~ headache

~asthenopia(fatigue, burning, tearing, aching, pain and pulling)

~photophobia 

~reading difficulty 

~nausea

~motility(diplopia)

Nervousness

~vertigo and dizziness

General fatigue

~distorted space perception

1.5% aniseikonia should result from 1 D of anisometropia 

TF to avoid over correction you should correct at  1% for every 1D of anisometropia

1.decide upon a frame(KEEP EYE SIZE SMALL)

2. make as much change in the eye wire as possibe(vertex distance)

3.change front curve as much as possible if it is effective (stay in a range from +10.00 + 2.00 and now what the lab has available)

4.make thickness changes per D1

5. make bevel adjustments as needed, this allows for differential changes in (vertex)

6.

vertex distance 

***note: contact lenses would be ideal 

Bevel changes only apply to minus lenses

~ decreased VA due to strabismic amblyopia

~decreased VA with crowding / interaction 

~binocular balance would NOT be conducted. Vertical prism may push the image out of the suppression scotoma and it is not clear what sensory response would be for each.

~it is a difficult percept for the patient

~ strab angle will manifest when both eyes are open so if the px has a large angle strab then there will be off axis error and prisms will be needed to compensate

~**** with an esotrope you need to find full amt of hyperopia, TF cycloplege is necessary

~ DO NOT TEST: 

1. Fusional limits. (*** note: UNLESS the px is intermittent, then test reserves in free space)

2. Fixation disparity(as above for intermittent)

3. Binocular accommodative facility (unless intermittent)

BUT 

Amplitude of accommodation and monocular accommodation facility can be conducted

1. intermittent fusion: (fusion at near and exotropia at distance w. suppression)

2. Suppression: Suppression can be broken down, BUT must be able to provide binocular motor allignment once suppression is broken down

3. ARC: more difficult represents a neural rewiring 

1. Suppression of the whole binocular field:

~viewed as an alternative to HARC

~found in large deviations 

~Deepest at the fovea

~evidenced in worth 4 dot 

2.Suppression in the area between the fovea and the anomalous point of HARC

~a trait of HARC likely pertaining to the remapping process

~seen with 4 pd loose prism test 

~ONLY as a part of the full restoration of strabismus

~MUST BE COMFORTABLE THAT MOTOR FUSION CAN BE RESTORED

~best prognosis is intermittent EXOtropia

~cosmetics: when angles are larger than 20-25pd they are noticable and may drive the desire for correction 

~stereoacuity: Likely underappreciated by those who have it .

possibility that it may be involved in enhancing motor tasks and driving 

depth perception 

TRUE 

~the most important thing is getting the vision increased in the ambylopic eye 

~onset from 0-6 months (differentiate from neonatal  misalignment)

~failure of binocular vision development (a primary strabismus. 

~large angle >30 pd 

~stable angle 

~ANGLE NOT CORRECTED BY HYPEROPIA

~Normal CNS 

~alteration with cross fixation initially 

~A or V in comittancy (overaction of the obliques, but not always)

~treatment: usually surgery(to large for VT)

~Significant amounts of hyperopia >+3.00D 

~high AC/A ratio 

~the typical age of onset is 2.5 years but can be seen in highly hyperopic infants as young as 6-9 months (there are 4 categories listed by evans 1.Full acc'd esotropia 2. partial acc'd esotropia 3. convergence excess 4. Accommodative insufficiency 

1. Fully accommodative: high levels of hyperopia over drive accommodative convergence, usually a high AC/A (but not a requirement), CORRECTION OF THE HYPEROPIA ELIMINATES THE EXOTROPIA, Requires a cycloplegic refraction (cyclopentolate or possibly atropine), should be monitored in infants and preschool children for the development of binocular vision

2. Partially Accommodative: Correction of the hyperopia reduces the angle of the esotropia BUT DOES NOT eliminate it. 

Measure gradient AC/A at 40 cm 

To ensure that hyperopia is fully corrected should atropine be used?

consider treatment with the use of orthoptics or near adds

3. Convergence excess (Strabismus): hyperopia is within normal ranges but the calculated leads to higher AC/A at 40cm than 6m

~correct distance RX especially if hyperopic 

~determine gradient AC/A

~minimum near add to align eyes at near 

~supplememt with orthoptics

4. Accommodative difficulty: Accommodative difficulty such as accommodative insufficiency,  shows low age related amplitudes of accommodation and leads to execessive effort of accommodation. 

~Normal positive angles kappa

Slight displacement of corneal reflexes but the displacement is symmetrical and in both eyes

****NOTE: the relative symmetry btw the eyes is what is impt 

1mm of offset = 22pd

At 6M: divergence excess(high exo), divergence insufficiency(high eso)

At Near: convergence excess, convergence insufficiency

*** Add to this basic eso or exo where deviation is present at both distances

True or false

All strabismus in children up to the age of 6 requires a cycloplegic refraction and a dilated fundus exam 

~cerebral palsy 

~down syndrome 

*** typically not treated due to organic cause 

~more common in women 

~deviation often only manifests at distance with fatigue or inattention

~few symptoms

~Photophobia and closing one eye in bright light 

~Large angle, can be trained with orthoptics 

Near vision exotropia (convergenve insufficiency)

now termed convergenve weakness type 

~Often seen in mid teens where high exophoria breaks down into exotropia 

~diplopia is reported

~orthoptic tx is effective with a negative add

~note AC/A could be low, prism may work due to limited compacity for prism adaptation 

~deviation is found at both 6M and 40cm to a similar degree

~depending on the time of onset and treatment orthoptics are possible

~large angle requires surgery

~Note the frequent association with vertical deviation 

~surgery 

~refractive 

~orthoptics

1. muscle weakening procedures 

~muscle resession: Move the muscle posteriorly 

~Marginal myotomy: Further weaken a previously recessed muscle (ie cut within the muscle itself)

Myectomy: Serve muscle without reattachment (often the most severe approach)

2. Muscle Strengthening Procedures

~resection: shortens muscle, normally recti

~advancement move a previously recessed muscle towards its insertion (this is a correction procedure if the first surgery weakened the muscle too much)

Tucking of a muscle or tendon, usually the superior oblique 

Subnormal binocular vision :

~orthophoria or asymptomatic heterophoria

~Normal visual acuity in both eyes

~fusional amplitudes

~Normal retinal correspondence

~Foveal suppression in one eye in binocular vision

~Reduced or absent stereopsis

~stability of alignment  

Microtropia

~reduced or no stereo

~anomalous retinal correspondence 

~central or parafoveal fixation 

~fusional amplitudes

~mild ambylopia frequent

~inconspicuous shift or no shift on Cover test

~no further tx except ambylopia prevention 

~some stablility of alignment 

Small angle eso or exotropia (<20pd)

~cosmetically acceptable 

~no further tx except amblyopia prevention 

~less stability of angle

~80% have ARC

1. Post operative diplopia (6<weeks)

 3.5%- intractable diplopia

2.Unplanned second operation

typically 6-21% in 10 yrs 

more complicated surgeries can be as much as 50%

3. oculocardio reflex (decrease HR during EOM contraction) temporary

4. sceral perforation 1-2%

1. neurogenic 

2. myogenic

3. mechanical

1. supra nuclear: frontal cortex, pons etc. eye movements are often conjugate but can not move in one direction (ex. vertical gaze palsy, supra and infra ductions are limited)

2. inter nuclear- ex internuclear ophthalmoplegia: effected eye has restricted ADDuction (lesion of the MLF btw CN 3 and 4)

~external ophthalmoplegia limited gaze 

3.Infra nuclear - common nerve palsies, SO LR, NOW patterns btw the eyes differ

~affecting the EOM directly 

ex. myasthenia gravis; 50% have ocular effects 

~more common in chinses than white ppl 

~can mimic neurogenic anomalies 

~ptosis common in ocular cases; cogan's sign is when you hold inferior gaze for 15 seconds then when px elevates the lids there will be a twitch of upper lid b4 ptosis resumes

~Duane's Retraction syndrome 

~MARKED RETRACTION OF THE GLOBE ON ADDUCTION

~More commonly unilateral 

Cause is not clear but a congenital lack of the CN6 nuclei 

type 1: 78% limited abduction, but fairly good adduction(easily confused with LR palsy)

type 2: (7%) Limited adduction, but fairly good abduction (mimics medial rectus palsy, highly unlikely)

type 3:(15%) limited adduction and abduction

Brown's syndrome: The muscl tendon btw the trochlea and its insertion on the globe is too short 

Limits SO relaxation so there is restricted elevation

~can be considered with IO palsy

The deviation becomes relatively more exo with upward gaze

~SO palsy or IO overaction 

The deviation becomes relatively more exo on downward gaze

~IO palsy and SO over action 

~IO palsy will give a positive result for IO with parks 3 step 

~will show overactions of ipsilateral SO and contralteral SR

~INcyclo deviation will be fun 

NOTE: None of these results will be present with Brown's syndrome 

This is when the px can not voluntarily initiate eye movement. (problem lies in the frontal area of the cortex where voluntary/ internally generated eye movements take place)

~px will have to turn head to change gaze 

 raised upper lid due to overaction of Müller’s muscle

~upper lid retraction

lid lag on downward gaze:

Upper lid does not follow the eye fully when changing fixation from up- to down-gaze

Reduced blink rate Poor convergence  

 in cases where the medial rectus is involved

manifestation of lid retraction and proptosis

~staring appearance

Other systemic conditions leading to neurogenic causes

1. diabetes

2. vascular HTN

3. Aneurysms

4. temporal arteritis (brushing hair, wearing hat, extreme pain)

5. MS

6. tumours

1. diplopia

2. dizziness and vertigo 

3. blurred vision especially when CN3 bc ciliary muscle effected

4. other sxs that point to underlying conditions 

5. injuries 

1. compliance(px and parents on the same page 

2. motivation (high motivation can often over come a poor visual prognosis)- intrinsic motivation may be strong for the parent but not the child, keep it fun, be supportive, introduce positive reinforcement 

3. communication of goals (must understand goals and timelines, parents needs to know that training is to achieve BV and may not improve school performance)

4. Preserverance (success will require the px and the practitioner to have preserverance

~later onset of strab >1yr 

~short duration, maybe a partial developmental esotrope 

~family hx 

~intermittent eso or exotrope (<20pd)

~Non ambylopic 

~central fixation

~Normal correspondence

~stable secondary fusion 

~stereopsis 

~good motor fusion 

~comittant 

~accommodative esotropia(refraction gives alignment)

~ensure that the functional non strabismic disorders needed opthalmic/orthoptic tx are managed. Provide refractive corrections and adjusts as needed 

~manage orthoptics on your own or refer to someone who does 

~make sure to rule out secondary organic causes and manage those cases when they arise 

1. manage cases where secondary causes are suspected

2. refer where appropriate for strab surgery

3. treat ambylopia 

4. provide ophthalmic correction for cases of fully accommodative and partially accommodative esotropia

5. manage orthoptics IF: favourable outcome, where motivation is high manage orthoptics for strabismus with less favourable visual profiles, management can ber referral to an orthoptic resources, optometric, ophthalmology

1. crowding 

2. spatial uncertainty(reduced vernier acuity)

3.Motion and direction deficits 

4. problems with shape determination/ differentiation 

***** ambylopia is a much more complex phenomenon than just a decrease in VA ( probably why not every px will react the same way to tx)

1. Congential cataracts (other things that would block sensory info of a clear image, corneal or ptosis) scarring 

2.Astigmatism  

3. anisometropia 

4. strabismus

**** note the first 3 types are considered deprivation and tend to show a dft patterns of visual deficit than strabismic ambylopia  

1. amt of anisometropia 

2. the duration of the uncorrected anisometropia 

****** however reduction in vernier acuity and crowding are reduced in proportion to their acuity loss 

It is amblyopia resulting from high amts of astigmatism in the early years of life.

*** large astigmatism over 2D persisting beyond 2 years of age can cause meridonial astigmatism 

~congential cataracts

~depends on there location, if the cataract is not located centrally there may be no ambylopia 

~the longer the cataract is present and not dealt with the more the VA will decrease

~crowding 

~vernier acuity and spatial uncertainty

~motion

*** in strabismic ambylopia vernier acuity is reduced more than VA

*** in anisometropic ambylopia it is reduced proportionally to VA

*** snellen letter(optotype) is decreased more than grating acuity

***strab reduced vernier and snellen letter more than grating 

*** anisometropia reduces all things in proportion to each other

1. patching 

2. spectacles and binocular vision approach

FALSE - it is actually easier to patch a child with glasses bc you can incorporate the patch into the glasses.

~usually more cosmetically pleasing 

NO more than half the waking hrs of the infant  (Most severe amblyopia)

~becomes the max for all ages now 

~the key is to minimal DAILY patching 

Patching for 2hrs per day showed to be equally effective as 8 hrs four months (pxs may vary)

*** higher # of hrs may get amelioration sooner for lower acuity group 

NOTE: downside of patching is that existing strab will be enlarged or px may become strabismic 

Birth to 7 years 

~the study showed no dfce btw 3-7 years, but after 7 years there was a decrease in successful patching 

~stereoacuity change correlated in change in VA

~deprivation ambylopia, nystagmus, strabismus and glaucoma

~autosomal recessive, can be associated with metabolic errors such as galactosemia etc and numerous congenital conditions 

1. There are changes within the brain activity with age. This gives rise to a critical period

2. loss of non amblyopic eye releases the inhibition previously placed on the ambylopic eye 

3. perceptual learning 

4. video gaming 

5. pharmacology 

1. where the cataract is located (centrally or peripherally)

2. how long was the cataract present b4 it was removed

1. cataract

2.unilateral infantile esotropia

3. large anisometropia 

4. high levels astigmatism 

The impact of these factors depend on:

~time the disruption occurred(3 weeks, 6mos etc)

~depth of disruption (strab vs anisometropia)

~whether the impact varies significantly btw eyes 

1. The degree to which the disruption can be removed

2. whether normal VA development existed before the disruption 

3. congenital vs later on in development

4. constant unilateral esotropia vs accommodative esotropia 

~bilateral cataracts 

~high astigmatism in both eyes

**** the impact is much greater when it is monocular. The VA dfce btw the 2 eyes tends not to be too large. BUT the problem is that the VA is lower in both eyes  

1. perception

2. visuo motor skills

3. spatial cognition 

4. attention

5. Decision making

~can only experience it when there is a filter on the non amblyopic eye that cause the CSF btw the eyes to be equal 

Px with normal BV the binocular summation would be the sqaure root of 2 

BUT in amblyopia(w. filters) there is NO binocular summation so the value can only be as high as the best eye tf =1 

1.Refraction: Now becoming the first step prior to patching. Allows binocular vision certainly in anisometropia 

THEN try 

2.patching 

3. penalization 

4. binocular training (where a balance is achieved through the contrast reduction of the preferred eye)

TRUE

*** in all cases of amblyopia px should be fully corrected BUT in some more complicated cases there many need to be patching etc 

1.single and crowded VA's 

2.Cover testing comittancy

3.sensory measures of binocularity; stereo acuity, suppression both foveally and peripherally 

4.in anisometropic amblyopia measure the amt of aniseikonia 

NOTE **** Follow up changes in refraction every 6 months in pre school children and younger 

Infants 3-4mos 

3-7 yrs showed better results than 7 -13 yrs 

But there was no dfce btw 3 yr olds and 7 yrs old responses

In order to attain a good prognosis when must a unilateral cataract be removed/operated on in a child?

bilateral?

unilateral must be removed by 6 weeks 

bilateral must be removed by 10 weeks

Correct with size lenses

**** there is increasig prismatic effect as you move away from optical centre

M: most minus lens

P: least minus lens 

~Goal Increase mag of M, decrease mag of P

~POWER FACTOR(has a bigger impact on -ve lenses than it does on +ve lenses)

~Moving M relatively closer to the eye, do this by altering the bevel

~decrease vertex(h) both eyes 

~decrease eye size which decreases S2, which will reduce h for both lenses

Manipulation of shape

flatten D1 of M, steepen base curve of P

increase the thickness of M and decrease the thickness of P (may not be realistic)

P: more plus lens, M: more minus lens

~decrease mag of P, increase mag of M 

power factors:

~adjust so that P moves closer to the eye and M further away 

~reduce vertex distance 

~decrease eye size (which decreases S2, which decreases h)

shape factors:

flatten D1 of P, steepen base curve of M 

~decrease thickness of P and increase thickness of M 

~ there optical properties of the spectacles

~their ability to adapt to mag dfces btw the eyes both static and dynamic