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It can be argued that vision is the major sensory input into the human brain, by virtue of the fact that about half of all afferent fibres projecting to the brain are from the eye and by the sophistication of the neural systems controlling visual processing. Brain damage disrupts these complicated processes, resulting in severe visual impairments including hemianopia. Patients with hemianopia complain mainly of difficulties with reading and scanning scenes fast enough to make sense of things as a whole. Consequently, they fail to notice relevant objects or avoid obstacles on their affected side and may collide with approaching people or cars. This has far reaching repercussions on their vocational and private lives. A small group are unaware of their defects until they are picked up on routine ophthalmic examination.1 Given the relative importance of vision as a sense, the treatment of hemianopia should assume a priority role for neurological rehabilitation programmes. In clinical practice, however, this has not been the case.
Pathogenesis of homonymous hemianopia
Forty per cent of homonymous hemianopias involve lesions in the occipital lobe, 30% the parietal lobe, 25% the temporal lobe, and 5% the optic tract and lateral geniculate nucleus (LGN).2 3The presence or absence of macular sparing is of no use in defining the site of the lesion and there is recent evidence to suggest that it simply represents a perimetric artefact.4 5 Patients with additional temporo-parietal dysfunction, especially neglect, are particularly difficult to rehabilitate from the point of view of their hemianopia.
Data concerning the pathogenesis of lesions causing homonymous hemianopia must be interpreted with caution because they are influenced by the way patients are selected.6 Allowing for this, 70% of lesions are arterial infarctions, 15% tumours, and 5% haemorrhages.1 2 Males aged 50–70 are most frequently affected, reflecting the …
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