von Noorden G K
Cullen Eye Institute, Baylor College of Medicine, Texas Children's Hospital, Houston 77225.
Eye (Lond). 1988;2 ( Pt 4):343-57. doi: 10.1038/eye.1988.65.
Several forms of esotropia with a different pathophysiology that meet the criterion of an onset early in life must be distinguished from essential infantile esotropia. A hypothesis is presented, according to which a delayed development or a congenital defect of retinal disparity sensitivity (motor fusion) in an otherwise normal infant with immature sensory functions causes esotropia under the influence of various strabismogenic factors. Some of these factors are genetically determined, hence the familial occurrence of essential infantile esotropia. The absence or marked decrease of stereopsis and the asymmetry of optokinetic nystagmus are interpreted as the consequence of ocular misalignment early in life rather than of structural anomalies in the afferent visual pathways of esotropic patients. The therapeutic results after surgery are classified into four groups: subnormal binocular vision, microtropia, small angle eso- or exotropia and large angle residual or consecutive eso- or exodeviations. Analysis of data from 358 operated patients with a documented onset of esotropia prior to the sixth month of life has shown that the probability of obtaining an optimal functional result is increased when surgical alignment is completed before completion of the second year of life. However, surgery after the age of two or even four years of life does not preclude the development of binocular vision on a subnormal or anomalous basis.
