Mr. President, Ladies and Gentlemen,—Last year I had the honour of delivering the Maudsley Lecture, and I brought forward a certain amount of evidence in favour of the genetic causation of dementia præcox. I have continued these investigations and published the results in papers entitled “Further Pathological Studies in Dementia Præcox, especially in Relation to the Interstitial Cells of Leydig,” Proc. Roy. Soc. Med., 1922, vol. xv (Section of Psychiatry), pp. 1–30; also “The Reproductive Organs in Relation to Mental Disorders,” Brit. Med. Journ., March 25, 1922. The former investigation included 27 cases of dementia præcox, the onset occurring in adolescence; also the results obtained in 9 cases of psychoses other than dementia præcox occurring in post-adolescence, and 4 cases of primary dementia, in which the demential symptoms came on in post-adolescence. From these investigations, and from others which I have been pursuing, I have come to the conclusion that it is better to speak of primary dementia, which may occur either in the pre-adolescent period, adolescence, or post-adolescence; moreover, I am of opinion that all the psychoses belong to one group and are genetic in origin. In those forms of psychoses in which recovery takes place—for example, confusional insanity or exhaustion psychosis, benign stupor, periodic insanity, or manic-depressive insanity—we may assume there is a suspension of neuronic function in the highest psychic level; but all these conditions I have found may end in a terminal dementia, in which the changes in the reproductive organs and in the brain do not differ from those met with in the primary dementia of adolescence, the dementia indicative of a suppression of function. In the primary dementias, naturally, the symptoms may be partially due to a suspension, and partially to a suppression of function, and I would explain partial remission of symptoms by a partial restoration of function in neurones in which the nuclear change was either not present or not advanced.
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