Abstract
To give the Montgomery Lecture is a great honour for any American but perhaps most especially appreciated by one from Boston. It was in this first port of call for the transatlantic ship lines that so many waves of your countrymen disembarked, and took prominent places in the development of that country of opportunity across the seas. We have much in common. To give the Montgomery Lecture is also a most humbling experience. When I look over the distinguished names of those who have preceded me on this platform I can only wonder at my good fortune in being included among those who have been challenged to uphold the traditions that surround this Lectureship. After recovering from the pleasant surprise of being invited, my first effort was to acquaint myself with the conditions of the lectureship. To this end I secured Dr. Somerville-Large's exquisite vignette, itself the 42nd Montgomery Lecture (Somerville-Large, 1960). I was delighted to read that the lecture was given by young investigators-although I was a little let dcwn when Dr. Somerville-Large subsequently added that this was in the earli4r 'eafs of the lectureship. I noted with some sympathy that the Dean of the Medical School was in the habit of coercing students to attend the Lecture so that the hall would appear full. But I was most impreisedy0t1 'tfact that the second lecture, or series of lectures, was given by Gordon Holmes (1919) on a subject which has preoccupied me of late, namely, some of the specific visual defects of cerebral lesions. In his lecture 45 years ago Holmes concluded that bilateral parietal lesions caused characteristic impairment of visual recognition and localization in space. I hope to deal similarly with some of the visual symptoms resulting from bilateral lesions affecting the visual associative and ocular motor areas. The present study is, in a sense, a sequel to that based on unilateral lesions in the parietotemporal region and previously reported (Cogan, 1960). I then pointed out, corroborating the many reports of others, that left parietotemporal lesions impaired recognition of visual symbols (alexia and agraphia) whereas right parietotemporal lesions impaired especially judgment of spatial relationships (topographic agnosia and constructional apraxia). Except for diminished optokinetic responses on
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