Abstract

In their March 24 commentary,1Moseley M Fielder A Improvement in amblyopic eye function and contralateral eye disease: evidence of residual plasticity.Lancet. 2001; 357: 902-903Summary Full Text Full Text PDF PubMed Scopus (19) Google Scholar Merrick Moseley and Alistair Fielder raise many important and fascinating issues about the functioning of the two eyes if one becomes amblyopic in early childhood.They draw attention to refractive errors or other pathology in the amblyopic eye and the likelihood of the non-amblyopic eye losing visual function at some later date, and use the term plasticity to explain the improvement in vision after such procedures as removal of a cataract. Disease processes are said to be nature's experiments, and this mechanism is a good example.While I was working at the Southeast Thames Metropolitan Regional Neurological and Neursurgical units, at the Brook Hospital, a man in his early 30s was admitted under the late George Northcroft. The patient had a squint from early childhood with an amblyopic right eye. He had a pituitary tumour and, during surgical removal, the left optic nerve had to be divided. Within a week or so after the operation, vision began to return to the amblyopic right eye, much to everybody's amazement, and continued to improve during the next 3–4 months. During this time, after the left-nerve division, the patient had no vision in his left eye.Some years later, at St Thomas's Hospital, London, at a retirement meeting for Hisako Ikeda, one of the speakers described an experiment he had done on a neonatal kitten, in which he had produced the same results. He had covered one eye of this kitten at birth for some weeks and the eye became amblyopic. He left the amblyopic eye uncovered and covered the opposite eye, after which the amblyopic eye regained vision.Moseley and Fielder thought this kind of visual plasticity was cortical in origin, but there might be a simpler explanation. In the visual pathway in the inferior colliculi and lateral geniculate bodies, there are “on” and “off” cells or neurons. The “on” cells respond to increasing light intensity and the “off” cells recognise decreasing light intensity. It seems to me that normal vision depends on a balance between these two systems, and this might be an important factor in whether vision returns to an amblyopic eye, even after as long as 30 years. In their March 24 commentary,1Moseley M Fielder A Improvement in amblyopic eye function and contralateral eye disease: evidence of residual plasticity.Lancet. 2001; 357: 902-903Summary Full Text Full Text PDF PubMed Scopus (19) Google Scholar Merrick Moseley and Alistair Fielder raise many important and fascinating issues about the functioning of the two eyes if one becomes amblyopic in early childhood. They draw attention to refractive errors or other pathology in the amblyopic eye and the likelihood of the non-amblyopic eye losing visual function at some later date, and use the term plasticity to explain the improvement in vision after such procedures as removal of a cataract. Disease processes are said to be nature's experiments, and this mechanism is a good example. While I was working at the Southeast Thames Metropolitan Regional Neurological and Neursurgical units, at the Brook Hospital, a man in his early 30s was admitted under the late George Northcroft. The patient had a squint from early childhood with an amblyopic right eye. He had a pituitary tumour and, during surgical removal, the left optic nerve had to be divided. Within a week or so after the operation, vision began to return to the amblyopic right eye, much to everybody's amazement, and continued to improve during the next 3–4 months. During this time, after the left-nerve division, the patient had no vision in his left eye. Some years later, at St Thomas's Hospital, London, at a retirement meeting for Hisako Ikeda, one of the speakers described an experiment he had done on a neonatal kitten, in which he had produced the same results. He had covered one eye of this kitten at birth for some weeks and the eye became amblyopic. He left the amblyopic eye uncovered and covered the opposite eye, after which the amblyopic eye regained vision. Moseley and Fielder thought this kind of visual plasticity was cortical in origin, but there might be a simpler explanation. In the visual pathway in the inferior colliculi and lateral geniculate bodies, there are “on” and “off” cells or neurons. The “on” cells respond to increasing light intensity and the “off” cells recognise decreasing light intensity. It seems to me that normal vision depends on a balance between these two systems, and this might be an important factor in whether vision returns to an amblyopic eye, even after as long as 30 years.

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