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
What is vision screening? and why do it?
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
26
Community screening, what ages
- 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
27
Community screening tests
- new born and 6-8 months- red reflex, corneal light reflex, inspection of eyes - VA - Power refractor - City Vision screener for school
28
City vision screener
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
29
Impacts and Consequences of vision screening
- 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
30
What is convergence?
- Coordination and simultaneous inward movement of the eyes. - Does not happen in isolation. - Accom essential for Binocular Visual acuity
31
What is accommodation?
- Ability of eye to focus dioptric power to obtain a clear image. - Does not happen in full isolation - essential for BV at near
32
Convergence insufficiency and cause and sx. order of correction
- 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,
33
Test for convergence insufficiency, and exercises
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
34
Convergence insufficiency vs convergence weakness/exophoria
- decompensated exophoria does not deduce convergence
35
Convergence paralysis, cause, sx, signs
- 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.
36
Accommodative insufficiency, cause, sx
-Inability to maintain adequate accommodation for comfortable NBVA -half of cases with AI have CI sx - blurred vision at near, asthenopia, micropsia
37
Accommodative Fatigue, what is it, cause, sx
-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.
38
Accommodative Infacility, what is it, cause, sx
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.
39
Accommodative paralysis
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
40
Convergence/Accommodation spasm, what is it, the muscles affected, causes, sx
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
41
Test for diagnosis of accom anomalies
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 ```
42
Dyslexia, cause, diagnosis, signs and sx, perception
unknown cause diagnosis by psych signs - closing and covering 1 eye, excessive blinking sx - headache, eye ache perception - move n float, blur, wobbly print
43
Visual factors which correlate with dyslexia, testing, improving, pattern glare
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
44
Visual stress in dyslexia and colorimetry
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
45
What is amblyopia? Types, when does it develop
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
46
Treating Amblyopia, pros and cons,
Pros - Better VA in this eye - if good eye damaged, then backup available Cons - BVA already good - may develop abnormal BV - may not work
47
Investigation of amblyopia and explained. how to test
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
48
Eccentric Fixation, process
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.
49
Amblyopia, steps for management, factors to consider
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
50
Refractive correction for amblyopia, occlusion therapy, MOTAS
- 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
51
Penalization, what is it, types and fogging method
- 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
52
Atropine advantages and disadvantages
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 ```
53
Other methods for treating amblyopia
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
54
What is accommodative Esotropia, how, ft, management | intermittent accommodative primary esotropia
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
55
Partially accommodative ESO | constant accommodative primary esotropia
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
Partially accommodative ESO | intermittent accommodative primary esotropia
Management - specs full time full rx, cycloplegic, bifocals, fresnel prism incorporated lens - botulinum toxin, cosmetic. repeated injections req
57
Non accommodative esotropia, types
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
Nystagmus blockage syndrome
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
Acquired non accommodative ESO
``` 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
Myopic Esotropia
CARRY ON LATER W THIS LEC
61
Intermittent distance exotropia, types, FT, Investigation, true vs simulated
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
Intermittent and non specific EXO, correction, monitoring, management
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
Near Exotropia, types, FT, management
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
Constant exotropia types, FT, management
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
Secondary Exotropia, FT, management
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
Residual Exotropia, what is it, management
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
Consecutive exotropia what is it, management
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
Sensory changes in strabismus
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
Mechanisms for ARC, Factors influencing the development of HARC Detecting HARC HARC management
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
Binocular sensory adaptation to strabismus
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
Modified mallet OXO for suppression and HARC
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
Microtropia, ft
- 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
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Primary Microtropia types
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
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Investigation of Microtropia
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
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Management of microtropia, Eccentric Fixation
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
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Eyecare for special needs, criteria, categories, early diagnosis and management, testing SEND px
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
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Examining with SEND
- 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
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Patterns as a result of vertical muscle action
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
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Alphabet Patterns, what is it, explained by, diagnosis
- 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,
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Patterns as a result of horizontal action
– 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
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A and V patterns as a result of anomalies
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
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Detecting and measuring alphabet patterns, why are they important?, treatment, surgical principles
- 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
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Hess test, How to perform
- 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
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Incomitant strabismus
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.
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Anomalous head posture in Incomitant strabismus
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
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Classification of incomitant strabismus
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
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Investigation of incomitant strabismus
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 ```
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Neurogenic Vs Mechanical strabismus (DD)
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
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Neurogenic strabismus, what is it, CN affected, FT, causes
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
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Causes of 3rd CN palsy, Complete, incomplete, ft, management, single muscles
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 -
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Cause of 4CN Palsy
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
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Causes of 6CN Palsy
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
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Investigation of neurogenic strabismus
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 ```
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Myogenic Palsy
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 ```
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Myasthenia Gravis
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)
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Chronic Progressive External Ophthalmoplegia
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
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Orbital Myositis
- 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
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Rhabdomyosarcoma
Highly malignant tumour of striated muscle px - young, squint, motility restriction, if rapid growth then PROPTOSIS RAPID DIAGNOSIS KEY Management - radiotherapy, chemotherapy, surgery
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Marcus Gunn - Jaw winking syndrome
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
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Mechanical anomalies, def, eg, characteristics
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 ```
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Duanes retraction syndrome
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
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Browns Syndrome
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
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Blow out fracture
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
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Thyroid Eye disease - Graves disease
- 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 ```
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Internuclear and supranuclear disorders
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
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Uni lateral and Bilateral INO
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
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INO
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
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One and a half syndrome
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
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Management of intraocular disorders
- Refer to HES, they will find cause. - Teaching Central head position to maximise movements - Prisms for diplopia, occlusion of incomitant
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Supranuclear disorders
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
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Supranuclear gaze palsies
- 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)
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Horizontal & Vertical gaze palsy & types
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
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nystagmus, what, types
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
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Physiological nystagmus
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
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Early onset nystagmus
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
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Infantile Nystagmus
- 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
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Acquired Nystagmus
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 ```
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Recording and testing
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 ```
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Management
- 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
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Pharmacological management of strabismus
- Memantine & gabapentin - reduce nystag and improve VA - Dexedrine - increase foveal duration, stereopsis, and improve VA - Brinzolamide - improve waveform
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Examination of children
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
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Age groups for examination
- 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 -
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Assessments
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 ```
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Cycloplegia
- 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
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Paediatric ocular exam
``` - External eye: Orbit and facial symmetry Head posture Eyelids Sclera Conjunctiva Cornea Iris Pupils Lacrimal apparatus ```
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specific aspects
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
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Further aspects paed oc exam
- 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
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Exam under anaesthesia - paed
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 ```
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Paediatric optom
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.
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Bifocal and prismatic bifocal specs
Clinical trial prism had minimal effect on progression Progression (D): SV- 1.55; Bifs - 0.96; Bifs/PC - 0.70
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Myopia control
- 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
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Myopia in practice
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
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Children with disabilities
wider range of Rx May not emmetropise Monitor frequently prepared to prescribe earlier
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review of controlled trials on visual stress | using Intuitive Overlays or the Intuitive Colorimeter
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
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Emotional Impact of Amblyopia | Treatment in Preschool Children
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
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Randomized Clinical Trial of Treatments for | Symptomatic Convergence Insufficiency in Children
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
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In-school eyecare in special education settings has measurable benefits for children’s vision and behaviour
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