This editorial considers whether the quality of care for people who present to clinical services in the UK following self-harm has improved or stagnated. Some real progress has been made in the areas of service provision and research, and self-harm has never had a higher priority in policy terms. However, major gaps remain. We need to enhance people's experience of services and improve access to high-quality assessment and aftercare.

Personality disorders affect up to 50% of psychiatric out-patients. Most treatment studies have been performed in patients with borderline personality disorder. Structured psychosocial interventions for people with borderline personality disorders appear to have similar efficacy. There is some evidence that non-structured, non-specialised treatments offered by psychiatric general services might be ineffective and possibly harmful in patients with personality disorders. Cognitive analytic therapy is a time-limited, integrative psychotherapy, which appears to be effective for a range of personality disorders and superior to treatment as usual. Its practical nature and relatively short time limit may make it suitable for front-line clinical services.

The past ten years have seen a spectacular increase in the number of psychologists who have elected to take up the type of work usually referred to as “clinical,” This increase has been most marked in the U.S.A., where now some 25 per cent. of the members of the American Psychological Association are employed in this field, and where Government regulations and training schemes set up under the V.A. (Veterans' Administration) make it almost certain that within a few years clinical psychology will constitute the main field of employment for psychologists (1). In Canada, too, there has been a similar growth, leading to all the problems of registration and certification which are currently being tackled in the United States (2). In this country, while psychologists have occasionally been employed in hospitals for the mentally ill, the development of “clinical psychology” in any formal sense may be said to have started in 1947 with the foundation of the Psychological Department at the Institute of Psychiatry (Maudsley Hospital), one of whose objects was to give a course of training in clinical psychology to graduate students of psychology (7).

It is evident from many reports published in the last four years that psychological changes can occur during the treatment of physical illness by Cortisone and corticotrophin (A.C.T.H.). There is no doubt, too, that similar mental symptoms have been occasioned by giving either of these agents in therapeutic doses. It is perhaps for this reason that most writers have not distinguished between them in this respect. Thus, the mild mood changes that often occur, and the relatively rare psychotic reactions are usually spoken of as complications of A.C.T.H. or Cortisone therapy. This implies that, in the individual case, these substances would be equivalent in their influence on the mental state; yet there are grounds for suspecting otherwise. The aetiology of these psychological reactions remains obscure, so that any evidence which serves to differentiate the psychiatric side-effects of the two drugs would be of interest.

Since the introduction of the electrically induced convulsion by Cerletti and Bini the history of this procedure has become too well known to record again; but certain clinical data have come to light that are worth noting, of which the most important is the now recognized fact that this treatment is of more value in the affective psychoses than in schizophrenia, for which it was early introduced. Most writers, e.g., Elfield, Metcalfe and Paul, are agreed upon this, and it would therefore seem worth while to examine the results of this therapy in one hundred such cases. Depressions are so much commoner than manias that it would take a long time to collect a sufficient number of the latter for reliable conclusions to be drawn. These remarks are thus confined to the depressive states.

In order to test whether a drug is an inhibitor of monoamine oxidase in the human subject, three main measures are available:

1. We can measure an increased excretion of the normal substrates of the enzyme, e.g. tryptamine (Sjoerdsma, et al., 1959b).

2. We can measure a decreased excretion of the metabolites resulting from the enzyme's action, e.g. 5-hydroxyindoleacetic acid (5-HIAA).

3. We can administer a loading dose of an enzyme substrate and observe how the subject deals with it before and after the drug, e.g. 5-hydroxytryptamine (Sjoerdsma et al., 1958), and epinephrine (N-methyl-C14) (Resnick et al., 1958).

Recent psychological investigations have left little doubt that considerable mental deterioration takes place with advancing age. The work of the United States Army Psychologists in the last war (22), of Beeson (1), Jones and Conrad (10), Weisenburg, Roe and McBride (21), Sorensen (18), Miles (11, 12, 13, 14), Ruch (17), Thorndike (19), Wechsler (20), Gilbert (7); Cleveland and Dysinger (3) and others makes it apparent that not only do the various mental abilities decline with age, but also that they decline at different rates.

The subject of the present communication arose from an incidental observation made during an attempt to establish a Symptom: Sign Inventory for use with all types of mental patients. For some time past all cases diagnosed by psychiatrists as suffering from depression, whether psychotic or neurotic, have been given this inventory. The observation made was that, within the group diagnosed as psychotic, those over 60 years of age did not appear from the inventory to have the same symptoms as those under 60.

The more modern and advanced opinion of the present day, not of necessity the most correct, regards toxic action as the most important factor in the pathogenesis of insanity. According to this view insanity is not regarded as primary disease of the brain, but secondary, and due to toxins derived from elsewhere acting upon the cortical nerve-cells, disordering their metabolism, and thus affecting their functional activity, damaging, or destroying them. The older psychologists are evidently disinclined to accept the toxic theories of the younger school, and cling with pertinacity to their opinion that mental disease is as a rule primary, and that the physical manifestations of ill-health result from a disordered central nervous system, and undoubtedly many of the facts they produce in support of their argument are difficult to refute; on the other hand, it is necessary for those who advance the theory of toxaemia as the essential factor in the production of insanity to marshal facts supporting their contention. By the term “auto-intoxication” we indicate toxins evoked within the body as a result of disordered metabolism, first, such as takes place in chronic Bright's disease, myxcedema, diabetes, etc.; and secondly, in the contents of the gastro-intestinal tract. Within the limits of this paper I propose only to deal with the second division, viz, auto-intoxication from the gastro-intestinal canal, for the cases coming under this group are by far the more numerous and important. For a long time I have strongly held the opinion, as a result of my own observations, that a very large proportion of cases suffering from melancholia are due to auto-intoxication resulting from the absorption of toxins from the alimentary tract, for in depressed states generally there are various symptoms referable to disordered metabolic processes in some part of the gastro-intestinal tract. The symptoms in question that I consider as evidence of a state of toxaemia are as follow: foul breath, coated tongue, indifference to and often refusal of food, marked constipation, foul stools, anaemia (varying in degree), a sallow dirty skin, profuse perspirations and of offensive odour, skin irritations, eruptions, disorders of sensation, often leading to flesh-picking, and headache. Of course we do not in any one case find all these symptoms, but there are several common to all cases of acute melancholia. It may be suggested that the signs and symptoms that I have mentioned as those of toxaemia are but those of lowered general health, and do not in themselves afford any direct evidence of the absorption of toxins, but I have observed that the signs and symptoms that I refer to as constituting toxaemia so commonly present in states of mental depression are constantly associated with the presence in the urine of indoxyl, in greater or lesser excess.

A review of the literature which is accumulating on the so-called tranquillizing drugs shows:

1. A relatively small number of adequately controlled trials with, in general, more conservative conclusions than those of the much greater number of uncontrolled trials (Foulds, 1958).

2. Diffuseness in patient selection, with subjects often being chosen for behavioural qualities (e.g. overactivity) or general characteristics (e.g. chronicity) rather than for diagnosis.

Iproniazid (1-isonicotinyl, 2-isopropyl hydrazine phosphate) was discovered by Fox and Gibas (1953) whilst working on new synthetic compounds for the treatment of tuberculosis.

Parental depression is a risk factor for psychiatric problems in children and adolescents. Exciting scientific developments have elucidated potential early mechanisms of intergenerational risk transmission and new models of intervention may help to prevent some childhood problems. However, caution is needed in interpreting such associations as causal and in targeting interventions appropriately.

There can hardly be a psychiatrist in this country who has not produced parkinsonism in his schizophrenics with reserpine or phenothiazines: Moore, who was among the first in the field in the use of reserpine, spoke of the parkinsonian syndrome, but there was one observation of his that received only passing attention, This was that a small number of his chronic schizophrenics lost their florid schizophrenic symptoms, to be replaced by a clinical picture that he found closely akin to retarded endogenous depression, to the point of contemplated or attempted suicide.

The following facts concerning West African witchcraft were observed and recorded by the present writer while working as an ethnologist in the Gold Coast. The writer had not, at that time, any psychiatric experience, but has since worked in British mental hospitals long enough for the facts to invest themselves with psychiatric significance.

Peripheral whole blood uridine diphosphate glucose (UDPG) has been found to be significantly elevated in psychotic depression (Hansen, 1969; 1972a, b), and this was related to an equally significant lowering of whole blood adenosine triphosphate (ATP). Addition to healthy human blood of UDPG accelerated the hydrolysis of ATP in vitro (Hansen, 1972a), and UDPG concentration dependently enhanced the activity of a vegetable ATP di-phosphohydrolase (EC 3.6.1.5), which was also inhibited by adenosine 3’, 5′-cyclic monophosphate (cyclic AMP) in a concentration-dependent manner (Hansen, 1972b). Other workers have recently published a similar inhibition of a rat heart ATPase by cyclic AMP (Dietze and Hepp, 1972), and another research group have found that sodium-potassium exchange pump changes and changes in erythrocyte membrane ATPase activity correlate significantly with mood alterations in psychotic depressive patients (Dick, Dick, Le Poidevin and Naylor, 1972; Naylor, Dick, Dick, Le Poidevin and Whyte, 1973). This paper reports a study of the relationship between blood ATP levels and mood in patients suffering from manic-depressive predictable (Jenner, 1971) short term cycle psychotic states, and in depressive patients receiving electroconvulsive treatment.

Almost all sleep-promoting drugs distort the natural pattern of sleep by suppressing rapid eye movement (REM) sleep, and cause a rebound to above-normal values on withdrawal which typically lasts about six weeks (Oswald, 1968, 1969). Furthermore, barbiturates reduce the number of eye movements per unit time in REM sleep (Oswald et al., 1963; Baekeland, 1967; Lester et al., 1968; Feinberg et al., 1969), with a rebound in eye movement (EM) profusion on withdrawal (Oswald, 1970). Non-barbiturate hypnotics do likewise, also with a rebound in EM profusion on withdrawal (Allen et al., 1968; Lewis, 1968).