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Amblyopia

 

Amblyopia

Amblyopia develops during childhood and results in the interruption of normal cortical visual pathway development. It is clinically defined as a difference in best-corrected visual acuity of 2 or more lines of acuity between the eyes.

Amblyopia is the unilateral or bilateral reduction of visual acuity which cannot be attributed exclusively to any abnormalities in the structure of the eye. This condition develops in childhood and causes disturbance in the development of normal cortical visual pathway. Clinically if the corrected visual acuity between two eyes is two lines or more, without any ophthalmic anomalies, it’s called as amblyopia.

Resulting from one of following:

  1. Strabismus
  2. Anisometropia or high bilateral refractive  error (Isoametropia)
  3. Visual deprivation

Prevalence: 2%-4% in the North American population

Commonly unilateral

Nearly all amblyopic visual loss is preventable or reversible with the timely detection and appropriate intervention.

Children with amblyopia or at risk for amblyopia should be identified at a young age when the prognosis for successful treatment is best.

Role of screening is important

Amblyopia is primarily a defect of central vision.

There is a critical period for sensitivity in developing amblyopia.

The time necessary for amblyopia to occur during critical period is shorter for stimulus deprivation than for strabismus or anisometropia.

Neurophysiology:

Cells of the primary visual cortex can completely lose their innate ability or show significant functional  deficiencies

Abnormalities also occur in neurons in the lateral geniculate body

Evidence concerning involvement at the retinal level remains inconclusive

Classification:

  1. Strabismus Amblyopia
  2. Anisometropia  Amblyopia
  3.  Amblyopia Due to bilateral high refractive error (isometropia)
  4. Deprivation  Amblyopia

 

Strabismus Amblyopia

·         The most common form of amblyopia

·         Strabismic amblyopia is thought to result from competitive or inhibitory interaction between neurons carrying the nonfusible inputs from the tow eye.

·         Which leads to domination of cortical vision centers by the fixating eye and chronically reduced responsiveness  to the nonfixating eye input.

 

Anisometropia  Amblyopia

·         Second in frequency

·         It develops when unequal refractive error in the tow eyes causes  the image on the one retina to be chronically defocused.

·         This condition is thought to result:

·         Partly from the direct effect of image blur in the development of visual acuity.

·         Partly from intraocular competition or inhibition

·         Mild hyperopic or astigmatic anisometropia (1-2D) è mild amblyopia

·         Mild myopia anisometropia (less than -3D) usually doesn't cause amblyopia

·         unilateral high myopia (-6D) è sever amblyopia visual loss.

·         The eye s of a child with anisometropic amblyopia look normaly to the family and primary care physician.

 

Amblyopia Due to bilateral high refractive error (isometropia)

·         Isometropia amblyopia result from large, approximately equal, uncorrected refractive error in both eyes of a young child.

·         Hyperopia exceeding 5D & myopia excess of 10 D è riskè bilateral amblyopia

 

Merdional amblyopia:

·         Uncorrected bilateral astigmatism in early childhood may result in loss of resoling ability limited to chronically blurred meridians.

Deprivation  Amblyopia

·         It is usually caused by congenital or early acquired media opacity.

·         This form of amblyopia is the least common but most damaging and difficult to treat.

·         In bilateral  cases acuity can be 20/200 or worse.

·         In children younger than 6 years, dons congenital cataract that occupy the central 3 mm. or more of the lens must be considered capable of causing sever amblyopia.

·         Similar lens opacities acquired after 6 years are generally less harmful.

·         Small polar cataracts & lamellar cataracts may cause mild to moderate amblyopia or may have no effect on visual development.

·         Occlusion amblyopia is a form of deprivation caused by excessive therapeutic patching.

 

Diagnosis

·         Characteristics of vision alone cannot be used to reliably differentiated amblyopia from other form of visual loss.

·         The crowding phenomenon is typical for amblyopia but not uniformly demonstrable.

·         Afferent pupillary defect are Characteristic of optic nerve disease but occasiinally appear to be present with amblyopia

·         Multiple assessment using a variety of tests or performed on different occasions are sometime required to make a final judgment concerning the presence and severity of amblyopia.

Binocular  fixation pattern:

·         It is a test for estimating the relative level of vision in the tow eyes for children with strabismus who are under the age of about 3.

·         This test is quite sensitive for detecting amblyopia but results can be falsely positive.

·         Showing a strong preference when sision is equal or nearly equal in the tow eyes, particularly with small angle strabismic deviations.

·         The modified Snellen technique directly measures acuity in children 3-6 years old.

·         Often, however, only isolated letters can be used, which may lead to under estimated amblyopia visual loss.

·         Croding bar may help alleviate this problem.

·         Crowding bar, or contour interaction bars, allow the examinator to test the crowing phenomenon with isolated optotype. Bar surrounding the optotype mimic the full of optotype to the amblyopia child.

Treatment

·         Treatment of amblyopia  involves the following steps:

·         Eliminating (if possible) any obstacle to vision such as a cataract

·         Correcting refractive error

·         Forcing use of the poorer eye by limiting use of the better eye.

·         Cataract removal

·         Cataracts capable of producing amblyopia require surgery without unnecessary delay.

·         Removal of significant congenital lens opacities during the first 2-3 months of life is necessary for optimal recovery of vision.

·         In symmetrical bilateral cases, the interval between operations on the first and second eyes should be no more than 1-2 weeks.

·         Acutely developing severe traumatic cataracts in children younger than 6 years should be removed within a few weeks of injury, if possible.

Refractive correction

·         In generally, optical prescription for amblyopic eyes should correct the full refractive error as determined with cyclopagic.

·         Occlusion and optical degradation

·         Full time occlusion of the sound eye:

·         Defined as occlusion for all or all but one waking hour.

·         It is the most powerful means of treating of amblyopia by enforced use of the defective eye.

·         The patch can either be left in place at night or removed at bedtime.

·         Spectacle-mounted occlussion or special opaque contact lenses can be used as an alternative to full-time patching if skin irritation or poor adhesion proves to be a significant problem

·         Full time patching should generally be used only when constant strabismus eliminates any possibility of useful binocular vision because è full time patching runs a small risk of perturbing binocularity.

Part-time occlusion:

·         Defined as occlusion for 1-6 hours per day.

·         The children undergoing part time occlusion should be kept as visually active as possible when the patch is in place.

·         Compliance with occlusion therapy for amblyopia declines with increasing age.

Penalization:

·         A cyclopagic agent (usually atropine 1% or homatropine 5% )è once daily to the better eye

·         This form of treatment has recently been demonstrated to be as effective as patching for mild to moderate amblyopia. 

Complication of therapy

·         Full time occlusion carries the greatest risk of this complication and requires close monitoring, especially in the younger child.

·         The first follow up visit after initial treatment should occur within 1 week for an infant and after interval corresponding to 1 week per year of age for the older child.

·         Part time occlusion & optical degradation methods allow for less frequent observation but regular follow up is still critical

The time required for completion of treatment depends on the following:

  1. Degree of amblyopia
  2. Choice of therapeutic approach
  3. Compliance with the prescribed regimen
  4.  age of the patient

Unresponsiveness

·         Complete or partial Unresponsiveness to treatment occasionally affect younger children but must often occurs in patients older than 5 years.

·         Primary therapy should generally be terminated if there is a lock of demonstrable progress over 3-6 months with good compliance.

·         Refraction should be carefully rechecked and the macula and optic nerve critically inspected for subtle evidence of hypoplasia or other malformation that might have been previously overlooked.

Recurrence

·         When amblyopia treatment is discontinued after fully or partially successful completion, approximately half of patients show some degree of recurrence,

Maintenance therapy: 

·         Patching for 1-3 hours per day

·         Optical penalization with spectacles

·         Pharmacologic penalization with atropine 1 or 2 day per week.

·         This may require periodic monitoring until age 8-10.

 

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