Microtropia

"A misalignment of the eyes with an angular deviation so small (less than 5 degrees) that it would usually be controlled except on dissociation of the eyes, in which case it becomes a phoria."

• Cosmetically fine and eyes work 'almost binocularly' (see later)
• Often no movement seen on cover test
• You could call it a strab that is 'perfectly adapted' - the EF and ARC are at the same point

Characteristic Features

• Freq presents betw 2-3 yrs but may be found later in life when VA in one eye slightly low
• Often made evident by crowding phenomenon
• Presence of HARC in small angle strabismus is assoc w/EF and amblyopia
• Normally ESO, EXO is rare

General Characteristics

• Small angle (less that 6 prism dioptres)
• Usually 1.50D anisotropia or more
• Amblyopia but usually reduced VA to 6/9 or 6/12 only
• EF always occurs. ANGLE OF ECCENTRICITY = ANGLE OF STRABISMUS thus no movement on cover test. The area on which the image falls in binocular conditions is the same as the eccentrically fixing area
• Harmonious ARC - retinal area where img falls in px's habitual vision = anomalously corresponding area = area used for monocular fixation = "Microtropia w/identity"
• Peripheral fusion which helps eyes to maintain their straight position
• Monofixation Syndrome: in many cases the angle of deviation increases on alternating CT or if one eye is covered longer than usual giving an ESOP superimposed on the microtropia.
  
• Stereopsis - low grade reported

Investigation & Diagnosis

• VA: presence of amblyopia in one eye is usually the first clue. Crowding phenomena present and letters on chart might be missed due to the central scotoma.
• FIXATION: EF (check using ophthalmoscope) present and may be assoc w/ ARC. Will be either (1) EF = angle of anomaly giving no shift on cover test or (2) EF doesn't equal angle of anomaly giving a shift w/CT
• CVR TEST: May find esophoria but not usually a strabismic movement
• 4D PRISM TEST placed before dominant eye - img moves across the retina and the eye moves to take up fixation. The non-dominant eye moves laterally (Hering's) in the same direction as it is not fixing so a VERSIONAL movement is seen and another recovery one when the prism is removed. If you put the same prism in front of the non-dom eye then there won't be any movement at all as the image has been moved across the retina and within the suppression area.
• AMBLYOPIA + NO CT MOVEMENT + POSITIVE 4BASEOUT TEST = MICROTROPIA
• BAGOLINI: Should get HARC - streak passes thru spot with or without a suppression gap.
• AMSLER: Scotoma may be demonstrated due to the EF

Classification of Microtropia

• Primary - remains constant throughout life and is rare
• A primary microtropia which become decompensated particularly between 1-3 years as a result of an accommodative element or superimposed phoria
• Secondary - optical or surgical correction of a concomitant strabismus

Lang's Classification of Microtropia

• Central Fixation
• Eccentric Fixation w/ARC where ang. of anomaly > degree of eccentricity
• Eccentric Fixation w/ARC where angles are the same

First two will show up on cover test. Third one gives a sensory adaptation to the deviation.

Eccentric Fixation

A failure of the eye to take up fixation with the fovea and using some other point on the retina instead. In strabismic patients this is only seen when the better eye is covered (unless the patient has microtropia with identity).

Between the two eyes there is 'relative localisation' which is based on each receptor having its own 'local sign' which determines the direction of objects in visual space. It's localisation with reference to each eye separately. In eccentric fixation the relative localisation could be normal or abnormal at the eccentrically fixing point or normal/abnormal at the fovea of the same eye. Usually if the eccentric point continues to be localised eccentrically and the fovea centrally then patients describe objects as being slightly to one side and this is known as eccentric viewing. This has a better prognosis for treatment that if the localisation is abnormal.

How EF is investigated

EF is nearly always present in strabismic amblyopia. The best way to investigate it in practice is with the ophthalmoscope w/the graticule on. If you get the patient to look straight into the light at the centre of the target the position of the fovea relative to that target can be noted. In esotropia the EF is usually slightly nasal. You can get a relative measurement by using the scale. NB graticule disc is 5x7 degrees. You induce accomodation using this method so cycloplegia/changing focus is useful.

The past pointing test involves touching the px's finger to the tip of a pen 25cm away, first with the good eye to increase confidence, then with the good eye occluded. If the patient's finger goes slightly to one side of the pen this indicates fixation doesn't coincide with the centre of localisation. The corneal reflexes can also be assessed by occluding one eye in turn. Relative displacement of the reflex in the bad eye by 1mm = about 11 degrees or 20PD. This is a gross test as eccentricity isn't usual that great. Other tests include the Bjerrum screen, Amsler chart, after image transfer test, Haidinger's brushes, acuity measurement and ND filters. The speed of accommodation is much slower in EF but also slower in other amblyopes.

Treatment of EF

As w/amblyopia treatment you have to encourage foveal fixation. Treatment of EF isn't done often and is far too time consuming for a mild effect.

• Direct occlusion alone may improve fixation but often a slight eccentricity remains
• Pleoptic treatment desensitises the eccentrically fixing area
• After-image transfer is used to locate foveal fixation

NB Established EF is real hard to remove. In amblyopia treatment VA won't improve beyond that expected for an eccentrically fixing point.

Critical Period In Humans

Von Noorden (him again) demonstrated that human amblyopia was accompanied by structural changes in the visual pathway. The LGN of a human amblyope was examined and cells in the parvocellular layers innervated by the amblyopic eye were about 18% smaller than the equiv from the other eye. The decrease in size was more pronounced in the layers receiving crossed fibres (1,4 and 6)

Preferential looking techniques have been used in thee past to monitor VA and stereo in both human and monkey infants w/convergent strabismus. Recent studies suggest VA is originally equal and coarse stereopsis is present. If strabismic infants below 2 are tested wearing prisms to correct the deviation then coarse stereopsis can be demonstrated but it can't without the treatment. The deviating eye doesn't actually develop amblyopia until after 6 months of age. Esotropia can be detected early w/a cover test.

Few deficits lead to amblyopia before six months of age. Emmetropisation sorts out refractive errors as long as they are modest within 6-12mths. An Rx needs to be persistent for two years or more from an early age before a permanent VA deficit occurs.

Cataract and other forms of stimulus deprivation (ptosis?) have a much more severe effect than anisometropia/astigmatism over a shorter period. If your baby has a congenital cataract then it needs to be removed pronto and the removal needs to be followed by a period of vigorous therapy. Weeks of deprivation can have a substantial effect between 6-18 months and months of dep can have an effect until 8 years of age.

In strabismic patients amblyopia and binocular function (w/stereopsis) must be considered. Amblyopia doesn't seem to develop in congen. esot until close to 1yr of age. Acuity differences didn't exceed normal limits until 9-11 months. The period of peak sensitivity lies between nine months and two years and then sensitivity declines until around the age of 8. Stereopsis in untreated esotropes is crude at best. If it's at worst alignment before 1.5 years can get it up to the dizzy heights of 'very crude'. Alignment after 1.5 years of age won't provide stereoscopic vision.

Occlusion therapy is the most common therapy in the treatment of amblyopia but its efficacy is unknown. Not good really. Retrospective studies have shown that 50% of patients show a marked improvement in VA following occlusion. These outcomes were independent of age. Occlusion must be administered with care to avoid the dreaded 'reverse amblyopia'. If the good eye is patched 50-70% of the time and both eyes open the rest of the time it can be avoided. The critical period for the cure of amblyopia seems to be longer than the critical period for its creation.

Summary

3 periods of development in the visual system

• Prestereoscopic (0-4 months) - acuity develops and direction and orientation specificity are refined
• Onset of Stereopsis (4-6 months) - stereopsis goes from zero to adult-like levels within a month at the same time as ocular dominance columns segregate
• Poststereoscopic (6-24 months) - acuity continues to develop

Restoration of BV may only be possible in the first 18 months of life although less dramatic improvement may be seen in px up to 3.

Restoration of VA depends on who you ask; Von Noorden thinks it's only really successful up to 5 years and Birbaum thinks 16! Experience suggests <6>10 little success.

Animal Studies of Abnormal BV Development

Studies have been limited. Well, not that limited but you can't just patch a babies eye, ruin its BV and then kill it to assess how the visual cortex has developed. It's not allowed. You can do it on cats and macaque monkeys though! That's probably still against many people's wishes but ho hum. Hubel and Wiesel did the most famous early work. Here's what they found w/cats

• VC of neonatal kitten possesses at least the skeleton of organisation present in adults. Orientation columns are present even before the eyes are opened but they subsequently become modified by experience.
• Disruption of binocular input via unilateral eye closure, alternating eye occlusion or artificial strabismus completely disrupts cortical binocular interaction
• Complete binocular deprivation actually has less effect than two monocular ones. It doesn't abolish visual responsiveness with the finality that monocular dep does.
• The physiological effects of abnormal visual experience are mostly confined to the cortex and aren't expressed to any great degree in the LGN. Changes in the LGN are probably due to suppression of the bad eye which in turn alters the neural connections between cortex and LGN.
• The effects of abnormal vis.exp. are only obtained during the moggy's critical period early in its life
• Short periods of occlusion produce severe changes, longer irreversible. When the cat reaches visual maturity, boom! Permanent changes!

The visual system is more plastic and stays more plastic at higher levels of processing. The retina is pretty much hard-wired but the output layers of the primary visual cortex are relatively very plastic indeed! Hubel and Wiesel also saw (when they used monkeys) that the critical period in the visual cortex for the magnocellular system ends earlier than that of the parvocellular system. When reverse suture was done at 3 weeks of age the open eye can reverse the effects of the initial deprivation for the parvocellular system but not the magnocellular system.

Critical period for monocular deprivation in cats starts at 3 weeks, monkeys soon after birth, peaks at one month and ends in one year. It's 0-3 years in humans. The critical period for ocular dominance changes starts soon after the eyes open and continues until some time near puberty.

The peak of the critical period for ocular dominance occurs when ocular dominance columns in V4 (which receives equal input from the right and left eye) are segregating and cells sensitive to disparity are being formed. These crucial peaks:

• Cats 4-6 weeks
• Monkey one month
• Humans 3-5 months

As you may have guessed functions requiring higher levels of processing have later sensitive periods. Interestingly some functions remain plastic until a far later stage in life. If some random human loses its good eye the amblyopic eye can show a marked improvement in VA.

Summary

• Mammals compensate for optical deficits occuring at a young age by anatomical and physiological changes @ the visual cortex. There's very little compensation at the retina and LGN.
• Animal studies have shown the plasticity of the immature visual system and the importance of a sharply focussed image in both eyes to normal binocular visual development.
• Early diagnosis/treatment of infants at risk of amblyopia is important!
  

Review of Pathway Underlying Vision

1. Partial decussation allows binoc interaction @ VC
2. Visual Cortex = first level of convergence of signals from the two eyes
3. Retina & LGN cells have circular receptive fields but cortex has rectangular visual fields which respond best to line stimuli at a particular meridian
4. Cells in the cortex are orientated in a columnar manner
5. Majority of cortical cells are binocularly driven but not equally influenced by each eye
6. Groups one and seven are monocular
7. Group four is equally responsive
8. When identical stimuli are presented to both eyes the firing rates of most cortical binocular cells exceed the sum of the individual firing rates for each eye. These cells may provide the basis for fusion.
9. There are binocular disparity cells. The optimal stimuli for a few of the binocular cells are not located at corresponding regions of the visual field of the two eyes - they are shifted horizontally. These cells may provide the basis for stereopsis.
   

Assessing Binocular Function in Children

Stereopsis

At birth the mechanism req. for binocular interaction is not present. At 3-4mths the binoc. cells in the cortex receive input from both the right and left eyes and gross stereo is present. This reaches adult levels at 6mths according to computerised preferential looking, w/a slower improvement in clinical tests. Sensitivity to pictorial depth info doesn't develop until after 6 months. Stereopsis is an important screening technique - loss of stereopsis can often mean development of strab/amb or blur from uncorrected refractive error. Gross stereo doesn't necessarily rule out the possibility of milder levels of amb/aniso/strab eg microtropia.

Accommodation

Newborn infants are capable of accommodation but aren't too accurate. They are fairly accurate by 3-4mths. Younger kids are fairly insensitive to blur compared w/older kids and adults.

Convergence

Appropriate vergence eye movements are found in infants below 2mths of age. The ability to maintain constant fixn (eg w/moving objects) and alter convergence over large ranges improves w/age. The response is well developed by 6mths but acc and conv systems aren't correlated until at least two months of age

Assessment of Infants

• Neonate is visually responsive
• Need to differentiate between normal and abnormal visual development
• Max info in the shortest time
• First do VA, Cover test, motility, stereo. If kid has good VA and stereo Rx not likely to be a problem
• Use appropriate tests and make it fun

INFANTS

• Simple obs. look for saccades etc
• Behavioural tests - alternate occlusion, visual cliff - stereopsis
• VA: <6mths>6mths pref looking @40cm, tracking (OKN), VEPs.
• Hirschberg - central + symmetrical. 1mm diff = 20D squint
• BV - 20D base out - eg base OUT in front of RE: eyes turn to left then LE converges - fusional movement
• Cvr test w/interesting targets and hand as occluder
• Stereopsis - LANG or Frisby if >7mths
• Ret - gross differences between eyes or large Rx, near ret, cyclo

1-2 YEARS OLD

• Cover test, motil, ret, ophthalmoscopy
• VA w/Cardiff cards prefer pref looking w/picture, vertical so better for px w/nystagmus
• Kay's Pics 18mths-3yrs

>3 YEARS OLD

• H+S, VA, motility, stereo, TNO, Frisby, Titmus
• Cyclo ret, ophthalmoscopy
• VA w/Sheridan Gardner - child points to letter, cambridge crowding cards, LogMAR crowded
  

More on Development

The visual system develops at all levels of the visual pathway after birth. From cortex to retina.

Retina

• At birth perip retina well developed (temporal bit more than nasal)

• Postnatally most important change is @ macula. Recent studies show development of fovea lasts beyond 3rd postnatal yr, when foveal width + cone diameter have reached adult levels.

• Much of the postnatal development of VA results from foveal cone maturation.

Myelination in visual pathways

• Incomplete at birth. Midbrain fully myelinated @ 3 months, Optic nerve/tract @ 2 yrs, extrastriate areas/intracortical neurones @ mid childhood

Cells

• Number of cells is complete @ birth but they grow in size/synapse numbers/interconnectivity especially during first 6 mths. Max density occurs @ 8mths-2yrs then declines to adult levels (60% of max) by age 11

How we objectively assess visual function

• Preferential looking - can do VA, stereo acuity, vernier acuity, colour vision, dark adaptation
• VEPs - w/flash & patterned stimuli, applicable to any age, VEP disappears when pattern can no longer be resolved
• OKN - repetitive eye movements induced by moving visual field VA = finest pattern that induces the movement

VEP data shows better visual performance in general as you aren't relying on the child to do something, merely recording the amount of activity in their cortex. VEP acuity levels are adult like at 6-8mths (PL @ 3.5yrs - correlates well w/data on cone density).

Contrast Sensitivity

• Newborn - 1 month don't show low freq attenuation. Sensitivity greatly reduced
• At 2-3 mths shape of function similar to adult one but is shifted to lower spat.freq. and lower sensitivities
• CSF nearly adult-like at seven months (VEP) or 3-5 yrs (behavioural data)

Refractive error

• Newborn around +2.00 with SD of +2.75
• 6-8 yr old +0.25 SD +1.00
• Passive emmetropisation occurs w/normal eye growth. Optical bits decrease in power to comp for eye growth, reducing Rx
• Active emmetropisation is less understood but it's the role of visual feedback in controlling eye growth. Visual system seems to recognise the value/direction of refractive error and guides the growth accordingly. Can be disrupted by congen.cat, ptosis etc
• 80% of full term kids hyperopic. Range of refractive errors tends to decrease during first year of life. Hyperopia declines in the first year onset 3-8 months. In 82% of children emmetrop. complete within 12 months
• Astig common during first 18 months. Most of it is corneal
• If emmet. fails and rx is +3.50 or more/+0.75 astig into the second year then incidence of amblyopia/strab is greatly increased.
• Anisometropia not the norm in kids older than 2-3months of age.
• Significant Rx after one year of age = +3.50 hyperopia, +1.00D astig, +1.00D anisometropia.
• Best to correct any myopia if significant in the second year. Premature babies tend to be more myopic

Causes of Dissociation of Ocular Motility (of)

1. DEVELOPMENTAL

• Failure of orientation fixn (anomalies in central vision, fov nervous system, occlusion, v blurred image, strabismus) - CONGENITAL NYSTAGMUS innate attempts to fixate
• Failure of conjgate fixn - COMITANT STRAB
• Failure of disjuntive reflex - ANOM OF CONVERGENCE/NEAR STRAB
• Stress of corrective fusion reflex - HETEROPHORIA
• Failure of conj. eye movements - CONGEN/INFANTILE INCOMITANT STRAB

2. ACQUIRED

• Pathological accident in neuro-muscular mechanism - NON COMITANT STRAB
• Path. accident in central mechanism - CONJUGATE DEVIATION (eg gaze palsy)
• Disruption of fixn/a postural mechanism - ACQUIRED NYSTAGMUS
  

Development of BV

Although all the visual apparatus is intact soon after birth BV is not inborn but must be acquired gradually during the first few years of life. Several factors affect the development of BV

Motor Mechanisms favouring development of BV are concerned w/maintenance of the two eyes in the correct position at rest and during movement

Anatomical factors: structure of bony orbit & contents, structure of eye and posn in orbit (eyes should be visually aligned correctly at rest - slightly divergent. This is only apparent when px is dead)

Physiological factors

• Postural reflexes - these show how the head and eyes work together, independent of visual stimuli. The eyes are maintained in their correct relative posn in the orbit so that the visual axes are correctly aligned despite changes in the head rel. to the body etc. Dolls head phenom. UNCONDITIONED REFLEXES THAT DEVELOP @ BIRTH
• Fixational reflexes - maintenance of two eyes in the correct posn in the orbit. Vis axes aligned as a result of visual stimuli reaching visual cortex. GRADUALLY DEVELOP OVER FIRST FEW YRS OF LIFE

Those fixational reflexes in mo' detail

1. Orientational fixn reflex - ability of each eye INDEPENDENTLY to fix a definite object. Depends on each retinal receptor having visual spatial sense (in turn need functioning retina & adequate FOV). NO BINOCULARITY INVOLVED. Is present @ birth feebly DEVELOPS AS MYELINATION OF NF DEVELOPS & IS COMPLETED W/IN 2-3 WKS. NB Vision at birth is less than 6/60 - the fovea is not developed @ birth - fixation reflexes are present but the VA is too poor for them to be brought into use.
2. Re-fixation reflex (saccades and pursuits) - develops shortly after fixn reflex - the ability of the eye to retain fixn of a moving object (passive) or change fixn from one object to the other (active). STILL NO BINOCULARITY. CAN DO THIS BY 10-12 WKS AT MOST
3. Conjugate fixn reflex - fixn reflex applied to both eyes at the same time - both eyes retain fixn during versional movement. USUALLY PRESENT WITHIN 5-6WKS OF BIRTH AND WELL ESTABLISHED BY 6 MONTHS. Should be able to do motility test then
4. Disjunctive fixn reflex - both eyes retaining fixn at same turn during vergence movement. Develops later than (3), WELL ESTAB BY 6 MTHS.
5. Corrective fusion reflex - elaboration of (3) & (4) - permits eyes to function binocularly even under conditions of stress. FUNCTIONS @ 1YR BUT ONLY FULLY AT 5 YRS. Should be able to do 20 base out prism test & see the fusional movement.
   

***Critical period for establishing cent. fixn = first 3 mths of life. Can easily be lost during this time. Plastic period is up to about 5 yrs.
***Critical period for BV is the first year, but can still go wrong in plastic period

Sensory Mechanisms (visual apparatus, extrinsic oc. muscles)

1. VA - adequate degree of central vision dependent on reasonable integrity of fovea & macular elements, refracting media of the eye, degree of refractive compatibility between the two eyes & adequate perip. vision
2. NORMAL CORRESPONDENCE betw retinal recep of the two eyes - stimulus of corresponding visual points despite existence of 2 separate patterns of stimulation
3. HEMI-DECUSSATION OF ON FIBRES @ CHIASMA enables nerve fibres from corres. areas of the two eyes to become associated with one another ultimately in visual area of occipital cortex. Become closely assoc in optic radiations & near termination of fibres in the visual cortex
4. PROPRIOCEPTIVE IMPULSES OF THE EXTRINSIC OC. MUSC. This provides brain w/sensory info. Not known if plays role in BV development

Central Mechanisms - act of fusion & cortical control of sensory movement

1. Fusion - single picture of obj built up by activity of the striate areas on both sides of the vis.cort. and the final analysis is implemented by the higher visual centres - the relatively crude visual image of the striate area is given meaning & is integrated w/other sensory inputs/past experience. ANATOMICAL/PHYSIOLOGICAL POTENTIAL PRESENT @ BIRTH, ESTAB. GRADUALLY DURING FIRST YEARS OF LIFE. All the different fixation reflexes need to be working properly for it to be maintained.
2. Cortical Motor Control - the integrity of parts of the cerebral hemisphere controlling cranial nuclei concerned in final efferent impulses to extrinsic ocular nuclei

Summary

All of the the above mechanisms develop side by side and each require the others to be functioning correctly - one visual system. They are all conditioned reflexes w/the exception of the postural reflex and depend on visual stimuli. If px has congenital cataracts you have to get rid of em fast!

Critical period(s)

• 2-3 months for fixation
• 2-3 yrs for VA

VA won't develop if the above factors aren't favourable and during the plastic period (up to about 5 yrs) any disturbance may break it down. After the age of 5 the reflexes start to acquire the fixity comparable to an unconditioned reflex. They will be maintained throughout life unless there's some serious kind of pathology

If BV isn't allowed to develop the neurons and cortical cells develop differently and the system is abnormally conditioned ie ARC & SUPPRESSION. These will become fixed at around 5 yrs also. EARLY DETECTION IS IMPORTANT FOR TREAMENT WHICH MUST AT LEAST TAKE PLACE DURING THE PLASTIC PERIOD TO BE SUCCESSFUL.

AMBLYOPIA #3: Management

When treating amblyopia you may have to use more than one method or change methods depending on how well they're working. The patient has to be told that he isn't likely to get full binocular function and may at best just get a good 'spare eye'.

Amblyopia can be prevented if detected at an early age - screening, identifying the risk factors (family history), correction of refractive errors esp. if px has full accommodative strabismus, anisometropia, high astigmatism. If px is less than 10 years old with VA of 6/24 or better the spec correction may improve the VA on its own. You would get the px to wear the new rx and reassess in 6-8 weeks.

Occlusion

• Total occlusion - excluding all light and form (patch, spec occluder, opaque contact lens)
• Total occlusion excluding form only - frosted glass
• Partial occlusion - allows form appreciation but diminishes acuity (clear nail varnish, ND filters, also near occlusion only)

Occlusion can be direct or indirect - occluding the amblyopic or non-amblyopic eye

• Bagerter and Cuppers thought indirect was best for amblyopia associated with eccentric fixation in an attempy to weaken the EF through disuse.
• Von Noorden found no evidence that direct occlusion reinforces eccentric fixation and found it superior to direct occlusion in children under 4.
• Schapero found that direct occlusion does not intensify EF. It's a simpler approach and should be the initial approach for all age groups
• Indirect occlusion could be of value to the px who doesn't respond well to direct occlusion or has steady EF prior to direct patching

Occlusion can be full time or part time

• The most common method of occlusion is direct & total excluding light but when binocularity is present as in small angle SOT, intermittent strab & anisometropia w/out strab partial patching is preferable
• For px under 4 part time occlusion for several hours a day is better and prevents deprivation amblyopia. It should be assessed every week at first
• For strabismic amblyopes over 4 years full time occlusion is best. It gets quicker results, is less disturbing to the Px and prevents ARC. Anisometropic Px can be patched full or part time.
• It's important to obtain maximum VA before the child goes to school.

Occlusion Amblyopia

• If there's no improvement after two weeks discontinue & check fields and VA with a view to determining an organic cause.
• When VA has stabilised remove occlusion gradually to prevent the amblyopia returning
• When doing direct occlusion it's best to give the Px a visual task like crossing out letter Es in newsprint or something like that.

Optical Penalisation/Fogging Method

This involves fogging the non-amblyopic eye for distance by sticking an additional +3.00 in front of it, sorta like a reading add. The amblyopic eye is then used for distance and the good eye for near. It can be worn either full time or in the evenings for tv. It's more acceptable cosmetically but not as effective as occlusion.

Drug Penalisation/Cycloplegia

This is achieved by using 1% atropine ointment on the non-amblyopic eye. This is the reverse of optical penalisation in that the Px uses the amblyopic eye for near and the non-amblyopic eye for distance. This treatment is good for supplementing or replacing occlusion but is rarely the first thing tried. It's good when co-operation is poor. Unfortunately it's only useful in mild/moderate amblyopia - if the amblyopia is too deep then the non-amblyopic eye will still be used. The lack of involvement of patching or glasses means it's good when cosmesis is a problem (ie in older kids).

If the patient has nystagmus with a latent component this method is also very good. If you patch the good eye and the other eye starts doing a nystagmus movement then it's obvious that you aren't going to get good 6/5 vision in that eye.

CAM Visual Stimulator

Px exposed to intense visual stimulation for short periods of time w/good eye occluded. Rotating grating of different contrast & spatial frequencies to stimulate large number of cells at one time. Method is better in anisometropic amblyopia rather than strabismic but the results are dubious.

Pleoptic Treatment

After-images - useful when EF is present. A large bright after image is produced in the amblyopic eye - a ring centred on and also sparing the fovea. It desensitises the EF point - Px then looks at a near fixation target with true foveal fixation. It requires a mydriatic and daily treatment is required. Very time consuming, not easy or popular.

After Image Transfer Method

This was first used for eccentric fixation but has been shown useful in amblyopia too. A central AI is created in the dominant eye and then transferred to the amblyopic eye. Px is then asked to locate AI at the point of fixation and to see the smaller fixation letters. This must be repeated as the AI fades. Best if VA is 6/24 or better esp when VA has deteriorated again following success with other orthoptic procedures.

Anti-Suppression

Useful in older Px w/good chance of binocularity

Mallett Intermittent Photic Stimulator Unit

Red light stimulation at 4Hz with an interesting detailed visual task for 20-30 minutes. One or two times a week. Results dubious again.

AMBLYOPIA #2: Investigating it

• Accurate H&S

Age of onset of strab, previous treatment (rx, occlusion, other - when given, for how long, successful? Why stopped?)

• Acuity assessment

Crowding: first thought to be specific to amblyopia. People demonstrate better acuity for widely spaced targets and when letters are brought closer together giving contour interaction acuity is reduced. VA must be measured w/optimum Rx. Try and measure line and single letter acuity under standard illumination etc

• Neutral Density Filters - Functional Vs Organic Amblyopia
  

VA is similar in each eye under mesopic vision but is reduced @ photopic levels. Von Noorden and Buren (1959) found that as luminance levels decreased the difference in VA decreased and at the lowest luminance levels the VAs were similar. Px w/functional amblyopia didn't see an improvement in the VA of the amblyopic eye from light to dark, but the VA simply decreased less than that of the normal eye. Px w/organic amb. --> VA decreased in similar manner both eyes.

The ND filter can also help differentiate between eccentric fixation and macular function type people.

• Dark adaptation

Wald & Burian found that dark adaptation is normal in amblyopes but there is a slight elevation in central threshold.

• Evaluation & Prognosis

If you're going to suggest treatment first think

1. Am I going to cause intractable diplopia?
2. Type of amblyopia - the relative importance of rx correction/strab correction
3. Age of px - younger is better, must be under 10, co-operation - understanding of exercises, ease of patching?
4. Duration of amblyopia - shorter = better
5. Acuity - poor acuity = worse prognosis

Treatment tomorrow.

Orbital Cellulitis

Bacterial Orbital Cellulitis is a life threatening infection of the soft tissues behind the orbital septum. It's most common in children. Most often the causes are strep. pneumoniae, Staph. aureus, Strep, pyogenes and H. Influenzae.

Causes

• Sinus related
• Extension of preseptal cellulitis through the orbital septum
• Local spread from adjacent dacryocystitis/mid-facial dental infection
• Haematogenous spread
• Post traumatic - develops within 72 hours of an injury that penetrated the orbital septum
• Post surgical - retinal, lacrimal or orbital surgery

Features

• Presents w/rapid onset of severe malaise, fever, pain and visual impairment
• Unilateral, tender, warm & red periorbital and lid oedema
• Proptosis, often obscured by lid swelling
• Painful ophthalmoplegia
• Optic nerve dysfunction

Complications

• Exposure keratopathy, raised IOP, occulsion of central retinal artery/vein, endophthalmitis and optic neuropathy
• Intracranial complications are rare but include meningitis, brain abscess and cavernous sinus thrombosis (rare but extremely serious - suspect if evidence of bilateral involvement and abrupt progression of clinical signs assoc w/prostration, severe headache, nausea, vomiting
• Subperiosteal abscess is most frequently located along the medial orbital wall. Serious as it can progress rapidly and extend intracrainially
• Orbital abscess (relatively rare)

Management

• Hospital! Needs frequency ophthalmological assessment
• Antibiotic therapy
• Monitoring of ON function with pupillary reactions, VA, colour vision and light brightness appreciation.
• Investigate white cell count, blood culture, CT scan of orbit, sinuses and brain
• Lumbar puncture if intracranial signs develop
• Surgical intervention if vision decreasing, px not responding to antibiotics, orbital/subperiosteal abscess
• It's usual necessary to drain the infected sinuses as well as the orbit.
  

Uveitis Intro

Someone mentioned Uveitis the other day and I realised that I didn't remember much about it save that it was inflammation of the uveal tract and caused a painful red eye, reduced VA and photophobia. So i'm going to learn a bit more about it.

In fact the term uveitis is now used to describe all kinds of ocular inflammation involving the uvea (choroid [between retina and sclera], iris, ciliary body [connects iris to choroid and includes ciliary muscles which change shape of lens]) and adjacent structures. It's classified anatomically, clinically and aetiologically (is that even a word?).

Anatomical Classification

• Anterior uveitis - Iritis or iridocyclitis where the anterior part of the ciliary body is equally involved
• Intermediate uveitis - posterior part of ciliary body, extreme periphery of the retina and the underlying choroid
• Posterior uveitis - inflam. of the choroid and retina posterior to the vitreous base
• Panuveitis - entire uveal tract

Clinical Classification

• Acute - sudden, symptomatic onset. Persists up to 3 months. If inflammation recurs following the initial attack then it's 'recurrent acute'
• Chronic - persists for longer than three months, with a more insidious asymptomatic onset. Acute/subacute exacerbations may occur though

Aetiological Classification

Exogenous uveitis is caused by external injury to the uvea or invasion by micro-organisms. Endogenous uveitis is caused by micro-organisms or other agents from within the patient.

• Assoc. w/systemic disease
• Infections w/bacteria (tuberculosis), fungi (candidiasis) & viruses (herpes zoster)
• Infestations w/protozoa (toxoplasmosis) or nematodes (toxocariasis). Worms!
• Idiopathic specific uveitis entities - group of unrelated disorders w/underlying system disease that need special descriptions of their own (Fuch's uveitis syndrome)
• Idiopathic non-specific uveitis entities - none of the above. 25% of cases.

ANTERIOR UVEITIS

Symptoms

Acute a.u. - photophobia, pain, redness, decreased vision, lacrimation
Chronic - asymptomatic, mild redness, perception of floaters

Signs

1. Circumcorneal (ciliary) injection in acute a.u. which may have a purple/blue hue

1. Keratic precipitates - cellular deposits on the corneal endothelium, most commonly form in mid and inferior zones of cornea thanks to convection currents in the ant. chamb. In Fuchs uveitis they're scattered throughout the endothelium.

• Endothelial 'dusting' - acute/subacute chronic
• Medium sized - most types of acute & chronic
• Large 'mutton fat' greasy/waxy. In graulomatous uv.
• Old KP are pigmented and may develop a 'ground glass' appearance

1. Cells

• <5>
• 5-10 = +1
• 11-20 = +2
• 21-50 = +3
• >50 = +4
• Hypopyon
• If you compare aq. cells with those of the ant. vitreous they should far exceed the number of vitreous cells if it's iritis.

1. Aq flare - due to scattering of light by proteins that have leaked into the aq humour thru damaged iris bv. On its own in absence of cells not indicative of active inflammation and doesn't need treatment. Faint/moderate/marked/intense.

1. Iris Nodules - feature of granulomatous inflammation

• Koeppe nodules - small, @ pupillary border
• Busaca - less common, away from the pupil

Anterior uv can result in complications. Posterior synechiae are adhesions between the iris and the anterior lens capsule which may form in acute a.u. or moderate to severe chronic a.u. If the synechiae go 360 degrees around then they prevent passage of aq humour from the posterior to the anterior chamber and you get iris bombé where the iris looks all stretched and bowed outwards. This in turn can lead to closure of the anterior chamber angle by the peripheral iris with 2ary elevation of the IOP. Glaucoma! Other complications include cataract and macular oedema.

INTERMEDIATE UVEITIS

Initially px sees floaters and later VA is impaired due to cystoid macular oedema. A sign of I/uv is cellular infiltration of the vitreous with fewer cells in the ant. chamb. Complications include cystoid macular oedema, cyclitic membrane formation and tractional retinal detachment.

POSTERIOR UVEITIS

Px sees floaters and vision is impaired. Visual impairment is minimal if the inflammatory lesion is in the periphery. On the other hand if it's in the fovea central vision will be lost and the patient won't notice floaters.

Signs

• Vitreous - cells, flare, opacities, PVD. Posterior hyaloid face may have inflammatory precipitates comparable to KP.
• Retinitis - retina has a white cloudy appearance with obscuration of retinal vessels. The outline of the inflammatory focus is indistinct so it's hard to tell where affected retina ends and healthy begins.
• Choroiditis - Deep, yellow or greyish patches with well demarcated borders. Inactive (old) lesions appears as white well defined areas of chorioretinal atrophy with pigmented borders
• Vasculitis - most commonly involves retinal veins and less commonly arteries. You get a fluffy white haziness surrounding the blood column and extending outside the vessel wall.
• Spill over anterior uveitis is common.

Complications

• Direct involvement of the macula (macular inflammation), cystoid macular oedema, macular ischaemia, epiretinal membrane formation, vascular occlusions, choroidal neovascularisation, retinal detachment and consecutive optic neuropathy. IE IT IS SERIOUS

Posterior uv can be focal w/ one lesion like in toxoplasmosis, multifocal like birdshot retinochoroidopathy or geographical in which there's a large confluent area of inflammation eg cytomegalovirus retinitis.

TREATMENT

This centres around preventing vision threatening complications, relieving discomfort and treatment of the underlying problem if possible. The drugs used these days are mydriatics, steroids and systemic immunosuppresive agents. Uv that is due to an infection should be treated with the appropriate antimicrobial or antiviral drugs.

1. Mydriatics

Short acting ones include tropicamide 0.5% and 1.0% w/duration of 6hrs, cyclopentolate 0.5% and 1.0% w/duration of 24hrs and phenylephrine 2.5% and 10% which lasts for three hours and doesn't have any cycloplegic effects like thee other twoo doo. Atropine is the sole long acting mydriatic used (1%) and the most powerful, lasting for two weeks.

These are indicated to promote px comfort - relieving spasm of the ciliary muscle and pupillary sphincter. Atropine is used but mostly only once - if after two weeks the inflammation appears to be subsiding then you can sub it for a short acting mydriatic. Short acting mydriatics are used to prevent the formation of posterior synechiae. They keep the pupil mobile so there's less chance of it adhering to the anterior surface of the lens cap. In mild cases it's best to instil the drug before bedtime to prevent difficulties during the day. Also the pupil shouldn't be constantly dilated by these drugs as pos. syn. can still occur if the pupil is dilated and stationary. NB in kids constant uniocular atropinization may cause amblyopia. You can also use atropine or phenylephrine to break down recently formed pos. syn. Subconjunctival injections of mydricaine are also used for that purpose.

2. Steroids

These are the main treatment for this sorta thing. They can be administered topically, by periocular injection, intravitreal injection or systemically. They should generally be started @ a high dose which is tapered as the inflammation becomes under control.

Topical steroids are only useful for ant. uv. They don't reach therapeutic levels beyond the lens. Stronger steroids like dexamethasone and prednisolone are better than wekaer ones like fluorometholone. A solution penetrates the cornea better than a suspension or ointment, although ointment can be inserted at bedtime. The frequency of instillation depends on severity. It varies hugely - from one drop every five minutes to one every other day.

Treatment of acute a.n. is relatively simple. Administration is initially very frequent (like every 15 minutes) and then tapered to q.i.d after several days. Once the inflammation is well controlled the freq is reduced to one drop a week and then discontinued altogether after five or six. Treatment of chronic is more difficult because the inflammation can last for months or even years. Acute exacerbations are treated in the same way as normal acute a.u. Following treatment the px should be examined after a few days to ensure the uv hasn't recurred.

Complications of the topical steroids include glaucoma, cataract, 2ary infection of cornea (uncommon), corneal melting (uncommon) and systemic side effects following prolonged administration, especially in children.

Periocular steroid injections

These allow therapeutic concentrations to be acheived behind the lens. Water soluble drugs that can't normally penetrate the cornea can enter the eye trans-sclerally via this method. A longstanding effect can be achieved with preps like triamcinolone acetonide or methylprednisolone. Injections are indicated in severe acute a.u. especially in px w/ankylosing spondylitis w/exudate in ant chamb/hypopyon. They are also used as an adjunct to topical or systemic therapy in resistant chronic a.u, intermediate uv, px w/poor compliance and at the time of surgery in eyes with uveitis.

First the conjunctiva is anaesthetised with a topical anaesthetic such as amethocaine at one minute intervals for five minutes, then a cotton bud with the same stuff on it is placed into the conj sac at the site of injection and left there for five minutes. The injection can be at the anterior or posterior sub Tenon.

Intravitreal Injection

Under review. Has been used successfully in resistant uveitic chronic cystoid macular oedema.

Systemic Therapy

Oral prednisolone 5mg is the main one. Indicated when the anterior uveitis is intractable - resistant to topical therapy and injections. Also for intermediate uv which has not responded to posterior sub-Tenon injections and certain types of posterior and panuveitis particularly those with severe bilateral involvement. Again it's a case of 'start with a large dose and then reduce'. A reasonable start is 1mg/kg/day in a single morning dose. If steroids are given for less than two weeks a gradual reduction isn't required.

The side effects depend on the duration of administration. Short term you may get dyspepsia, mental changes, electrolyte imbalance and rarely hyperosmolar hyperglycaemic non ketotic coma. Long term could cause osteoporosis, limitation of growth in children, reactivation of stuff like TB, cataract and increase in severity of existing conditions like diabetes and myopathy.

AMBLYOPIA #1

Amblyopia is yet another sensory adaptation that may be present in strabismus. It's some kind of monocular adaptation occuring in the strabismic eye in cases of unilateral strabismus. The adaptation remains when the good eye is covered. Features:

• Reduced VA
• Normal fundus & good optics
• Strabismus, anisometropia or form deprivation in early life

You can divide the causes up into passive and active factors, both of which are involved in unilateral amblyopias.

• W/passive factors good VA never develops. It results from deprivation of form vision due to dense congenital cataract (complete deprivation) or a defocussed image (partial deprivation).

• W/active factors VA is actively suppressed. This is the result of abnormal binocular interaction or competition ie confusion caused by strabismus or incompatible images in anisometropia.

During development, neurones from both eyes compete for control over cortical connections. The neurones from the better eye succeed at the expense of the crap eye and the unwanted image is suppressed and amblyopia occurs. Amblyopia only develops in the critical/plastic periods. The neural plasticity makes the entire system vulnerable to any sort of abnormal experience. The most damaging period is between 0 and 18 months - if VA doesn't develop then it may never do so. The depth of amblyopia depends more on the length of time the px has a strabismus rather than the age of onset.

The retina has been found to be basically uninvolved in amblyopia. Cortical mechanisms involved in form and shape perception are thought to be involved.

Strabismic and anisometropic amblyopia seem to have different characteristics which could mean that they have a different physiological basis. To this very day the mechanism causing amblyopia is still unknown. Anisometroptic amblyopia usually occurs in the eye with the highest refractive error.

If anisometropia is responsible for amblyopia then the cause could be a combination of monocular contrast reduction and image size differences.

In the optic tract there are sustained/X cells and transient/Y cells. The X cells give a continuous response to a grating stimulus and the transient Y cells give an initial response but then return to their unstimulated state. The receptive field capacity of sustained cells is best for fine spatial discrimination so provide a basis for visual acuity. They respond poorly to large low contrast stimuli. Transient cells have large receptive field centres and weak surrounds and are poor spatial discriminators but are very sensitive to large objects w/high contrast fluctuations in time. They are more commonly found in the peripheral retina whereas the X cells are in or around the area centralis. Hawerth and Levi (1978) showed that amblyopic eyes had normal activity in the transient detection channels but reduced activity in the sustained detection channels.

Measuring contrast sensitivity at various spatial frequencies may also indicate the presence of amblyopia. Hess and Howell (1977) suggested a two type classification

• Amblyope w/only a high spatial freq. abnormality
• w/ significantly depressed CSF for all frequencies but a more severe reduction @ high

SUMMARY:

The visual deficits in amblyopia

• Reduced VA
• Reduced contrast sensitivity
• Reduced positional acuity

Spatial misperception has been measured using gratings and after-images.
Cortical undersampling of amblyopic eye: "the eye is partially disconnected from the cortical machinery required for the normal processing and interpreting of visual information" (Horton & Stryker 1993)

There hasn't been an awful lot of amblyopia testing on humans brain-wise: w/animals we can induce amblyopia and then kill em an analyse the brain! Meanness in the name of science. Monocular deprevation studies have been done on monkeys and cats. The majority of cells respond to the non-deprived eye but there was a change in the relative widths of ocular dominance columns - Shrinkage in the ODC of the deprived eye. There was also a shift in cortical dominance away from the deprived eye in severely affected animals. Hubel & Wiesel were the pioneers of that sort of stuff.

The human tests are less in-depth. Through analysis of CSF Bradley, Levi & Hess found that low spatial frequencies were spared but high spatial frequencies were affected w/accompanying loss of VA. I've already typed that above.

The cortical undersampling in humans gave misperception of vertical gratings. Patients were asked to draw what they saw. It's been argued (Barret et al 2003) that the ODC shrinkage would selectively distort the the orientation representation and lead to the patients' perceptual errors. Bedell and Flom (1983) found that strabismic amblyopes report distortion of visual space when viewing with their amblyopic eye but anisometropic patients do not but more recent research has suggested that amblyopia really varies more in severity than in kind. As you can read this is all very confusing/conflicted and more research will probably make better sense of the condition in the future.

CONCLUSIONS

• The old view that strabismus/anisometropia was the cause of amblyopia is too simplistic
• Amblyopia might actually be the cause of anisometropia rather than the other way around
• Evidence is building that residual binocular interactions are omnipresent in the amblyopic cortex
• Form deprivation and strabismus have different effects on the development of cortical binocular connections

Soft Lens Problems

When doing aftercares the patients (hopefully) turn up with their lenses in but it's also helpful if they bring their case and care system with them too. You can make them demonstrate how they clean their lenses and inspect the mankiness of the case. Even if they are using the solutions etc correctly if they then put the lenses into a manky case they are undoing all the good work. They should really be using the case that's designed to go with the solution too. Someone using a peroxide system will have a barrel case with air vents so the oxygen produced in the process has somewhere to go. Obviously using the peroxide based system and using a flat sealed case ain't going to work as well.

Yet again we have to stress the importance of records. Record all the advice you've given to the patient in case of sueage/gettinghauledupinfrontoftheGOCage. For example if you write down "Advised Patient To Come Back In A Month" at the time and then they don't turn up after you'd sent them the reminder then you have a point from which to defend yourself.

The receptionist should be taught to prioritise contact lens problems. People who should be squashed in as quickly as possible include those with acute red eye, painful eye, sticky eye/discharge, blurry vision and someone with a lens stuck in their eye.

The four main problems encountered in practice are

• Hypoxia
• Toxicity
• Mechanical Insult/Trauma
• Infection

HYPOXIA

eg Px ok but can't wear lenses as long as they used to (12hrs down to 10hrs). NB Ask how long they can wear the lenses comfortably. Patients will often tolerate uncomfortable lenses for a lot longer. You want to try and get an accurate estimate. Also VA is often a bit reduced towards the end of the day. There are three mains signs of hypoxia:

1. Striae - vertical colourless lines running parallel in the centre of the cornea. They are an indicator of corneal oedema. Short term oedema to be precise. When you wake up in the morning your cornea has swollen by 4%. This reduces back to zero as the day goes on. When swelling goes up to 7% or over then striae will appear. The number of striae give an indicator as to the level of oedema.
2. Epithelial Microcysts - These are cysts made up of cellular debris. Their presence suggests that the hypoxia has been there for several weeks. NB complete epithelial turnover in the cornea all the way down to the Bowman's layer takes 2-3 weeks. When a bit of damage is done to the uppermost layers that can be sorted in a couple of hours but an entire regeneration takes longer.
3. Corneal Neovascularisation - Suggests that hypoxia has been there for a few to several months. It takes some time for new blood vessels to form. NB When the hypoxia is sorted the ghost vessels will remain and should be visible. The new vessels are usually spotted at the top and the bottom of the cornea covered by the lids.

Management of Hypoxia

There are several options

• Change the lens type - higher water content (better O2 transmission), thinner, higher Dk material. Silicone hydrogel?
• Reduce wearing time - difficult to get people to cooperate. Needs to be a reduction of 30%-50% for any difference to be noticed. Which is a lot really for people who wear their lenses all the time. And inconvenient.
• RGPs - Smaller, better O2 transmission. But people don't like em.

Remember that there's 21% oxygen in the air, so an eye without a lens is exposed to all of that. Any lens that allows less than 10% of oxygen to get to the cornea is likely to have hypoxia. NB There are different concentrations of oxygen at the edge, centre etc depending on the thickness of the lens, whether it is high + or - etc

TOXICITY

If a patient reports a stinging sensation on inserting the lens that clears up as the day goes on and doesn't have any real other symptoms then it's likely to be a toxic reaction. Ask when the stinging first occurred and if anything changed at that point in time. Here are some problems that don't involve the contact lenses in any way that could have occurred

• New makeup, aftershave, whatever
• Px shaved his beard off at the same time as stinging began - having to use shaving products and aftershave now which could be getting into his eye
• New dog. New dog that px is allergic to
• New quilt with feathers in it that px is allergic to

So basically don't assume that it's the solution causing the problem straight away. Again check how the patient is cleaning the lenses - they might just be doing it wrong. Slit lamp examination could reveal non-serious shallow diffuse corneal punctate staining - same in both eyes. Again this suggests a toxic reaction.

Management

• Get them to get rid of their new quilt/care for the lenses better
• Replace the solution - patient may have developed allergy to the preservative. Choose one with a different preservative, duh. There's no point otherwise. Eg chlorhexidine to polyhexanide to preservative free
• Change the lens type. Pxs aren't usually allergic to a component of the lens, but if you suspect it then you'd be looking to change to a non ionic lens which is more deposit resistant BUT will have a lower water content. So consider that.

MECHANICAL

Painful eye, made more painful when lens is taken out. This suggests damage to cornea from a foreign body or a defect on the lens. The lens will act as a 'bandage' in this case shielding the cornea from the lids and reducing the painful sensation. You could also consider dry eye, especially if the patient is older. Checking TBUT would be a good idea. 10 secs and upwards will probably be ok. You need to compare it to the blink frequency. If the px blinks every 8 seconds then a TBUT of 12s would be ok.

Management of dry eye

• Artificial tear - gel is the best. Watch preservative! Unit dose best but expensive
• Punctal plug
• Decrease wearing time
• Blinking exercises. These never work
• Change lens type - make it thicker and decrease water content to reduce evaporation. Or Si-H. High water content lenses dry much faster.

Management of foreign body

• If on surface of lid remove w/moist cotton bud or nylon loop or sterile needle, forceps
  
• Irrigate (NB always nasal to temporal and with px tilting head down)
• Refer to hospital if it's embedded in the cornea

INFECTION

It's really easy to pick up an eye infection. Discard lenses and start anew! If the infection is painless then it may be herpes - reduced corneal sensitivity - px might not even know there's a problem.

Dispensing - Wot I (re)learned 26/11/08

Effectivity! The effective power of a thin lens

If you increase the distance of the lens from the eye the effective power becomes MORE POSITIVE or LESS NEGATIVE

ie the dispensed lens is going to need less plus power if it sits further away from the eye than it did in the trial frame. Or more minus. This ties in with my contact lenses being -4.50/-4.75 when my prescription is closer to -5.00/-5.25.

The optom should quote the BVD from lenses in trial frame to eye if the power is +/-5.00.

What the dispenser needs to do is measure the BVD in the patient's chosen frame (do a bit of fitting first) and then transpose the prescription into cross cyl form, for example

+8.00/+2.00x180 transposed into minus cyl form is
+10.00/-2.00x90 transposed into cross cyl form is
+8.00x90/+10.00x180

Then both the +8.00 and the +10.00 need to be adjusted for the new BVP
Let's say it's 8mm in the trial frame and 15mm in the spec frame.

The focal length of the lens must be reduced by the difference between the trial & spec frame BVP.

d=7mm.

so focal length of the lens = f'-d

effective power = 1/(f'-d) or 1/[(1-F')-d]

so in this example:
@ 90 F=1/[0.125+0.007] = 7.57D
@180 F=1/[0.100+0.007] = 9.34D

So you'd end up giving +7.50x90/+9.25x180 or
+7.50/+1.75x180

Goldmann Tonometry

Stuff to remember

The tonometer head is 3.06mm across
Set up correctly - two bits the tonometer clicks into depending on which eye you're doing!
Focus the eyepieces fool
View of the rings is monocular, duh
Wide, full cobalt blue beam @ the axis that gets best illumination
Lights off
x16 magnification is best so head fills as much of view as possible
If px has big cyl (over 4.00) angle head so cyl axis lines up with red line (need to check what this means) and should give a better reading theoretically
Set pressure reading to expected median value (ie about 15) before starting so only a small amount of knob twiddling is needed on the eye

Talking of ON THE EYE

• If your rings are a bit off (not central, top one bigger) MOVE OFF THE CORNEA, adjust and move back onto it again. Have to move off the cornea!1!
• If your rings are off centre in any way you have to move the slit lamp in the direction of the wrongness and that'll sort it. Eg if bottom ring is bigger and the whole picture is shifted to the right, move towards the bigger ring and to the right. Then it should be central.
• If rings are too thick, too much fluorescein!
• If rings are too thin you ain't pressing hard enough. Careful now.
  

The anaesthetics you could use are

• Proxymetacaine 0.5% minims w/0.25% flu (doesn't sting as much due to pH being less acidic, is more expensive and needs to be kept in fridge)
• Lidocaine 4% w/flu 0.25% (for px allergic to proxymet's NH2 benzoic acid esters & for when longer duration of action required)
  
• Amethocaine 0.5% and 1.0% (aka tetracaine, needs fridge)
  
• Oxybuprocaine 0.4% (should be kept cool but doesn't need fridge)

More to be added here most probably!

Suppression #3

Ok, we're back with the Whole Treatment Shebang. Treatment of suppression involves training the patient to be aware of the suppressed image. Normally corresponding points must be stimulated to do this - you don't want to be enforcing ARC. So you have to treat the strabismus and totally correct the angle before proceeding. In practice the first thing you'd need to do would be to do an accurate refraction to minimise the angle of strabismus and maximise clarity (this would make the suppression less strong and easier to overcome). Then and only then try one or more of the following:

Stereoscope. The classic 'bird and cage' setup could be used. The practitioner needs to reinforce the prescence of the bird as it won't be seen initially. A variable prism stereoscope can be used to correct angles of >10 degrees. In a Holmes stereoscope the card distance can be changed. Fusion cards (eg incomplete block of text) can be used as well as a G series card (this is a black box with a binocular lock and red/black writing inside - can be used with a red filter). It's better to use 'simultaneous vision' cards w/strabismics because it encourages normal retinal correspondence.

Wire/bar reading. This again needs to be done having already fixed the strabismus. TRY IT YOURSELF. Put a pen in front of some text just above the page. You should be able to see the text between 'two' pens. The patient practices reading the text in between the pens. You need binocular vision to see the text properly.

Red Filter method. Stick a red filter over the dominant eye and trace a picture with a red pen. This again trains the suppressing eye to see whatever you're drawing. A similar exercise would involve sorting coloured beads. The red filter distorts the colour of the beads so the patient would have to use the other eye to see the difference in colour. NB it's important that you don't reinforce ARC and the monocular acuity has to be good enough for the task you're attempting.

Physiological Diplopia. Bit of string and beads/nuts/needles/whatever. The patient finds the point at which the lines 'intersect' and is trained to recognise points further away and nearer in physiological diplopia. This is a long, drawn out process and the chance of it being done these days is fairly slim.

So that's that basically.

Suppression Things to Remember

1. Suppression can transfer from one eye to the other eg in alternating convergent strab
2. It's probably initiated cortically but there may be a retinal component.
3. It eliminates confusion and indeed diplopia if the area extends far enough.

In most people with strabismus from an early age both ARC and suppression are present. Form vision is suppressed both at the macula AND at the nasal retinal point receiving the image. The localisation of an object in space is modified across a more extensive peripheral area (ie larger scotoma) of strabismic eye to avoid diplopia.

NB ARC and Suppression are both binocular adaptations - they only occur when both eyes are being used. Normal correspondence returns and there is no suppression when the fixing eye is occluded and the strabismic eye takes up fixation.

There are two more adaptations that could be present in patients with strabismus, Amblyopia and eccentric fixation. I'll deal with them in a bit.

Suppression #2

SUPPRESSION'S GOT A HOLD O'ME! SUPPRESSION! GOTTA BREAK FREE!

There are a series of tests that can be done to measure the extent of a suppression scotoma. You have to investigate it under binocular conditions. There are two possible scenarios: one - you have two suppression scotoma - one at the fovea and one at the point receiving the image OR you have one big one because they've joined together. That happens if the strabismus is large angle or longstanding.

Here's another one of those things that you read about but never actually have to do in your life ever. It is Suppression Scotometry and it involves the Bjerrum screen. So y'all know it is old hat. The px sits in front of the Bjerrum screen in the corner of the room and a small mirror is mounted at 45 degrees in front of the fixing eye. This stops the eye seeing the screen but the eye can see a small marker to one side of the px at the same distance away as the screen. This allows the scotoma to be plotted with both eyes open throughout. You use the usual bjerrum targets and pins and crap.

You gonna see suppression of the nasal retina in esotropia and suppression of the temporal retina in exotropia. As you may have noticed the test is difficult to set up and takes ages so is not often done.

Something that is often done is the Prism Bar Method. The px fixates a spotlight with the dominant fixing eye and the prism bar is put in front of the suppressing eye. When the image of the spot has moved off the suppression scotoma the patient sees two spots. Simple yet effective. You can get a quantitative estimate of the angular extent of the scotoma by calculating the difference between the angle of strabismus (you've already got that from a prism cover test right) and the amount of prism which moves the spot out of the scotoma. You could do vertical deviations with that method anarl.

Sort Of Conclusion

The deeper the suppression and greater the extent across the retina the more difficult it is to treat. Take into account the age of the patient, the duration of the strabismus and how co-operative the patient is likely to be before even trying man. You must only treat suppression if the deviation can also be eliminated and if there's a strong chance of BSV occuring. Basically this boils down to only young kids where the strab can/has been corrected and binocularly driven cells can still develop. Otherwise you may end up with intractable diplopia which is very rubbish indeed. Suppression is an adaptation to prevent diplopia and confusion so if you try and treat it and the patient ends up with diplopia and confusion then he/she will be angry.

If it's suppression in conjunction with anisometropic amblyopia it can also be treated in a similar way in combination with Rx and amblyopia treatment. I will do the whole treatment shebang tomorrow.

Suppression #1

Suppression is another adaptation to strabismus that occurs before 6 years of age and like ARC turns up in order to avoid diplopia or confusion. It's an extension of normal visual processing that takes place at the cortex and prevents images in the strabismic eye reaching a conscious level. Again this is good and bad - no double vision but it makes restoring normal sensorimotor function harder.

It usually occurs in tandem with ARC in smaller strabs of 25 dioptres or less and dominates proceedings in larger ones.

There is a thing which needs to be considered here and it is called Retinal Rivalry. When different images are presented to two corresponding points on the retina either the strongest image or dominant eye dominates. If the eyes are equally dominant there is what is known as an alternating rhythm of change between the two eyes ie it can't make its mind up. For example an F and an L overlapping and making an E. Or two squares with diagonal lines orientated 90 degrees to each other creating some sort of thatched pattern.

Obviously when you have a strabismus your corresponding points are always receiving different images and the retinal rivalry you would have had previously with normal BV (looking into a synoptophore or whatever) would cease to exist. You would only see one image. This loss of form in the deviated eye prevents confusion.

Suppression also occurs without strabismus in amblyopia. See later.

The optician (or more likely orthoptist?) can investigate suppression in various ways. We mainly look to determine the depth of suppression and the extent of retina being suppressed (aka size of the suppression scotoma).

Existence & Depth

A neutral density filter bar can be used to assess how deeply ingrained suppression is. If the px has strabismus we instruct him/her to look at a spot and the palest filter is put in front of the non-suppressing eye and the density increased until two lights are seen. How dark the filter is at this point is a measure of the depth of suppression. Sometimes when this point is reached fixation swaps over to the other eye as if we'd put up an occluder and the suppression swaps over again resulting in no diplopia. A stereoscope can also be used with various cards featuring images of different sizes etc. If fusion cards such as interrupted passages of text are used and can be read normally then the suppression is said to be more shallow.

The infinity balance/septum test can be useful in anisometropia, heterophoria and small angle strabismus. If one eye is found to be suppressing then it may be overcome if you occlude the other eye for a moment.

A more widely used technique for determining the size of the suppression scotoma is Bagolini striated lenses. You place the lenses with the streaks at 90 degrees to each other and ask the px if both of them are seen, for a start. Then you can ask if there is a central gap where the lines cross. If one streak is missing or there's a central gap then you can use the neutral density filter as above to test the depth of suppression. Tests like this are more widely used than stereoscopes etc partly because they don't totally dissociate the eyes and are closer to 'real life' in that respect. The maddox rod could also be used but it dissociates the eyes a lot. The polarised lines on the Mallet unit dissociate to a lesser extent.

Yet another test is often seen in orthoptics departments in hospitals: the Worth Four Dot Test.
There it is. It's viewed through red and green goggles. So with a red filter on the right eye and a green filter on the left you can get the following possible results

• Px sees all lights - normal fusion
• Px sees all light but has strabismus - has ARC
• Px sees two red lights - LE suppressing
• Px sees three green lights - RE suppressing
• Px sees two red lights and three green lights -diplopia
• Px sees green & red lights alternating - alternating suppression

This test is not 'mazing. For a start the eyes are well dissociated by the red and green goggles so if a patient with unstable but functionally useful BV tries it then he/she might exhibit a suppression response (ie a false positive). Also the dots are actually so far apart that a small scotoma could be missed in between em.

Mysterious loss of suppression in heterophoria is usually down to suppression. The TNO test has a suppression plate. I can't find a picture of said plate. So i'm just going to stop this post right now.

The Joy of Abnormal Retinal Correspondence

Hello there, I thought if I blogged a wee bit about some optometry related stuff that I found a bit confusing it might make more sense. So here we are. I named the blog after a Chrome song because it had the word 'eyes' in it. If you are coming here from the music blog TURN BACK NOW.

Okay, back down to business. Binocular vision isn't innate - it develops in the first three years of life and is 'established' by the time the kid is 5 or 6. The 'plastic' period where everything could go horribly wrong ends there. The reflexes that develop in the first three years that cause development of binocularly driven cells in the cortex become unconditioned at that point.

If a strabismus develops before three years then an 'adaptation' to normal development occurs which prevents symptoms (double vision/confusion) and this leads to abnormal unconditioned reflexes developing by six. The kid won't see any symptoms and left untreated has a sort of binocular vision, but not true binocular vision. If the strabismus develops between three and six then symptoms will occur. However the system is still plastic at this point so adaptations do develop and again the child ends up with no symptoms. From six onwards a strabismus is going to cause symptoms, no doubt abouddit.

The problems that occur with this strab i'm typing about are as follows;

1. DIPLOPIA - Image of an object falls onto the fovea of the dominant eye but onto the periphery of the other eye. This gives two images. The visual system has two visual directions because the images aren't falling on corresponding points on the retina as they should be.

2. CONFUSION - The two images are superimposed but the brain can't fuse them as they are different (think about an X and and O near each other on a test chart - the brain might see the X directly on top of the O). This leads to retinal rivalry and what we're calling 'confusion'.

If it is plastic enough the brain copes with these problems in two ways - ARC and suppression.

ARC is the name of a condition in which two originally non-corresponding areas of the retina start to co-operate and produce a form of binocular single vision (not a particularly good one). So for example in the above strab the dominant eye's fovea enters into correspondence with a peripheral point on the retina of the other eye as if it was the fovea. It seems quite clever, and it is, but it's not ideal. For a start vision will obviously be worse in the non-dominant eye as peripheral VA isn't usually as good as foveal VA due to receptor cell density. Although it's preferable to diplopia it still isn't ideal. The definition of ARC is as follows:

"The two foveas have different visual directions." OR
"The fovea of the fixating eye has acquired an anomalous common visual direction with a peripheral element in the deviating eye."

That sounds fine to me. But then it gets a bit more confusing, splintering off into Harmonious and Unharmonius ARC. Harmonious ARC is when the angle of the anomaly is equal to the angle of strabismus. If you're going to have ARC this is the one to have. Unharmonious ARC has an angle of anomaly that's greater than zero but less than the angle of deviation. So patients with this still have some diplopia. Bummer. Annoying me even further at this point is a third type - Paradoxical ARC or PARC in which the angle of anomaly is in the opposite direction to the strabismus! I don't know what this ARC is trying to pull. Anyway PARC is rarely seen and is usually after strab surgery.

Back to ARC in general. I was getting at this bit before - because there is no longer 'point to point' correspondence on the retina there's a loss of resolution - we aren't 'bang on' the fovea in one eye so vision simply isn't going to be as good. The ARC may occur at various levels (people ain't sure yet) - retinal horizontal cells, the LGN or the cortex. In effect what it does is produce an enlarged 'pseudo-Panums' area in the duff eye centred on the point receiving the image. This corresponds with the fovea of the other eye.

So IN ARC THE IMAGES OF THE OBJECT OF REGARD ARE GIVEN THE SAME VISUAL DIRECTION DESPITE THE STRABISMUS. THEREFORE THERE ISN'T ANY DIPLOPIA AND SOME LOW-GRADE BV MAY BE PRESENT.

CONDITIONS FOR DEVELOPMENT OF ARC
1 Strab before about 4 years
2 Delay in treatment
3 Small constant strab angle
4 Esotropia more likely than exotropia
5 Unilateral more likely than alternating.

Theories of ARC tomorrow I think.