Unifying concepts in mechanism of amblyopia.

Most of the evidence of formation of amblyopia is derived traditionally from electrophysiological studies. Recently, there have been many discoveries from genetics, histopathology, biochemistry, immunology and interventional studies. On the basis of evidence gathered in the last five years, the various types of amblyopia (strabismic and non-strabismic amblyopia) can be seen not only as disturbance of the development of the visual system at different points but as basically different pathologic processes. It is postulated here that strabismic amblyopia is initiated as a maladaptive differentiation in the ocular dominance columns, whereas the non-strabismic amblyopia may be initiated from the ganglion cell population of the amblyopic eye. The total clinical picture is confusing because of secondary changes in other parts of the central nervous system. The manifested features can be due to a slower, more enduring type of change (pooling, loss and re-wiring of the neurones) as well as a more transient, adaptive type of response (such as suppression of diplopia). Neurotransmitter replacement has a potential therapeutic application.