There have been reports that low doses of the dopamine-agonist apomorphine, which may inhibit dopamine neurotransmission, are of therapeutic benefit in schizophrenia. We conducted a placebo-controlled study of acute and chronic schizophrenics in which videotaped interviews were blindly rated. No specific therapeutic effect was demonstrated for apomorphine other than a reduction in anxiety in acute schizophrenics. Furthermore, there was no difference in the frequency of side-effects of apomorphine between schizophrenic patients and controls, and no specific effect of apomorphine on blink-rates. These findings emphasize the importance of placebo-controlled studies in schizophrenia research.

The hormonal effects of apomorphine, a direct-acting dopamine receptor agonist, in schizophrenic patients are of interest in view of the therapeutic efficacy of dopamine receptor antagonists. In this study, apomorphine (0.75 mg s.c.) and placebo were administered to unmedicated acute and chronic schizophrenics and controls. Apomorphine-induced prolactin suppression did not discriminate between the groups. However, an inverse relationship between basal prolactin levels and the severity of positive symptoms was detected in the patients with acute schizophrenia, consistent with a role for dopamine in the genesis of these symptoms. Growth hormone increments after apomorphine administration were blunted in the chronic schizophrenic patients, particularly those with ‘negative’ symptoms. It is argued that this blunting is not due to previous neuroleptic therapy and may represent evidence of structural change in the hypothalamus in this group of patients.

This clinical research report identified 4 subcategories of the hospitalized borderline personality disorder: developmental, affective disorder, attentional deficit/learning disabled, and organic. Developmental and affective disorder subcategories are predominantly composed of females, while males are overly represented in the attentional deficit/learning disabilities subcategory. Comparison of the borderline patients with schizophrenic and affective disorder control groups supports the hypothesis that the borderline personality disorder is a diagnostic entity distinct from schizophrenia, but perhaps not from affective disorders.

About a quarter of the psychiatrists at the Maudsley Hospital use the diagnosis of ‘borderline’ personality. The description of the borderline patient obtained in this study does not overlap with any existing ICD personality disorder but has characteristics of the schizoid, paranoid, hysteric, explosive, anankastic and antisocial personalitities. The item that discriminated best between borderlines and controls was ‘brief, unsystematized, psychotic episodes', which is not included in the DSM-III definitions of borderline diagnoses. Items of the DSM-III ‘schizotypal’ set—e.g. ‘suspiciousness' and ‘ideas of reference'—discriminated better between borderline cases and controls, whereas items of the DSM-III ‘borderline personality’ set—e.g. ‘impulsivity’ or ‘unpredictability'— scored more frequently in both groups. These are similar to American findings.

Thirty-eight patients suffering from severe depression were given a course of ECT (Electroconvulsive therapy) in one of three waveforms. These were high-energy sine wave (HS), high-energy pulse (HP), and low-energy pulse (LP). Patients were assigned to one of these treatments on a double-blind basis. The patients were given a battery of memory tests before ECT commenced, after three treatments, at the termination of treatment, and two weeks after the last treatment. The marked improvement in both verbal and nonverbal memory scores was attributed to the lifting of depression. No significant differences were found between the memory scores of the three treatment groups at any point during the treatment period.

A signal detection analysis was used in a recognition memory task involving material of varying hedonic tone. Major differences were found between the control and depressed states. Although overall recognition rates were the same, pleasant material was recognised less and unpleasant material more easily by depressives. Neutral material was recognised equally well by both groups. In the depressed state, response biases were altered such that unpleasant material was handled in a preferential way to neutral or pleasant material.

The study investigated the retrieval deficit hypothesis of forgetting in senile dementia, using a cued recall technique. Memory for lists of words was tested with either no cues given at the time of recall, or alternatively by cueing the patient either with the word's first letter or its semantic category. Results do not support a retrieval deficit explanation of forgetting in dementia, but instead suggest the possibility of a processing deficit at the acquisition stage.

Ratings of behaviour and family relationships were made on the basis of (a) a non-schedule standardised interview, (b) direct observation of family interaction during a meal time and (c) direct observation of mother-child interaction during free play. A number of scales met a battery of reliability and other criteria, and possible generalisation of these ratings across methods (interview versus direct observation) and settings (meal time versus free play) was assessed. For the vast majority of scales this was low. Reasons for this, together with some clinical implications, are discussed.

The 25-item Hopkins Symptom Checklist (HSCL–25) was used on two occasions four weeks apart to identify self-reported symptoms of anxiety and depression in patients attending a family planning service. Only 28 per cent of patients classified as anxious to start with remained so four weeks later, but 62 per cent of those with high depression scores and 74 per cent of those with high depression and high anxiety scores maintained significant levels of depression. The implications of these findings for routine screening are discussed.

Cognitive therapy for depression is a psychological treatment designed to train patients to identify and correct the negative depressive thinking which, it has been hypothesised, contributes to the maintenance of depression. General practice patients meeting Research Diagnostic Criteria for primary major depressive disorder were randomly allocated either to continue with the treatment they would normally receive (which in the majority of cases included antidepressant medication) or to receive, in addition, sessions of cognitive therapy. At completion of treatment, patients receiving cognitive therapy were significantly less depressed than the comparison group, both on blind ratings of symptom severity made by psychiatric assessors and on a self-report measure of severity of depression. At three-month follow-up cognitive therapy patients no longer differed from patients receiving treatment-as-usual, but this was mainly as a result of continuing improvement in the comparison group.

Recent clinical investigations have shown that long term treatment with the tricyclic antidepressants desipramine and amitriptyline reduces the sensitivity of the alpha-2 adrenergic autoreceptor. In order to determine whether the tetracyclic antidepressant mianserin also has this action, the effect of clonidine, an alpha-2 adrenergic receptor agonist, on plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenlethyleneglycol (MHPG), blood pressure, and patient-rated sedation were measured in fifteen depressed patients before and during mianserin treatment. Postsynaptic alpha-2 adrenergic receptor function was assessed by measuring the growth hormone response to clonidine before and during treatment. Mianserin had little or no effect on the ability of clonidine to lower plasma MHPG and blood pressure, and to increase sedation and growth hormone secretion. The findings of this investigation indicates that long term mianserin treatment does not produce significant subsensitivity of the alpha-2 adrenergic receptor and suggests that a reduction in alpha-2 adrenergic autoreceptor sensitivity is not a necessary action for all effective antidepressant treatments.

The growth hormone and hypotensive responses to clonidine have been measured in six drug free severely depressed patients before, and at two weeks after, the surgical procedure of stereotactic sub-caudate tractotomy. The responses were unaltered two weeks after operation, by which time a small clinical improvement was evident. These findings are discussed in relation to central a adrenoceptor functions in depression, and the effect upon this of antidepressant treatment.

In order to explore the possibility that prolactinomas may be caused by prolonged under-inhibition of prolactin-secreting cells we examined the pituitary fossa in 69 patients on long-term phenothiazine treatment. The average duration of treatment was 12.5 years and 55 (80 per cent) of the patients had persistently raised serum prolactin levels. The incidence of radiologically detectable pituitary fossa abnormalities was not significantly different to that in control populations. In 62 per cent of patients the skull x-rays from an earlier admission were available. Comparison of these with earlier films did not show a higher incidence of pituitary fossa abnormalities after prolonged exposure to phenothiazines.

A case of obsessional disorder is described in which a combination of tranylcypromine and thought stopping was effective in markedly reducing obsessional ruminations. Thought stopping appears to have had a major role in preventing relapse on withdrawal of the tranylcypromine. Isberg (1981) and Jenike (1981) have reviewed the literature regarding the response of obsessive compulsive disorders to monoamine oxidase inhibitors, the results of such treatment may be quite dramatic but there is a tendency to report positive results and not to report treatment failures.

We have recently demonstrated that some patients with atypical bipolar affective disorders, characterized by psychotic manias and depressions, have fluctuating and episodic high urinary phenylethlamine (PEA) excretion. We treated a 30 year old woman, who has this disorder, with 200 mg/24 hours of carbidopa. Her psychosis was ameliorated and the urinary PEA output stabilized to a low normal level. Upon withdrawal of carbidopa her psychosis worsened and improved again when carbidopa treatment was reinstated. Carbidopa did not affect the duration or severity of the patient's mood cycles.

One of the central paradoxes of the Victorian reforms in the treatment of the mentally ill was the curious fact that the “scientific” discovery of mental illness and the adoption of a more rational approach based on this discovery—an approach which aimed at treating and curing the lunatic, rather than neglecting him or incarcerating him in a gaol or workhouse—were associated with an explosive growth in the number of insane people. Edward Hare's recent Maudsley Lecture raises again the interesting question of whether or not this reflects a true increase in the incidence of mental illness in nineteenth century England. As he correctly notes, the aggregate data collected at the time do not allow a “decisive answer”, but I am pleased that his reassessment of the probabilities led him to endorse my prior conclusion that its incidence was indeed increasing. (Scull, 1979).