Recent interest in the problems of long-stay mental hospital populations has led to a number of studies which have been concerned with rehabilitation and particularly the re-activation of chronic, deteriorated patients by deliberate and systematic modification of their environment. In some of these studies, attention has been focused on the hospital ward itself, both as the background against which personal and social deterioration may be assessed, and as the means of re-building desirable patterns of behaviour (Cameron, Laing and McGhie, 1955; May, 1956). Another group of rehabilitation studies has been concerned with the value of specific work programmes. Industrial-type workshops in Dutch mental hospitals have been discussed by Carstairs et al. (1955), and the value of industrial and productive work in hospitals in this country, as well as some of its therapeutic effects, have been described in other publications (Baker, 1956; Stern, 1959; Collins, Fynn, Manners and Morgan, 1959). Considerable developments in the rationale and organization of sheltered as well as financially viable industrial workshops or factories for chronic mental patients have been made more recently (Wadsworth, Scott and Tonge, 1958; Early, 1960; Cooper and Early, 1961; Wadsworth et al., 1961).

Most patients with endogenous depression who receive electroconvulsive treatment (E.C.T.) recover completely or improve considerably. However, it is evident that the effect of E.C.T. varies in different individuals. In some cases more treatments are necessary than in others and sometimes the final result is unsatisfactory even after a great number of treatments. Many attempts have been made to explain these variations.

Haloperidol is a comparatively new tranquillizing drug synthesized by Janssen et al. (1959). It is chemically unrelated to other drugs acting on the nervous system. It is a substituted butyrophenone whose formula is 4-fluro-4(1-[4-hydroxy-4-(4-chloro)-phenyl-piperidino]) butyrophenone.

Amitriptyline hydrochloride is 5–(3 dimethylaminopropylidine)–dibenzo (a,d) (1,4) cycloheptadiene hydrochloride. Structurally it is not related to the hydrazines and is not a monoamine oxidase inhibitor. It bears some resemblance to the phenothiazines and its chemical structure is related to imipramine, in which the central seven numbered ring is azepine, nitrogen replacing the partially unsaturated carbon of the amitriptyline cycloheptadiene ring (Dorfman, 1960; Vernier, 1961).

Former attempts to restore weight loss in psychiatric patients have included hyperalimentation (Weir Mitchell, 8) and sub-coma insulin therapy (Debenham et al., 2; Sargant and Craske, 5; Sullivan, 7). The aim of the present trial was to compare weight gains in a group of patients given repeated small doses of insulin with two other groups to whom oral hypoglycaemic agents were administered, and with a control group. The drugs used were tolbutamide and chlorpropamide, both of which are sulphonylureas used in the management of diabetes mellitus, and known to induce hypoglycaemia in non-diabetic subjects (Hoenig and Gittleson, 4; Cardonnet et al., 1; Garcia Reyes et al., 3). Pharmacologically there are no qualitative differences in their mode of action. Stowers et al., (6) found the half-life of tolbutamide to be 3·5 hours and that of chlorpropamide 34·5 hours. The prolonged action of chlorpropamide permits once daily dosage, but tolbutamide, being a shorter acting drug, was given in divided doses to maintain depression of blood sugar over the 24 hours.

Since the introduction of anti-depressant drugs into general use in the psychiatric field, there have been several statements to the effect that such a drug administered concurrently with electrical treatment reduces the number of shocks required to achieve a satisfactory response. This has been claimed by Sargant (1961) but without experimental support. Dunlop (1960) has published a comparison between the number of electrical treatments given with the anti-depressant drug during a particular attack, and the number of treatments without the aid of a drug in an earlier attack in the same patient: however, comparison of treatments in the same group of patients at different times is unreliable because there may be other factors to account for the differences noted. A controlled trial is necessary to ensure that all factors are constant other than the one under consideration.

SKF 7261 is a low dosage phenothiazine derivative belonging to the piperazine group, other members of which include trifluoperazine (“Stelazine”), prochlorperazine (“Stemetil”) and perphenazine (“Fentazin”, “Trilafon”).

The mono-amine oxidase inhibitors, of which phenelzine (“Nardil”) is one example, were introduced for the treatment of depressive illness as a result of the observation that iproniazid, which is a mono-amine oxidase inhibitor, produced euphoria and increased mental alertness in some tuberculous patients to whom it was given. Trials of iproniazid in mental illness were carried out (Loomer et al., 1957; Cesarman, 1959), but it was found to be very liable to give rise to side-effects, being particularly toxic to the liver. Other less toxic mono-amine oxidase inhibitors such as phenelzine, which is chemically related to iproniazid, were later developed.

Frank Fish's paper, published in The Journal of Mental Science in September 1961, pp. 978–985, deals with issues which are fundamental for psychiatry. He examines the different approaches used in existential psychology and especially the philosophical basis of existential psychiatry. In his conclusion, he denies its value. His paper demands a reply, since it contains misrepresentations.

In view of the reports of Mendigutia et al. (6), Delay et al. (3), Kamphausen (5), Harenko et al. (4), Alleva (1), that haloperidol was very effective in controlling manic states, it was decided to treat a number of cases with this diagnosis using this new preparation.

Thioproperazine is a phenothiazine compound with a piperazine nucleus in the side chain. The pharmacological investigations of Courvoisier et al. (1958) indicate that it is much less sedative than other phenothiazines and that it has weak anti-adrenaline, anti-histamine and anti-serotonin activity. Clinical reports by Delay et al. (1958), Perrin et al. (1958), Denber et al. (1959), Levy and Maarek (1960) and Perret et al. (1961) indicate improvement in schizophrenic patients, but their papers described trials of this drug in which both recent and long-term cases or other diagnostic groups were included. Denham and Carrick (1961) reported the total remission of symptoms in 32 of 58 chronic schizophrenics treated by the discontinuous method with significant improvement in a further 25. Their acceptance of the view that improvement was correlated with the occurrence of hypertonic syndromes and that failure of treatment was likely if anti-parkinsonism drugs were used to suppress the hypertonicity, excludes the possibility of the type of continuous treatment employed with other phenothiazines. Denber et al., however, advocated the suppression of these drug effects and Perret et al. reported 47% improvement using the continuous method in another mixed group of chronic patients.

At the International Symposium on Niamid (nialamide)—1-/21—(benzylcarbamyl) ethyl/2-iso-nicotinoyl hydrazine—a mono-amine oxidase inhibitor, held in Lisbon in November, 1959, T. S. Davies reported that a 35-year-old mongol of imbecile grade, who had previously been inert and who had never spoken, gradually began to speak in monosyllables and, after two months on the drug, was able to converse in short sentences, showed increased physical activity and was able to undertake simple domestic tasks. It is not clear exactly what dosage of Niamid this patient received, but it was within the range of 30 mgm to 75 mgm daily. This report received wide publicity, out of its context, in the lay press, with its inevitable tendency to give the impression that a treatment of mongolism had been discovered, an impression which it is perhaps unnecessary to say Davies had certainly not intended to give.

Since its introduction in 1938, electroconvulsive therapy (E.C.T.) has shown itself to be a dramatically effective, unusually safe treatment for severe depressive states (“melancholias”, “endogenous” or “psychotic” depressions). Nevertheless, it is repugnant to many patients and psychiatrists, produces a troublesome, if transient, amnesia—especially in older individuals—and is occasionally complicated by fractures and dislocations as well as by anaesthetic and relaxant misadventures. Worst of all, as early studies showed, of the 80–90 per cent. of severe depressives who respond to E.C.T., some 30 per cent. relapse (Huston and Locher, 1948 a, b). Recent work suggests that the rate of relapse may often be higher still—thus of 94 per cent. of a group of patients who had responded to E.C.T., Kiloh and Ball (1961) reported that 46 per cent. had relapsed during the six months following the cessation of treatment. For these reasons, the trend to chemotherapy initiated by the advent of effective antidepressant compounds in 1957 continues to develop, and signs are becoming manifest that within a few years E.C.T. may be replaced by pharmacotherapy.