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!
  

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.