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[page 7 of handout]Some extracts from Zeki (1993) “A Vision of the Brain”
(This is given as reference, but substantive points made in this book do not differ from those in the Scientific American article: as the examples below show, the book is partly a history of controversies over cerebral localization of function, which are equally well covered in the Brain articles which are available online).
Later on Zeki discusses other cases and says:
“The first important point to note about achromatopsia is that the retinal mechanisms mediating colour vision are intact in this condition... The fibres carrying the messages from the retina to the striate cortex are also intact. Hence the defect is entirely central, due to a specific lesion in the cerebral cortex. In brief, with achromatopsia, we witness a condition in which the signals relayed to the brain are normal but the mechanism used to construct colours is defective.” (pp 267-8)
Mackay, G. and Dunlop, J.C. (1899) The cerebral lesions in a case of acquired colour-blindness. Scot. Med. Surg. J. 5, 503 -12.
Zeki, S. (1990) A century of cerebral achromatopsia. Brain, 113, 1721-1777. (available in the UCL Clinical Sciences Library, entrance on University Street or via the BK elibrary | log on first for access outside the College.)
Chapter 10, p 82 A motion-blind
patient.Zihl et al (1983) described a patient who had suffered
a vascular disorder, which
produced bilateral lesions outside the striate area. She had
several problems including
difficulties in calculations and mild aphasia. But her inability
to see objects in motion was very
striking. She had difficulty in pouring tea or coffee because the
fluid appeared to be frozen, like
a glacier. She complained of difficulties in following speech
because she could not see the
movements of the mouth of the speaker, and, when crossing the
road, was only aware of cars in
isolated individual positions, either near or far away.