D-Lysergic acid diethylamide (L.S.D.-25) was first prepared by Stoll and Hoffmann in 1938 (35) as a derivative of rye ergot. Its profound effects in minute doses were discovered accidentally by Hoffmann and reported by Stoll (34) along with additional observations by the latter on 16 healthy controls and six schizophrenic patients. With a dose of 30–130 γ (0.03–0.13 mgm.) Stoll (34) noted motor inco-ordination, disturbances of visual perception with illusions and hallucinations, clouding of consciousness, and affective changes principally in the direction of euphoria and distractibility. Subsequent clinical reports have confirmed these findings (6, 38). Becker (1) using doses of 30–40 γ in healthy controls attempted to predict the quality of the resulting psychosis from the constitutional somatotype of the subject; he contrasted maniacal hyperkinetic states with those showing inhibition and depersonalization and drew attention to the pattern of the visual perceptual disturbances, which were principally those of differences in size, clarity and perspective. Becker's attempts at somatotypological correlation were less successful than those of Condreau (4) who used mentally ill patients as well as healthy subjects and found that L.S.D.-25 did tend to reinforce pre-existing personality characteristics, especially with regard to mood changes. Rinkel and others (30, 7) with doses of 20–90 γ in mixed healthy and psychiatrically disturbed populations stressed the scotopic nature of the hallucinations and the greater frequency of illusions of rippling or wavy lines evolving at times into geometrical designs. Affective blunting with a lack of spontaneity was commoner than the production of major delusions. In epilepsy apparently visual hallucinations are more frequently concomitants of L.S.D.-25 administration than in other mental disorders (31).

The purpose of this paper is to outline the application to various psychiatric conditions of a test which measures peripheral capillary oxygen saturation and to discuss the significance of the findings. It is convenient to commence with a brief review of some previous work concerning the relevance of anoxaemia to psychiatry.

The acute cerebral haemodynamic effects of modified ECT were monitored by electrical impedance piethysmography in four patients with schizophrenia and three with depression. A total of 20 recordings were made on these patients; of these, 19 involved the following segments, in sequence: a rest period of 25–115 min, a short period in which Atropine, Brietal, and succinylcholine were given by injection, administration of the ECT, monitoring of post-ECT effects for 10 min, and, finally, a recovery period of up to 120 min was recorded. An identical procedure, save for the omission of ECT in one of the patients, formed the 20th recording. Results were considered significant if they were given by a majority of the 19 ECT recordings. No impedance changes took place during the pre-drug resting period nor following the pre-medication drugs. The acute effects of ECT were shown by electrical impedance changes during the 10 min immediately following it. These implied a surging increase in CBF and persisted during the recovery phase. No such changes occurred when ECT was omitted, and the results suggested that these cerebral circulatory changes formed part of the therapeutic action of ECT.

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