye at all distances
  • optimum correction to normal eye
  • strong convex lens in good eye to blur all distances
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52
Q

Atropine advantages and disadvantages

A

Advantages -
cosmetically good
as good as occlusion
useful when px refuses patch

Disadvantages -
allergy 
not useful when severe
not suitable for older presbyopes
not used when heart defects
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53
Q

Other methods for treating amblyopia

A

1) Dichoptic training - different and independent
- target for each eye. Tasks require both inputs
- amblyopic eye - higher contrast, to overcome
- suppression and. As progress, contrast is reduced
- until eyes match.

2) Strabismic amblyopia
- full time specs wear for 4 weeks, only give full correction if partial not accepted
- then occlusion
- if eccentric fixation, occlude amblyopic eye for 2 weeks constantly then switch to normal eye. (promoted foveal stimulation)
- warn about intractable diplopia

3) Anisometropic amblyopia
- Full rx 4 weeks for young, partial for older
- refraction, fundus, cl for high rx and anisometropia
- when no improv, occlusion 2 hrs. For poor VA increase time

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54
Q

What is accommodative Esotropia, how, ft, management

intermittent accommodative primary esotropia

A

DUE TO:
uncorrected hyperopia or a high accommodation convergence/ accommodative ratio or a combination

1) FULLY ACCOMMODATIVE
Accommodative exerted to overcome hyperopia
F/T
- 2-5 yrs, uncorrected hyperopia, child may lose interest in near activities, noticeable when tired, untreated then strabismus

Management
- full Rx and full time, cycloplegic refraction

  • Orthopic exercises - (up to +1DC, +3DS, <25D)
  • diplopia recognition,
  • control of eso (fusion),
  • improvement in BVA - via negative fusional reserves with -sph
  • Surgery - if decomp still w specs, rx surgery for hyperopia and for those who cant tolerate (adults)

2) CONVERGENCE XS
-occurs at near fixation despite correction,
due to excessive accommodative convergence

-F/T - 2-5yrs, AC/A ratio of 6:1, uncorrected rx, noticed when tired,
non accommodative near target doesn’t deviate

Management - Rx full correction, cycloplegic refraction.
- surgery - >20D and 8:1> AC/A, after 6 yrs
- Bifocals - reduce need to accommodate, decreasing accom convergence.
Min reading add to maintain BSV, month follow up,
- increase add if req,
- if no control then discard.
- If good, then progressively decrease until none

  • Orthopic ex NOT FOR:
    AC/A >6:1, dev constant at near, exceeds 20D
    Use for small dev and same methods
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55
Q

Partially accommodative ESO

constant accommodative primary esotropia

A

non accom element results in deviation when it is corrected

FT - 1-3 yrs, anisometropia and astig, strabismic or anisometropic, assoc w vertical dev

56
Q

Partially accommodative ESO

intermittent accommodative primary esotropia

A

Management

  • specs full time full rx, cycloplegic, bifocals, fresnel prism incorporated lens
  • botulinum toxin, cosmetic. repeated injections req
57
Q

Non accommodative esotropia, types

A

not from uncorrected hyperopia,
Infantile - could be congenital (before 6 months)

ft - stable, exceeds 30D, alternates, emmetropic

Unique ft -

  • Nystagmus and asymmetric
  • dissociated vertical deviations-inferior oblique
  • overaction, acquired 18 months to 3 yrs.
  • Compulsory head posture to compensate for nystagmus and abduction limitation

management - correction of rx, amblyopia treatment, botulinum toxin, surgical treatment

58
Q

Nystagmus blockage syndrome

A

Results from eye converging to block manifest nystagmus and improve VA

  • stays same even if one eye closes,
  • when eye abducts (away) it gets worse
  • head turns to fixating side

management
- rx correction, occlusion therapy, surgery

59
Q

Acquired non accommodative ESO

A
after 6 months
-> 6 - 24 months, assoc strabismus,  
prism, botulinum, surgery.
-> 2 - 8+yrs, intermittent that becomes constant, diplopia initially, could be assoc w brain tumour.
prism, botulinum, surgery
60
Q

Myopic Esotropia

A

CARRY ON LATER W THIS LEC

61
Q

Intermittent distance exotropia, types, FT, Investigation, true vs simulated

A

10D larger at distance than near

1) intermittent distance exo with normal AC/A
- N matches D when one eye occluded
- 10D> at D

2)intermittent distance exo with high AC/A
- N matches D when measured with +3.00DS, not
occlusion

3) True intermittent distance exo
- No change in N

4) Intermittent Near Exo
- Prism CT 10D greater at near

5) Non specific intermittent EXO
- CT difference does not exceed 10D

FT - high illumination, deviated eye closes in bright
light, px may be unaware.
They manipulate accom and vergence to control dev

Investigation
VA - equal
CBA (VA with BSV) - indicates quantity of control
- examiner observes px alignment whilst chart
reading
- end point when dev noticed or blurred/double
CT - D AND N
Convergence - should be good
motility - decrease dev on lateral gaze

True VS Simulated

1)Occlusion test
   strabismic eye occluded for 45 mins, suspends 
   tonic FR.
   Do CT:
   if D and N matches, then normal AC/A
   If no change, then high AC/A or true

2)+3.00 ADD N test
CT 30cm +3.00 lenses,
if dev same, high AC/A ratio
if no change then true intermittent

62
Q

Intermittent and non specific EXO, correction, monitoring, management

A

Fully correct myopia, leave >+3.00 hyperopic

Monitoring
VA - reduc in monoc, strabis present most of time
CBA - reduced control of dev
NPC - poor control, risk of dev becoming more constant

Orthoptic exercises
- red/green septum filters -
awareness and can eliminate
- control - positive FR by BOUT
- positive vergence by Pos sph
- positive converg by -3.0

Optical and surgical correction

  • minus lenses up to -3.00 stimulate converg
  • prisms BIN full comp of exo
  • tinted specs as bright light is a factor
  • botulinum toxin in LR
  • surgery 6+
63
Q

Near Exotropia, types, FT, management

A

1)Simulated intermittent near
occlusion increased D to match N

2)True intermittent near
occlusion has no effect

FT
- less common than D and non specific,
- some have no sx
- differ from:
- convergence palsy - no ability to converge,
doesnt respond to BOUT.
-convergence insufficiency - no tropia present
- accom converg insuf - w reduc in accom amp

Management
 - Correction RX
 - Orthoptic exercises <25D
   pos FR and recog, prism BIN
 - surgical treatment - no success of others and dev huge
64
Q

Constant exotropia types, FT, management

A

D and N

1) Decompensated infantile exotropia
decomp of D or non spec - results in constant

FT

  • constant with suppression and no diplopia
  • eq VA
  • excellent potential for BSV post treatment

2) Infantile exotropia
first year of life, D and N

FT

  • rare, resolves by 3 months
  • secondary to pathology
  • early onset - server craniofacial abnormality

Management
-if early, refer to paediatric ophthalmologist
- correct RX
-surgical treatment- main if constant
Botulinum toxin classed as a surgical type

65
Q

Secondary Exotropia, FT, management

A

Exotropia from severe vision loss which disrupted fusion mechanism.

FT -
vision loss unilateral
secondary to pathology
retinoblastoma could be primary reason

Management
treat cause, then prisms, toxin, surgery

66
Q

Residual Exotropia, what is it, management

A

Remains after surgery
May be planned, if so, no further treatment req.
If unplanned, further treatment req

Management
full rx, negative lenses for less that 25 D
Majority have BSV so no treatment req
BIN lenses
botulinum toxin
67
Q

Consecutive exotropia what is it, management

A

previous history of esophoria or esotropia, usually from surgical overcorrection
usually no diplopia

Management
discontinue plus in young px with low hyperopia
perm prism in lenses
botulinum toxin

68
Q

Sensory changes in strabismus

A

Binoc -
Global suppression - likely to suppress the whole VF of strabismic eye. If young with plasticity, develop ARC

ARC - both retinas correspond to same point normally. The eye develops new corresponding point which is the angle of strabismus (angle of anomaly) . Called HARC
CORTICAL PHENOMENON

Monoc -
Amblyopia -
Eccentric fixation -

69
Q

Mechanisms for ARC,
Factors influencing the development of HARC
Detecting HARC
HARC management

A

1) - Remapping of Panums area, small angle strabismus.
2) - Enlargement of Panums area.
3) - Bifoveal assumption abandoned, each eye position registered seperately, large angle strabismus.

 - 
Age of onset - younger, greater chance
 - constant and unilateral - most likely
 - small angle likely to develop HARC
 - likely to be ESOT
 - horizontal more common that vertical
  • Has to be techniques w little distruption/dissociation otherwise it will break down before test.
  • Sensory function - new foveal point is zero
    point. When good eye covered, HARC
    eye returns to true fovea. CT will pick up
  • Local suppression -
    HARC comes from small receptive fields and zero point
    If HARC not in these places then suppression
    Greater strabismus angle, greater remapping req
    Hence greater suppression
  • Stereopsis in HARC
    compensate for strabismus and produce stereopsis and stereoacuity.
    Deeper HARC more likely to have it
  • Motor function in HARC
    Objective angle = angle of strabismus measured by the examiner.
    Subjective angle = angle of strabismus perceived by the patient from any diplopia they may have.

Angle of anomaly = objective angle - subjective angle
NRC= anomaly angle is 0 HARC = Subjec = 0

HARC Management

  • sol to a problem
  • must be BV specialist if req
  • superficial - correction of motor dev
  • deep HARC, less likely to respond to treatment
  • Unstable HARC can break down and may req treatment

rx, motor dev treatment, small dev orthoptic exercises, if strabis >20 then ask surgeon,

70
Q

Binocular sensory adaptation to strabismus

A

1) Diplopia

 - WORTH 4 DOT TEST
lights off, glasses on, then target
4 lights in diamond formation
green on sides, red on top, white at bottom
px asked what they see

Results -
BSV if seen as is/ slightly pink on white.
LE suppression - all red, RE suppression - all green
3 green left, 2 red right - ESO
2 green left, 3 red right - EXO

2) Global suppression
3) ARC

DIFFERENTIAL DIAGNOSIS BETWEEN SUPPRESSION AND HARC
- correct rx

Bagolini striated lens
- plano lens with gratings on dev eye
- px looks at spotlight, streak should pass through
- streak appears to pass through the spot - HARC
- if streak has gap around spot, local suppression
Examiner observe movements and CT to ensure dev
Dont repeat as break down
Alternating strabis, lenses in both eyes, 45 and 135

3/12/21 SLIDE 10

Depth of HARC with bagolini
Filter Bar with increasing absorbtion in strip, 0.3 steps
deeper filter req to suppress, deeper ARC, worse prognosis
-

71
Q

Modified mallet OXO for suppression and HARC

A

Use distance fixation mallet unit at 1.5m

  • if strabismic eye has no strip - suppression
  • UARC, NRC - diplopia or confusion
  • neutral density bar between eye and visor
    examiner check if breakdown, if does then question daily life may reveal sx for treatment
72
Q

Microtropia, ft

A
  • Small angle dev where: ARC, normal motor function & reduced/normal stereoacuity are present
  • primary or a result of treatment

FT - less than 10D, anisometropia ( VA diff greater than 1.5D), amblyopia, EF, ARC, low stereopsis, little sx

1) Primary - No prior history of large dev

2) Secondary - Large dev reduced by treatment
Fully accommodative SOT controlled to micro-SOT
Dense suppression

73
Q

Primary Microtropia types

A

1) With Identity
Loss of central vision, scotoma, HARC
No CT movement

2) Without identity
-Non absolute eccentric fixation
Unstable EF, shown in CT

-Central suppression and periph fusion
NRC, no ED, shown in CT

3) Primary decompensated microtropia
1-3yrs, accommodative, hyperope, deviation decompensated to larger angle

74
Q

Investigation of Microtropia

A

VA - reduced in deviated eye, may show crowding
Rx - Anisometropia
CT - with identity - no dev seen may be heterophoria
without identity - identified on unilateral CT

4 Prism Dioptre test

  • isolated target on featureless background
  • 4 BOUT in 1 eye, observe movements
  • small initial vergence movement normally
  • if put in strabis eye, moves to suppression area
  • if put in normal eye, both eyes verg movement but strabismus eye will fail due to scotoma

HARC tests
Stereopsis tests

75
Q

Management of microtropia, Eccentric Fixation

A

Best RX, treat amblyopia, if assoc decomp phoria (exercises),
Adults dont usually benefit

Eccentric fixation - monocular condition in which a point on the retina other than the fovea is used for fixation (in the deviating eye)

  • greater EF, worse VA
  • amblyopia always present with EF
  • often assoc with ARC

Why amblyopes have EF?
Diff theories
deep absolute central scotoma,
- px fix with surrounding areas on fovea with greater VA.
- Change of area of localisation as scotoma develops
- leads to error focussing ahead when req monoc

76
Q

Eyecare for special needs, criteria, categories, early diagnosis and management, testing SEND px

A

Criteria to diagnose:

  • intellectual impairment (IQ)
  • social or adaptive dysfunction combined with IQ
  • early onset

Categories
1) SEN - Special education needs
2) SEND - Special education needs and disabilities
Can effect the px ability to learn, socialise,
read/write, concentration and physical ability

Early diagnosis crucial, eg improve handwriting and they are likely to have other abnormalities

1) Child friendly environment
- adapt room
- avoid waiting
- allow time
- tools and toys
2) Communicate well
- terminology
- explanation loud and clear
- verbal and written advice
3) Fit the test to the patient
- earlier recalls, diff tests, objective

77
Q

Examining with SEND

A
  • VA charts may not be appropriate
  • CT may not be appropriate, use corneal reflex and
    alignment
  • NPC - perform objectively, when one eye doesnt converge with interesting target
  • Accom - dynamic ret while px fixates on near target, move target back n forth until neutral. Ask q about target to pay attention
    Mohindra -px likely to be sensitive to
    cycloplegics. 50cm dark, wait for max dilation
    adjust WD to comp for accom:
    1.25 for adults
    1.00 for children over 2 years
    0.75 for infants under 2 years
78
Q

Patterns as a result of vertical muscle action

A

Adduction: non-primary action of the SR and IR
Abduction: non-primary action of the SO and IO

-> V-pattern
• V-esotropia
Congenital acquired.
Decreased of ESO deviation in up-gaze by:
- Increased abduction: over-action IO muscles
- Decreased adduction: under-action SR muscles

Increase of ESO deviation in down-gaze by:

  • Loss of abduction: under-action SO muscles -
  • Increased adduction: over-acting IR muscles

• V-exotropia
Congenital
Increase of EXO deviation in up-gaze by:
- Increased abduction: over-action IO muscles
- Decreased adduction: under-action SR muscles

Decrease of EXO deviation in down-gaze by:

  • Increased adduction: over-action IR muscles
  • Decreased abduction: under-action SO muscles

-> A-pattern
• A-esotropia
Congenital, associated with mechanical disorders of ocular motility, eg Graves
Increase of ESO deviation in up-gaze by:
- Decrease of abduction: under-action IO muscles
- Increased adduction: over-action SR muscles

Decrease of ESO deviation in down-gaze by:

  • Increased abduction: over-action SO muscles
  • Decreased adduction: under-action IR muscles

• A-exotropia
Increase of EXO deviation in down-gaze by:
- Decrease of adduction: under-action IR muscles
- Increased abduction: over-action SO muscles

Decrease of EXO deviation in up-gaze by:

  • Decreased abduction: under-action IO muscles
  • Increased adduction: over-action SR muscles
79
Q

Alphabet Patterns, what is it, explained by, diagnosis

A
  • Signif changes in horizontal dev when looking up or down.
  • Eg. Strabismus, Congenital, acquired paralytic strabismus, muscle innervation disorders, mechanical restriction of ocular movement.
  • V - >15D from Up to Down
  • A - >10D from down to up

Alphabet common in comitant strabismus
V more common than A
seen in many vertical muscle palsys

EXPLAINED BY:

  • abnormal vert, horizontal muscle action
  • anatomical anomalies, configuration of orbit, muscle pulley, mechanical limitations
  • Disorders of innervation
  • Anomalous insertion of muscle tendons
  • Sensory torsion

Diagnosis:
- CT,

80
Q

Patterns as a result of horizontal action

A

– Related to V-pattern
• V-esotropia may be due to over-action of the MR muscles
• V-exotropia may be due to over-action of the LR muscles

– Related to A-pattern
• A-esotropia may be due to the under-action of the LR muscles
• A-exotropia may be due to the under-action of the MR muscles

81
Q

A and V patterns as a result of anomalies

A

1) Anatomical -
- orbital config
- muscle pulleys
- mech limitations

2) Disorders of muscle innervation-
- Eg Duanes

3) Anomalous insertion of muscle tendons
- A different muscle insertion,

4) Sensory Torsion

  • Infantile strabismus - High incidence of V A ESO
    before 6 months
  • Duanes - High incidence of V A in Duanes
    retraction syndrome
  • Browns - Y pattern, increased abduction, IO
    inhibited
  • Acquired 4CN Palsy - underaction of SO, V eso
  • Graves - A pattern
  • Craniocytosis - V strabismus
82
Q

Detecting and measuring alphabet patterns, why are they important?, treatment, surgical principles

A
  • Observation - head posture, children is
    intermittent.
  • CT - primary, up and down gaze, distance and
    near, measure using prism
  • Ocular Movements - look at under/over action of vertical muscles
  • Binoc fx - Baggolini lenses - pos of least dev
  • Hess Chart - inwards/outward slope of the fields
  • Influence diagnosis, prognosis, management of strabismus
  • management allows BSV
  • Certain patterns have signif:
    Large V - bilat 4CN palsy
    Infantile A SOT - dissoc vertical dev
  • Most req no treatment
  • influence choice and extent of surgery
  • if >14D diff, then surgery
  • aim - Comitance on gazes, BSV, better alignment

1) correct oblique muscle dysfunc if present
2) this allows surgery to correct al[habet
3) both eyes

83
Q

Hess test, How to perform

A
  • Investigating incomitant strabismus, under/over action
  • accurate record of ocular motility

HOW TO PERFORM

  • both eyes open
  • red-green specs.
  • One eye fixates at a time,
  • fixating eye - directed in positions of gaze (red lights) This will be seen by the eye with the red filter. Position of non fixating eye recorded.
  • px shine green torch where red light perceived (assess pos of non fixating eye). Plotted on chart
  • Do all 9 pos
  • FIlters swapped and repeated

TEST REQUIREMENTS

  • NRC, if ARC measurement will be incorrect
  • No suppression
  • No red green colour defect

PERFORMING THE TEST

  • 50 cm away
  • chin and forehead rest
  • dim light

INTERPRETING HESS CHART, show the effects of:
- Hering’s Law - same direction movements,
Equal and simultaneous innervation flows to corresponding muscles to contract.
Yoke muscles = contralateral synergist

  • Sherrington’s law - During contraction of muscle, equal and simultaneous signal is sent to the ipsilateral synergist
  • Primary Dev - angle of dev when normal eye fixating
  • Secondary Dev - angle of dev when affected eye is fixating

POSITION of field -
OUTwardly displace = EXOdeviation
INwardly displace = ESOdeviation
lower field - lower eye

SIZE
- Smaller field, the affected eye
- UNDER-ACTION - interior to normal field
displacements
- OVER-ACTION - Displacements of exterior to
normal field
- NARROW FIELDS - Mechanical origin

SHAPE
- Slopping fields - indicate A/V pattern

84
Q

Incomitant strabismus

A

Limitation of movement, angle of dev increases when looking is direction of limitation. Decreases in opposite.

Primary dev - dev when fixating with normal eye
secondary dev - dev when fixating with affected eye

Main FT - Secondary deviation has greater angle than primary deviation,
abnormal head posture, development of BSV, Limitation of movement affecting 1 muscle/1 direction. Followed by muscle sequelae.

85
Q

Anomalous head posture in Incomitant strabismus

A

AHP

Purpose -
Place eyes in pos of least dev, BSV
Centralize field of BSV
Obtain foveal fixation

Components -

  • Head tilt - compensate cyclotropia & vertical dev
  • Face turn - place eyes away from direction of underaction
  • Chin elev/depres - place eyes in pos of least dev & avoids discomfort

Modifications -

  • If ocular movement improves
  • extension of fusional amplitude
  • sensory adaptation
  • AHP difficult or painful to maintain
86
Q

Classification of incomitant strabismus

A

Paralytic (incomitant) strabismus, characterized by cause:

Neurogenic - CNPALSY 3,4,6
Mechanical - elements within orbit causing
Myogenic - Muscular Origin

Terms
Paralysis - loss of muscle function
Paresis - Partial loss of muscle fx
Palsy - both paralysis and paresis

87
Q

Investigation of incomitant strabismus

A

Aims:

  • Neurogenic or Mechanical (differ)
  • Which muscles (over and underacting)
  • Differentiate congen and recent onset
  • most appropriate treatment
  • Permanent record

CN Palsy

  • Adults - Poor health, loss of VA in 1 eye, decomp of palsy resulting in sx
  • Children - Parents notice AHP, manifest strabismus

Acquired Palsy

  • Adults - present with sx, mainly diplopia
  • Children - present w sx or manifest strabismus

H/S -
Nature, when, sudden/gradual, change since onset

Q’s -
direction of diplopia, assoc sx, constant/intermittent, variations in day, whether it is overcome by tilts

Observe -
AHP, facial asymm, injury, dev of axis, difference in pupil size, ptosis, difficulty in speech/hearing/commun

-VA - N&D mono, bi
-CT - N&D with and without AHP
-Version, duction, vergence movements
-measurement of dev angle, prism CT
-Hess test
Referral

Congenital vs Acquired (importance)
 - Acquired - usually further investigation req to find and treat cause, time given to allow spontaneous recovery
Aq - 
aware of AHP, 
may just be overaction and no underaction, 
larger difference in field size, 
smaller vertical fusion range
small BSV field
no suppression in adults
AMBYLOPIA ONLY IF CHILDHOOD
URGENT REFERRAL
Fresnel prism
Surgery can be done when static for 3 months
88
Q

Neurogenic Vs Mechanical strabismus (DD)

A

N - can be marked in primary gaze, diplopia same in all gazes, Head tilt usually vertical, Movement greater on duction then version

M - to small to see in primary, diplopia may reverse (swap), Head tilt rare, chin up/chin down used to compensate

REFER NEUROGENIC quicker, poss serious cause.
eg tumour,
Mech - cause eg Duanes, Thyroid, Browns syndrome

89
Q

Neurogenic strabismus, what is it, CN affected, FT, causes

A

1+ Cranial nerves supplying an extraocular muscle affected

III - Oculomotor
IV - Trochlear
VI - Abducens

FT - 
Unilateral/bilateral
isolated or multiple ocular motor nerves
Underlying systemic disease
Neurological disease

Causes of acquired-
tumour, trauma, vascular, inflam, Viral, demyelination, Ophthalmoplegic migraine

Tumour -
(Meningioma, Pituitary tumour, craniopharyngioma)
Closed (IV, VI,), Often Bilateral
6 - passes over petrous temporal bone (prone to traction damage) causing pressure, fracture of skull base
4 - exits brainstem then goes round to join cavernous sinus
3 - Can be caused by trauma

Vascular -

  • Aneurysm of BV around circle of Willis - 3rd
  • Subdural Haematoma - head trauma, bleeding in subdural space
  • Microvascular - Diabetes, diab is sx for 3&4 palsy
  • Systemic hypertension - hypertension

Inflam -
Giant cell arteritis - inflam of artery, ischaemic optic neuropathy, 60+
headaches, fatigue, weightloss, 4&6 palsy, emergency

Viral -
Benign 6 CN Palsy
Herpes Zoster Ophthalmicus - rash of face following division of 6(trigeminal) and 3rd
Meningitis and encephalitis - viral/bac, CN affected

Demyelinating
MS - 16-40yrs, More than one demyelinating event at a time, then additional tests for diag, Optic Neuritis most common. 6th Nerve

Ophthalmoplegic migraine -
Rare - inflammation of the cranial nerves
hemicranial headache, sudden onset vomiting and nausea, 3CN palsy ipsilateral

90
Q

Causes of 3rd CN palsy, Complete, incomplete, ft, management, single muscles

A

COMPLETE

  • Posterior communication artery aneurysm
  • Microvascular disease
  • Pressure from space occupying lesion

FT -
Complete Palsy -
upper and lower div and all extraocular muscles innervated by 3CN
- Exotropic, hypotropic, intorted eye w (dilated and ptosis)
- crossed diplopia, AHP
- ocular movement limited

Management - 
Spontaneous recov likely
May recover due to aneurysm after treatment
ptosis crutches fitted to specs
surgery when stable
Botulinum toxin

INCOMPLETE 3CN PALSY
FT -

  • Superior div -
    SR elevator congenital, if acquired its by an aneurysm
    Hypotropia with ptosis
    Management - only if diplopia, prisms, upper specs lens occlusion, surgery
  • Inferior - IR, MR, IO -
    Rare, XOT, interted and hypertropic, accom affected
    Management - Prisms and sector occlusion unlikely to be successful, surgery better

Single muscles
Isolated palsy,
SR - bilateral, V pattern, same as superior palsy management
IR - congen/acq, DD: Myasthenia gravis, prisms, surgery
IR -

91
Q

Cause of 4CN Palsy

A

UNDERACTION OF SUPERIOR OBLIQUE

  • Closed head injury, microvascular disease, pressure from space occupying lesions, Myasthenia gravis
  • FT - UNILATERAL
    Congenital,
    AHP since early, facial asymm, diplopia, small horizontal dev, head tilt to opposite side

management - Spontaneous improvement, if px comfortable with AHP then leave,
sectorial occlusion, prisms, surgery

FT - BILATERAL
V SOT, AHP (lower chin) -
Bielchowsky head tilt test positive at either side of head tilt,
Similar management to 4th

92
Q

Causes of 6CN Palsy

A

UNDERACTION OF LR

Demyelination, vascular disease, tumours, nucleolus, fascicular damage
Closed head injury - compression of nerve by pituitary tumour, meningioma
Intercranial pressure

BILATERAL
FT - Eso in greater in distance (same for long standing) , head turn to affected side, no AHP at near.

Management (unilateral/bilateral)
Non surgical early, aimed to reduce diplopia and AHP
prisms if mild
Fresnel prisms - divided between eyes, can be attached to upper half of specs
occlusion, botulinum toxin, surgery for later stages

93
Q

Investigation of neurogenic strabismus

A

H/S -
Particular attention - nature of sx, whem, sudden/gradual, any change since onset

Q’s related - direction of diplopia, any assoc sx, constant vs. intermittent, variation, chnages in diplopia since onset,

Observation of px -
AHP, facial asymm, dev in axis, difference in pupil size, difficulty with speech/hearing/locomotion

Comprehensive exam -
VA, CT, motility, measurement of angle of DEV prism CT, Hess chart

Indications of referral -
All acquired neurogenic palsies referred

Treatment - 
Alleviate sx - prisms, teach, occlusion, surgery
Consider occlusion, partial
surgery after 6 months stability
Botulinum toxin
94
Q

Myogenic Palsy

A

Paralytic strabismus:
congenital/acquired, ocular movement limited so incomitant deviation.

Types:
Neurogenic
Mechanical
Myogenic - Weakness of ocular movement due to a primary problem such as lesions affecting the muscle

eg
– Myasthenia Gravis
– Chronic Progressive external Ophthalmoplegia
– Orbital myositis
– Rhabdomyosarcoma
95
Q

Myasthenia Gravis

A

Autoimmune, disorder of neuromuscular transmission

1) Reduced ACH receptor sites at motor plate
2) Lack of muscle contraction
3) Striated muscles fatigue early

  • Classification
    1) Paediatric
  • Neonatal - MG mother, self limiting
  • Congenital - Non MG mother
  • Juvenile - Develops with infancy

2) Adult
- Ocular - Limited to eye muscles, if limited to eye muscles for 2 yrs, unlikely to become generalized
- Generalised:
- Mild To Moderate - slow onset, less likely to
affect respiratory
- Acute Fuliminating - Rapid onset, early
respiratory muscle involvement
- Late - Severe, 2 yrs after muscle weakness

3) Drug related secondary
- Caused by drugs for immune disorders such as rheumatoid arthritis

Signs

  • Ptosis - Usually unilateral, asymm if bi, increases with fatigue, fluttering on elevation
  • Cogan’s Lid - Moving from down to primary pos, lid twitches up and overshoots before settling
  • Low lid entropion -
  • mimics palsy
  • fatigue and nystagmus when checking for saccades
  • diplopia

Diagnosis
- Tensilon test - short acting ACHE, improved condition for 5 mins, 2mg +8mg =10mg injected
Atropine if Side effects
monitor fatigue and systemic changes with Hess changes.
Pos response indicated MG

  • Blood test for acetylcholine receptor sites
  • CT scan - can be assoc with thyroid eye disease which have enlarged thyroid
  • Chest X ray - enlarged thymus
TREATMENT
immunosuppressant
longer lasting ACHE
antibody circulation reduction therapy
surgery
  • ptosis props
  • occlusion therapy (frosted lens etc)
96
Q

Chronic Progressive External Ophthalmoplegia

A

Progressive disorder where eye and brow movement lost

Hered - bilateral loss of motility, between infancy and 50, Bilateral ptosis
Diplopia - starts off as asymmetry, then progresses
Pupillary responses normal

Diagnosis - muscle biopsy

If diplopia, can treat with: Prisms, occlusion therapy, surgery

97
Q

Orbital Myositis

A
  • Inflammation in orbit caused by anterior globe displacement, confirmed by CT
  • ocular motility issues in one muscle
  • unilateral and painful
  • PROPTOSIS
  • ptosis
  • Conjunctival chemosis
  • Self limiting, resolves in 8 weeks, steds can speed
98
Q

Rhabdomyosarcoma

A

Highly malignant tumour of striated muscle

px - young, squint, motility restriction, if rapid growth then PROPTOSIS
RAPID DIAGNOSIS KEY
Management - radiotherapy, chemotherapy, surgery

99
Q

Marcus Gunn - Jaw winking syndrome

A

Eye lid retraction evoked by jaw movement

  • complete to variable ptosis in primary position
  • ptosis increases when jaw moved on same side
  • Congenital

Management

  • self disguise - leave untreated
  • ptosis props
  • bilat levator muscle surgery alongside bilateral brow suspensions
100
Q

Mechanical anomalies, def, eg, characteristics

A

Factors in the orbit which interfere with muscle action, preventing free movement in the globe.
– Duanes Retraction Syndrome (Congenital)
– Browns Syndrome (Congenital)
– Blowout Fractures (Acquired)
– Thyroid Eye Disease (Acquired)

Characteristics
 - Forced duction test - 
Limitation of passive movement is pos
 - Globe retraction - 
occurs when gaze directed away from lesion, seen in version, if looking at px from side or above
 - Ocular motility - 
Duction movements equally limited to version movement
 - Muscle sequelae
Overaction of contralateral synergist
101
Q

Duanes retraction syndrome

A

Due to (mechanical):

  • thin elastic muscles
  • muscle bound to anterior wall
  • inelastic LR muscle

Due to (innervation):

  • Absence of 6CN
  • Partially formed 6CN in 8th week of preg

Classification
Browns:
A - Limited abduction and less degree of adduction
B - Limited abduction and normal adduction
C - Limited adduction and less degree of abduction

Hubers:
1 - Limited abduction
2 - Limited adduction
3 - Limited abduction and adduction to a lesser degree

H/S - Birth history
CT - look for dev in primary position, test with and without AHP, elevates and abducts slightly when attempting to adduct
Motility - looking for A OR V or up and downshoots on adduction, globe retraction
PCT, CONVERG, HES, BSV, RX,FUNDUS

Management
If BSV maintained and AHP cosmetically acceptable, then leave
Poor AHP or dev in primary, surgery

102
Q

Browns Syndrome

A

Congen - Short SO tendon sheath, Tight/short tendon, swelling or nodule on SO
Acquired - inflam of trochlear, rheumatoid arthirits causing nodule on SO tendon

fx - Limitation on elevation when adducting, down drift of affected eye

  • No muscle sequelae
  • Pain or discomfort in trochlear region
  • clicking felt and heard when attempting adduction and elevation over action of IO
  • AHP - chin up and tilt
  • Hess chart - dog ear shaped

HS - birth history, absence of diplopia
AHP, VA
CT - dev in primary, with and without AHP
ocular movement - AV, Downward drift on adduction, feel and listen for clicking of SO nodule when elevating in adduction
PCT, BFX,
HESS - dog eared shape
BSV, RX, FUNDUS

Management
sometimes spontaneous resolve
AHP - acceptable & BSV, then leave
- px are sx free and dev in primary pos well compensated, intervene rare
- poor AHP cosmesis, poor dev cosmesis, diplopia then surgery/injection

103
Q

Blow out fracture

A

Blunt trauma

1) Soft tissue - Oedema, bruising, haemorrhage
- recov without intervention, espec if no fracture
- May initially cause diplopia
2) Bony
- Orbital rim normal, one or more orbital walls fractured
- Force applied from object larger than rim, compresses orbital contents, increases IOP, thus fracture of thinnest walls
- Sporting injuries/ fights
- if orbital rim also damaged, car accident

Sx -

  • Diplopia - muscle entrapment at fracture site, prevents globe from moving in opp direction
  • Pain on movement - trapped tissue, worse when attempting to look away from lesion
  • Loss of vision - pressure on ON

Signs -

  • Limitation of movement - oedema, bruising, haemorrhage, tissue trapper,
  • Displacement of globe - displaced backwards.
  • Retractions of globe - when eyes move opp direction to lesion
  • Facial asymmetry - orbit displaced, if rim damaged
  • Infraorbital anaesthesia - loss of sensation if infraorbital nerve involved

Investigations
H/S - date, cause of injury - indic management and type
AHP, VA, CT,
MOTILITY - Limitation, globe retraction
HESS, BSV, CV, enophthalmos, IOP, FUNDUS, CT/MRI

Management

  • If lot involvement - immediate surgery
  • less sev, monitored over 2 weeks every 2 days
  • Referral GP if l severe
104
Q

Thyroid Eye disease - Graves disease

A
  • Disturbance of autoimmune system due to defective antibodies
  • Thyroid gland in lower neck and synthesizes thyroid hormones

Impacts:

  • physical/mental development, nerve stability, metabolic rate, heat and energy production, healthy skin, hair
  • Inflam response around orbit

1) Hyperthyroid
- muscle watsing
- high pressure
- rapid pulse
- heart palpitations
- proptosis

2) Hypothyroid
- Gaining weight
- decreased temp and BP
- oedema
- fatigue
- decreased mental and metabolic rate

Mild - lid lag, lid retraction
SEVERE
- Wet - muscle oedema and enlarged, fibrotic, proptosis, corneal exposure, VF loss, chemosis
- Dry - inflam reduces, so does proptosis, scar tissue round muscles, fibrotic muscles limit ocular motility can cause diplopia

SIgns
Vertical dev, proptosis, corneal oedema, corneal erosion, chemosis, AHP TO INC BSV

Sx
No signs/sx
Only sx
Soft tissue involvement
Proptosis
EOM involvement
Corneal exposure
Sight loss due to ON compression
  • Diplopia - vertical, worse in morning and may reverse from elev to depr
  • Painful, gritty eyes - corneal exposure, conjuc oedema, proptosis
  • Loss of VA - Dry eyes secondary to corneal exposure, decreased blood supply to ON
Investigation
H/S - gen thyroid probs
AHP, VA
CT - with and without AHP
Motility, hess, bsv, cv, contrast sensitivity, exophthalmos measure, IOP, corneal exposure, fundus, VF, MRI CT
Management
thyroidectomy, steroids, thyroid drugs to inc/dec activity, lubricant, botulinum toxin
surgery - 
 - decomp to reduce proptosis, inc space within orbit
 - enlarge bsv, allevating diplopia
 - relieve uncomfortable AHP
 - improve cosmesis
 - help lid retraction
105
Q

Internuclear and supranuclear disorders

A

Internuclear ophthalmoplegia (INO) - paralysis of 1 or more eye muscle
cause - Medial Longitudinal fasciculus (MLF) lesion
ft - Loss of adduction in 1 eye, gaze evoked nystagmus of the other

MLF - pathway linking 6CN to 3CN,
Right LR links with Left MR, hence eyes move together
- The lesion breaks this connection
- Thus loss of adduction

DIFFICULTY - saccadic, smooth pursuit, VOR
partial or total, uni or bilateral
sx - x diplopia by gaze movements, blurred, tilting/upside down images

106
Q

Uni lateral and Bilateral INO

A

Unilateral INO signs:

  • Lag of ipsilateral MR of gaze movement (add)
  • Smaller and slower saccadic movement
  • Nystagmus of abducting eye
  • Vertical nystagmus

Bilateral INO signs:
- Discrete lesion - eyes normal: primary, converging. paralysis elsewhere.
CAUDAL lesion
- Larger lesion - affect convergence centre in upper midbrain (next to 3CN nucleus)
Adduction and convergence affected, eyes XOT due to ROSTRAL lesion

Abducting nystagmus.
- Affected eye fixates laevo,
Right side INO, extra innervation sent to affected MR, as a result, excessive innervation of contralateral LR,
- The convergence system is being innervated at the same time so abducting nystagmus

107
Q

INO

A

FT - XOT OR XOP in primary gaze, bigger in affected MR, starts off with saccadic movements being affected

Causes - MS <50Yrs,
50+ - Vascular,
UNIlateral - Old px, small vessel occlusion (vascular)

DD -

  • Myasthenia Gravis - check for fatigability, involvement of vertical muscles, see if Tensilon helps
  • Duanes

Investigation
VA - If MS cause: see less spatial frequency, CV defects, due to optic nerve demyelination
CT - XOT/XOP
Motility - MR underaction when abducting nystagmus
if space occupying lesion - adduction deteriorates

108
Q

One and a half syndrome

A

Unilateral INO - same side horizontal gaze palsy

  • lesion in PONS: affects PPRF(responsible for saccades) AND MLF
  • MR in each eye and affected LR not innervated

ft

  • Only horizontal movement is Abduction, (LR is normal)
  • If left sided PPRF lesion, head turn to left, causes right eye to abduct (fixing it)

Cause

  • Vascular
  • MS
  • Space occupying lesion
109
Q

Management of intraocular disorders

A
  • Refer to HES, they will find cause.
  • Teaching Central head position to maximise movements
  • Prisms for diplopia, occlusion of incomitant
110
Q

Supranuclear disorders

A

Isolated supranuclear motility disorders result in palsies of conjugate movement systems. This can effect multiple movement systems

Lesion for supranuclear motility RARE, can affect nuclear and intranuclear components req for eye movement. As a result, mixed poor motility disorders DIPLOPIA

Eye movements
saccadic, pursuit, vergence, optokinetic, vestibular ocular reflex

  • Saccadic - fast eye movements. Voluntary or involuntary. Visual, audible, tactile stimuli.
    Responsible for fast components of optokinetic nystagmus
  • Pursuit - stable eye tracking, combined eye and head. Counteracts slow movements of target which may destabilize retinal image
  • Vergence - maintain binoc alignment, BS
  • Vestibular and optokinetic - maintain stable retinal image in head movement

Conjugate eye movements, the anatomical pathway

  • X Saccades -
    1) frontal eye fields
    2) Supplementary eye fields
    3) Parito-occipital cortex
    4) Superior colliculus
    5) Cerebellum
  • Vertical saccades -
    1) Bilateral frontal field stim
    rostral interstitial nucleus of medial longitudinal fasciculus (riMLF)
  • 3&4CN
  • Smooth Pursuits -
    1) Started in visual cortex
    2) parieto-occipital cortex
    3) frontal fields descend fibres to doral pontine nuclei
    4) info relayed to cerebellum then sent to 3,4,6CN
  • Vergence -
    1) pathway not confirmed
    2) striate cortex, responds to image disparity
    3) signals sent to mesencephalic reticular formation, then converge round 3cn
  • Vestibulo- ocular reflex -
    1) mediated by: semi circular canals, otolith organs, saccule and utricle in ear, 8CN
  • Optokinetic -
    Maintain stable retinal image while head and body moving, non confirmed pathway
111
Q

Supranuclear gaze palsies

A
  • Saccadic palsy - Accident in frontal lobe or space occupying lesion,
  • Lesion in right front eye field, loss of saccades in left OKN
  • Ocular motor apraxia - Inability to do horizontal saccades, head thrusts used to initiate (CONGENITAL)
  • Smooth pursuit palsy - vascular accident or tumour in parieto-occipital lobe.
  • Smooth pursuits replaced by small amplitude saccades (cog wheel)
112
Q

Horizontal & Vertical gaze palsy & types

A

Horizontal gaze palsy -
Unilateral - damage to VIN nucleus, severe damage to LEFT PPRF, so eyes cannot move to left.
Cause = MS, Vascular accidents, space occupying lesion

Vertical gaze palsies
Bilateral supranuclear control
- Lesions in riMLF, and nucleus of Cajal
- Saccades, smooth pursuits, affected
- VOR reamins normal unless lesion affecting brainstem CN8

Parinaud’s syndrome

  • Initially saccadic up gaze
  • loss of up gaze smooth pursuits
  • Finally loss of down gaze saccades and smotth pursuits
  • Convergence and retraction ‘nystagmus’

Cause - Pineal gland tumour is most common cause

        - Vascular accidents in rear midbrain
        - Papilloedema

Parkinson’s Disease - Usually up gaze lost or impaired, slow saccades, convergence insufficiency

investigation
H/S, ASSESS ALL 5 SYSTEMS, VA, VF, PUPIL REACTIONS

113
Q

nystagmus, what, types

A

Nystagmus in a constant, involuntary, oscillation of the eyes
• One component of the oscillation is a slow phase drift away from the assumed
position of gaze
• The other component is a fast phase that returns the eyes to the initial position
of gaze

Physiological, acquired, early onset

114
Q

Physiological nystagmus

A

Normal healthy adult,
Optokinetic Nystagmus - used to minimise retinal slip triggered by larger moving stimuli. Can be triggered with OKN drum

End point nystagmus - Extreme positions of gaze

115
Q

Early onset nystagmus

A

First few months of life or trauma/tumour

1) Latent nystagmus - 1 eye closed/covered, beat direction to fixating eye.
If RE occluded, both eyes beat to left
If LE occluded, both eyes beat to right

2) Spasmus nutans - in first yr
High freq, low amp nystagmus with:
AHP and irregular nodding
Resolves spontaneously in 2 yrs

3) Infantile nystagmus -Constant horizontal
First 6 months and persists
aetiology unknown
ERG, VEP, OCT req, hospital

116
Q

Infantile Nystagmus

A
  • Waveforms - pattern of eye movement, varies between px’s and different gaze angles
    Jerk - slow away from fixation, fast corrective
    Pendular - equal slow movement velocity

FT of waveform

  • Amp - degrees, extent of movement
  • Freq - no of beats
  • Foveal period - area when eye velocity is min and VA is maximal

Null zone - Gaze angle where nystagmus is nullified

  • 10 Deg of primary position common, hence precise head posture to facilitate this. Espec if more than 20 deg outside
  • Convergence reduces the nystagmus usually
  • VA most comfortable in this position

Oscillopsia - Perception of world moving back and forth, most px dont have

  • May get when tired/ill
  • More likely to be in acquired

Physiological factors, head shaking

  • Change dependent on fatigue & attention, stress, anxiety
  • Some px oscillate head, inc w intensity then trying to focus

Rx -
- High rx, usually myopic, WTR astig, inc w age

Idiopathic - All other causes ruled out
Common eg - high ametropic w strabismus without pathology is still idiopathic

117
Q

Acquired Nystagmus

A

Pathological may develop from disease, injury to vestibular or CN

eg - MS, stroke
prompt referral if suspected - neuroophthalmological exam
URGENT ref first time

FX -
asymm eye move
signif vertical component
oscillopsia
saccadic oscillations without slow phase
118
Q

Recording and testing

A

Recording
Eye tracking -

H/S - How long, oscillopsia?, History of strabismus, FOH
Assess - inc w occlusion?, sym?, direction changes dependent on which one covered, head shaking, convergence reduces nystag, null zone?

Testing
no phoropter
use null zone
wide aperture lenses
give time
Fog and do Binoc rx instead of monoc
CT may be dificult
119
Q

Management

A
  • Oscillopsia (illusory motion of world), reduced VA early onset
  • Social and emotional difficulties
  • May want reduction for cosmesis
  • TREAT, CORRECT, MINIMIZE INTENSITY

Hospital first, low vision assessment, support awareness (nystagmus network)

1) Latent Management
- RX, surgical alignment - can turn it into
LATENT LATENT NYSTAG - improving BV
- Surgical alignment of AHP
- special consideration - worsen w patching, atropine instead

2) Acquired nystag management -
all of the IN points, but may be a result of pathology, so if suspected then immediate referral.
Botulinum toxin - temp muscle paralysis, less oscillopsia for 13 weeks.

3) Infantile management
- Lifelong but we can reduce
- full rx, good dispense, mark AHP caused by null zone. Eccentric point will induce prismatic effect and aberrations
- CL - less periph aberrations and prismatic effect

  • Prism therapy - allow px to see null point of gaze whilst not physically looking there
  • eccentric positions, high prism, heavy
  • alternative fresnel stick on, but looks bad
  • If convergence null zone, BOUT
  • if divergence null zone, BIN
  • this aids AHP and recover neck pain/prevent
  • Surgical
    1) AHP correction
    2) Treat assoc strabismus
    3) Improve visual function

severe surgeries
1) – Kestenbaum surgery - move null zone to primary gaze, reducing AHP. Recession and resection of rectus muscles

2) – Artificial divergence - for convergence induced, this surgery can induce exodeviation.
3) – Recession of all horizontal recti - reducing lever arm of muscle action. Recessions of 4 horizontal recti
4) – Tenotomy and reattachment - modify proprioceptive loop in muscles, broadens the null zone. severing horizontal recti at muscle insertion then reattachment at original site
5) – Combination surgery - comb of above procedures, while correcting strabismus

120
Q

Pharmacological management of strabismus

A
  • Memantine & gabapentin - reduce nystag and improve VA
  • Dexedrine - increase foveal duration, stereopsis, and improve VA
  • Brinzolamide - improve waveform
121
Q

Examination of children

A

H/S - reason, sx, ocular history, medical history, birth history, lifestyle, educational details

Key q's
Difficulty seeing tv?
Difficulty reading?
Does child have visual habits?
Does child rub/blink often?
Squint?
  • School
    progress at school well?

5 birth q’s - was it difficult

122
Q

Age groups for examination

A
  • Up to 9 months
    address child as well, friendly environment, dont spend too long on each task
  • 9 Months to 3 years
    Stranger fear, prevent distraction, may need several appointments
  • 3 to 5 yrs
    Greater H/S involvement
  • 5 to 11 yrs
    School related questions more signif
    Ask child questions
  • 11 to 18 yrs
    Like adults, may want specs
    Px confidentiality

-

123
Q

Assessments

A

Acuity - monoc and binoc for children
CT - D & N, interesting target

Rx - ret, cycloplegia,
In infants - hand held lenses and hold fogging, small pd so can hold both with 1 hand
Slightly older - paediatric trial frame

1) static ret - distance fixation target and keep
talking, use interesting target, ie toy
If asleep, hold eyelids open and perform

2) Dynamic ret - put target at wd, should be neutral here, maybe a small with.
Lag of accom between 0.25 and 1.00D
D corrected
If greater lag, uncorrected hyperopia which requires correction.
Diff in lag between eyes = uncorrected anisometropia
Diff in lag between merid = astig

3) Mohindra technique
Dark, near fixation ret, 50cm, occlude one eye at time.
-1.25D taken away from result, Mohindra derrived this.
less accurate for high rx

Subjective
little until 4 - 6 yrs, keep simple
+ lenses until reduction in VA
large dioptric intervals intially and then small ones to clarify

 - Autorefractor
older children
size can scare children
Can use a hand held autorefractor
power refractor - +5.00 to -7.00D
124
Q

Cycloplegia

A
  • Cycloplegia
    essential:
    low acuity, low stereopsis, strabismus, SOP unstable, amblyopia, hyperopia, eye turn, anisometropia, poor accom, poor cooperation, argue the need even if they dont have any of this list.

Pros
latent hyperopia reveales
aids fundus exam

Cons
risk of AR
photophobia
distress when installing
reduce near ability

CN - pupil size before and 10 mins after, rresidual accom <2D

PROCEDURE
end of exam before fundus
do non cyclo ret first
consent req
cycloplegic drug
px sit until max effect
ret

Which drug
cyclopentolate 0.5 ( >12 yrs and <3 months) &1% (<12 yrs)

AR - restlessness, drowsy, disorientation, rare allergy

125
Q

Paediatric ocular exam

A
- External eye:
 Orbit and facial symmetry
 Head posture
 Eyelids
 Sclera
 Conjunctiva
 Cornea
 Iris
 Pupils 
 Lacrimal apparatus
126
Q

specific aspects

A

Pupils - Neonatal, small, poor to react until 3 months, iris permanent colour by 12 months
- Red reflex via Bruckners - 1m from oph and
look for asymm between pupil size
brightness and colour, compare reflexes
seperately at 30-40cm.

Slit lamp - 
Anterior seg
trans illumination detects albinism
cataract type and pos
infants - held by parents
toddlers - parents lap
children - standing

Internal ocular health -
Combination of direct and indirect ophthalmoscopy

Indirect ophthalmoscope -
open babies eyelids, quick glimpse then lid squeeze
- +20D lens – useful overview of fundus
- +28D – wider field of view
- +14D – greater detail
- disadvantage of bio is bright and dilation

127
Q

Further aspects paed oc exam

A
  • Abnormal blinking, eye closure -
    unilateral closure - learnt
  • Excessive blinking - usually benign
  • Large phoria - blinking to control
  • Blinking Tic - onset between 6 to 10 yrs, lasts up to a yr
  • Child who closes 1 eye
    • acute - eyelid swelling, watering, photophobia
    • long standing - Tics, intermittent XOT, diplopia
128
Q

Exam under anaesthesia - paed

A

Ocular examination
Refraction

IOP - lower in children
Neonates - mean approx 9.5mmhg
5 yrs - mean 14mmhg

   -Tonopen - anaesthesia, portable
   - Icare - no anaesthetic, good for non compliant 
                 px

Keratometry
Corneal diameter
Contact lens fitting

Burton Lamp with fluorescein
- red eyes, cl patient, give parent torch to take home

If no pathology, check for:
reduced vA
if alert
if fixate at light
unexplained visual loss
ocular albinism
colour vision testing
129
Q

Paediatric optom

A

Uncorrected Rx may interrupt normal visual development
1 yr old - >3.5D hyperopia in 1 merid
4 year old - >2D hyperopia in 1 merid
1-4 yr olds with increasing ametropia.

Emmetropisation generally complete by 6 years of age

Controlling myopia
pharm- atropine, pirenzepine, 7 MX
specs - PALs, bifocals, single vision
CL - ortho-K, multifocal
Behavioural - time out doors 
Effects of lenses
positive lenses 
1 - retinal blur
2 - myopic defocus
3 - eyegrowth slows
4 - induced hyperopia
Negative lenses
1 - retinal blur
2 - hyperopic defocus
3 - eyegrowth increases
4 - induced myopia

Near work
hyperopic blur drives elongation

Myopic correction trial (COMET)
- reduced progression with PAL 0.2D

Hyperopia, astigmatism and anisometropia – correct
if asthenopia, difficulties with reading, headaches,
reduced VA.

130
Q

Bifocal and prismatic bifocal specs

A

Clinical trial
prism had minimal effect on progression
Progression (D): SV- 1.55; Bifs - 0.96; Bifs/PC - 0.70

131
Q

Myopia control

A
  • Correct central myopia with standard lens
    1) hyperopic blur peripherally
    2) Acts as stimulus for axial growth
  • Correct central myopia and induce periphery myopic blur.
    1) No peripheral stimulus for growth
132
Q

Myopia in practice

A

predicting who will become myopic

  • < +0.75 at 8 yrs
  • SOP at near
  • large accom lag

Advise

  • Myopia control - multifocal soft CL
  • encourage reading distance
  • encourage reading breaks
  • outdoor play for 2 hrs a day

Contact lenses:
Dual Focus: MiSight, CooperVision
Two correction zones (refractive correction)
– Two treatment zones (2.00D myopic defocus)
NaturalVue - Extended depth of focus lens
• Increase in plus power
towards periphery

Orthokeratology - slow myopia progression

SPECS
myosmart - 50:50 D:N ratio, 2 year myopia control effect:
59% refraction,
60% axial length

Essilor - Relative positive power micro-lenses arranged in concentric rings around a clear central area

133
Q

Children with disabilities

A

wider range of Rx
May not emmetropise
Monitor frequently
prepared to prescribe earlier

134
Q

review of controlled trials on visual stress

using Intuitive Overlays or the Intuitive Colorimeter

A

coloured filters lack evidence?
study shows methods of prescribing coloured filters

20% experience visual stress -
perceptual distortions, headaches, and eyestrain

when viewing repetitive patterns, it improves reading performance in people with visual stress
BUT NOT DYSLEXIA

RESULTS
- FOR VISUAL STRESS, INTUITIVE OVERLAYS REDUCED IT

limitations
- recruitment strategies are based on participants experiencing reading difficulties or dyslexia. Not so much VS

  • diagnosis of VS needs further research. Few diagnostic processes have perfect sensitivity
135
Q

Emotional Impact of Amblyopia

Treatment in Preschool Children

A

Overview - emotions of children undergoing active treatment for 177 children of monoc visual impairment
Starting at 4 years

Method -
5 categories of px:
receive either glasses with or without patches, glasses alone, or treatment deferred for 1 year.

A questionaire was sent on 3 topics:
1. The experience of treatment for the child and family
2. The child’s general well-being since diagnosis
3. Possible psychopathology associated with amblyopia treatment
Each was a rating out of 5
questionaire given out 3 times: before, after,
There were less replies as time went on, with drop outs to patching etc

3 hours of daily patch wear made it more flexible

Limitations

  • Most parents reported having difficulty with patching their child, children were unhappy with patching
  • Those with dense amblyopia had less compliance
  • Harder to patch those of 4 years, some saw as punishment and damaging to relationship

Conclusion
Hard to implement, but no impact on the child’s global well-being or behavior. No severe emotional distress

136
Q

Randomized Clinical Trial of Treatments for

Symptomatic Convergence Insufficiency in Children

A

4 groups for testing
1) Home based pencil push up
2)home-based computer vergence/accommodative therapy and pencil push-ups
3)officebased vergence/accommodative therapy with home reinforcement
4) office-based placebo therapy
with home reinforcement
221 children, aged 9 to 17 years, >4D EXO

therapist contacted the patients by telephone on
a weekly basis to log and motivate

follow-up visits were conducted after 4 and 8
weeks of treatment

Results
3 was the lowest (best) and improved near point of convergence and positive fusional vergence. 73% improvement
All showed improvement

CONC
3 - near point of convergence and positive
fusional vergence and a greater percentage of patients reaching the predetermined criteria of success

limitation
12 weeks- short duration
control group with no treatment not included

137
Q

In-school eyecare in special education settings
has measurable benefits for children’s vision
and behaviour

A

Comprehensive in school eye care benefits children in terms of visual status as well as behaviour.

200 pupils, some with learning difficulties, tests and dispensed in school
visual history and status, behaviour, records reported before and after (2-5 months) by teachers

Results
Large range of ametropia was found (32%)
- Almost half presented visual deficits which were unidentified
 - Classroom engagement increased
 - VA improved

Conclusion
huge benefit etc, helps engage with learning material…

CN

  • majority who had underaccom had a previous eye exam but wasnt reported. Optoms need to be more thorough
  • A lot of spectacle wearers failed to bring them to school
  • Environmental changes advised as problems which could not be resolved.eg CS