The memory loss that follows a series of electroconvulsive therapy (ECT) treatments has been well documented. The amnesia appears to involve an impairment in the ability to acquire new memories, an impairment of memory for events that occurred shortly before ECT (Dornbush, 1972; Williams, 1966), and an impairment in the ability to recall material from remote memory (Janis, 1950; Squire, 1974a). Several characteristics of the anterograde amnesia produced by ECT have been the subject of contradictory reports. For example, it has been reported that memory functions can improve markedly or even return to pre-ECT levels within hours after the last of a short series of treatments (Brengelmann, 1959; Zinkin and Birtchnell, 1968; Zirkle, 1956). Yet, it has also been found that amnesic effects of a short series of treatments can be detected for weeks (Cronin, Bodley, Mather, Gardner and Tobin, 1970; Halliday, Davison, Browne and Krieger, 1968). Moreover, some reports suggest that memory recovers at the same rate following each of the first few treatments in a series (Brengelmann, 1959; Zinkin and Birtchnell, 1968), whereas other reports demonstrate that the effects of the first few treatments on memory can be cumulative (Bidder, Strain and Brunschwig, 1970). One explanation for such variant findings is that different memory tests have been employed in these studies. To obtain accurate estimates of the effects of ECT on memory, tests used to assess memory should be as sensitive as they can be to memory impairment. This point is particularly relevant, of course, to the evaluation of long-term effects of ECT on memory. Patients who had sustained partial temporal lobectomy could perform normally in tests of immediate reproduction from memory, but were markedly impaired in tests that imposed long delays between learning and retention (Milner, 1958). Apparently tests involving delayed reproduction from memory are a more sensitive index of organic memory dysfunction than tests that involve immediate reproduction. The present study assessed the ability of patients receiving ECT to retain newly learned material for 30 minutes and 24 hours. The results of these delayed retention tests demonstrate that recovery from anterograde amnesia is quite gradual and that the effects of the first few ECT treatments on memory are cumulative; and underscore the value of such tests as sensitive indicators of possible long-term effects of ECT on memory.

In 1959, J. M. Roberts claimed that in 50 depressed women aged 40–60 years the response to the intravenous injection of 15 mg. methylamphetamine differentiated significantly between those diagnosed as ‘psychotic’ and those diagnosed as ‘neurotic’. Following the injection each patient was observed closely for two to three hours, and in the great majority one of two responses occurred. Either the patient experienced a ‘sustained period of general uplift of mood and a feeling of greater well-being'—the ‘normalization’ response; or the patient showed ‘an immediate, or almost immediate, intensification of symptoms, particularly a worsening of any agitation present, often together with a deepening of the depressive affect'—the ‘intensification’ response. In only two patients, both with neurotic depression, was it not possible to classify the response.

Systematic desensitization using bodily responses other than relaxation as the specific anxiety inhibitor has produced positive results in phobic states. Jones (1924) used feeding, Wolpe (1969) advocated motor activity using a conditioned motor response, Ventis (1973) described a case where induced laughter was effective and Orwin (1971) paired the respiratory relief obtained after maximum voluntary respiratory arrest with the anxiety evoking stimuli. A derivation of this latter technique utilized the autonomic excitation caused by the vigorous physical exertion of running, to compete with the anxiety response in the agoraphobic syndrome (Orwin, 1973). This brief report describes an unusual situational phobia treated by this latter method (‘the running treatment’), following previous experience with simple claustrophobia.

All the papers about flat dwelling (Central Housing Advisory Committee, 1952; Hopper, 1962; Hird, 1966; Fanning, 1967; Gunn, 1968; Gilloran, 1968 and Stewart, 1970) except one (Sheerboom, 1962) state that it has an adverse effect on mental health. They are almost unanimous in naming the care of children as a cause. The best study from a scientific point of view (Fanning, 1967) showed a significantly higher rate of psychiatric consultations among those living in the same flats as in the present study. This was thought to be due to social isolation caused by the nature of the flats and being confined in them by children. A widely held belief that bad housing can cause or aggravate mental illness is not justified by the evidence. Three investigations (Martin, Brotherston and Chave, 1957; Wilner, Walkley, Schram, Pinkerton and Tayback, 1960 and Hare and Shaw, 1965) failed to show any benefit to mental health from new housing. The only one (Taylor and Chave, 1964) to find an improvement studied new housing which was socially planned. All four studies failed to allow for two other variables. One was the adverse effect of the move itself (Maule and Martin, 1956; Hall, 1964 and Shepherd, Cooper, Brown and Kalton, 1966) on those in new housing. The other was moving to better old housing among controls (Wilner et al., 1960).