We interviewed 128 women regularly during pregnancy and the first postnatal year. Psychiatric interviews identified eight ‘cases' of psychiatric disorder (6 per cent) in early pregnancy and twenty ‘cases' (16 per cent) at six weeks after birth. Postnatal affective disorder, which accounted for 15 of these cases, was significantly associated with dissatisfaction with the marital relationship and also with previous psychiatric history. The implications of the term ‘postnatal depression’ are considered in terms of the course of the disorder in the 29 women (23 per cent) who had episodes of affective disorder at some time during pregnancy and the postnatal year. We found that the majority of episodes of affective disorder could be understood in terms of previous psychiatric history and/or reaction to life-events, including the stress of childbirth itself.

There is growing evidence of a connection between the metabolism of monoamines and severe depressive illness, but the exact role of these substances in affective disorders has yet to be defined. We know that reserpine depletes the brain of monoamines and that a proportion of patients treated with this compound develop a depressive illness. Conversely a number of compounds which raise the levels of amines in the brain by blocking the enzyme monoamine oxidase have been used in antidepressant therapy. The knowledge that loss of amines may be associated with depression, and that their replenishment in the brain may induce recovery, immediately leads to the question as to which of the biogenic amines is responsible for the affective changes. Pollin, Cardon and Kety (1961) observed the effect of giving various amino acids together with a monoamine oxidase inhibitor (M.A.O.I.) to patients suffering from chronic schizophrenia. They found that only tryptophan, the precursor of the monoamine 5-hydroxytryptamine (5HT), produced an elevation of mood. On the basis of their results, Coppen, Shaw and Farrell (1963) treated a number of patients suffering from severe depressive illness with M.A.O.I. and half of this group also received an oral dose of a suspension of D L-tryptophan (214 mg./kg. body weight) for one week. The patients taking tryptophan and M.A.O.I. recovered more rapidly than those receiving M.A.O.I. alone both while they were on tryptophan and also subsequently. One explanation for these findings was that the combination of M.A.O.I. and tryptophan increased the amount of amines derived from tryptophan in the brain, and that it was this which was responsible for the therapeutic effect. If this were so, then there were several possibilities. The first was that the level of 5HT in the brain was low in depression and the combination of amine precursor and enzyme inhibitor brought it back to normal. Alternatively it may be that recovery occurred as a result of the presence of abnormally large quantities of 5HT in the central nervous system or even following the production of tryptamine, another amine derived from tryptophan.

Regional cerebral blood flow was measured with H215O positron emission tomography in four patients with obsessive–compulsive disorder. Patients were scanned on 12 occasions in the same session, with each scan paired with brief exposure to one of a hierarchy of contaminants that elicited increasingly intense urges to ritualise. The relationship between symptom intensity and regional cerebral blood flow (rCBF; an index of neural activity) was subsequently examined in the group and in individual patients. The group showed significant positive correlations between symptom intensity and blood flow in the right inferior frontal gyrus, caudate nucleus, putamen, globus pallidus and thalamus, and the left hippocampus and posterior cingulate gyrus. Negative correlations were evident in the right superior prefrontal cortex, and the temporoparietal junction, particularly on the right side. The pattern in single subjects was broadly similar, although individual differences in neural response were also observed. A graded relationship between symptom intensity and regional brain activity can thus be identified in obsessive–compulsive disorder. It is hypothesised that the increases in rCBF in the orbitofrontal cortex, neostriatum, global pallidus and thalamus were related to urges to perform compulsive movements, while those in the hippocampus and posterior cingulate cortex corresponded to the anxiety that accompanied them.

Depressive personality and depressive illness are examined from an evolutionary adaptationist standpoint. It is postulated that the depressive state evolved in relation to social competition, as an unconscious, involuntary losing strategy, enabling the individual to accept defeat in ritual agonistic encounters and to accommodate to what would otherwise be unacceptably low social rank.

A representative sample of 105 women were assessed by Goldberg's Standardised Psychiatric Interview (SPI) on two occasions during pregnancy and twice more in the puerperium. Total SPI scores increased significantly after childbirth. Thirteen out of the sample had a severe postnatal depression and a further 17 women had milder depression, which in 15 lasted at least four weeks. Marked deterioration of their marital relationships was reported by the depressed women but no other social or obstetric characteristics of postnatal depression were found. Women with severe postnatal blues were particularly at risk of developing persistent depressive symptoms subsequently. The only two women referred to a psychiatrist had personality disorders rather than depressive illnesses.

Schizophrenic patients were recruited into a trial of a prophylactic behavioural intervention with families. Families with at least one high Expressed Emotion (EE) relative were randomly allocated to one of four intervention groups: Behavioural Intervention Enactive; Behavioural Intervention Symbolic; Education Only; Routine Treatment. Patients from low-EE families were randomly allocated to two groups: Education Only or Routine Treatment. Relapse rates over nine months after discharge were significantly lower for patients in the two Behavioural Intervention, compared with Education Only and Routine Treatment groups. There was little difference between the two low-EE groups. Patients returning to high-EE relatives showed significantly higher relapse rates than those returning to low-EE relatives, in groups not receiving active intervention. Changes from high to low EE occurred in the Behavioural Intervention groups, and similar although less extensive changes occurred in the Education Only and Routine Treatment groups. Changes in criticism and marked emotional over-involvement (EOI) occurred generally in high-EE groups but were larger in magnitude in the Enactive and Symbolic groups. Reduction of hostility only occurred in the Behavioural Intervention groups. These results give partial support for the causal role of EE in relapse. There were no significant differences between the groups with respect to contact with the psychiatric services or medication.

The role of central serotonergic (5-HT) system dysfunction in the regulation of aggression in both animals and man has been investigated for more than the past two decades. Evidence for reduced central 5-HT in the mediation of aggression comes from both behavioural and correlative studies. Functional reduction and augmentation of 5-HT activity is respectively associated with increased and decreased aggression in various animal models of aggression. While similar studies in man have not been performed, strong and consistent associations between indices reflecting reduced pre-synaptic 5-HT activity and aggression have been reported. Evidence of post-synaptic receptor upregulation in the brains of suicide victims has also been reported leaving the functional status 5-HT activity in such patients an open question. However, reduced neuroendocrine (i.e. prolactin) responses to fenfluramine, a 5-HT uptake inhibitor/releaser, which activates both pre- and post-synaptic sides of the 5-HT synapse, strongly suggest that overall central 5-HT activity is reduced in mood and/or personality disorder patients with history of suicidal and/or impulsive aggressive behaviour. Preliminary data with the 5-HT receptor agonist m-chlorophenylpiperazine further suggest that reduced activity of post-synaptic 5-HT receptors may be an important correlate of impulsive aggressive behaviour. Pharmacological agents with potent 5-HT pre- and/or post-synaptic augmenting effects should be tested clinically to determine their efficacy in the treatment of impulsive aggressive behaviour in psychiatric patients.

The two major follow-up studies of children suffering from infantile psychosis, that of Kanner's cases (Kanner, 1943 and 1949; Kanner and Eisenberg, 1955; Eisenberg and Kanner, 1956; Eisenberg, 1956; Kanner and Lesser, 1958) and that of psychotic children seen by Creak (1962, 1963a and b) have shown the generally poor prognosis for these children. In both studies about half the children were in full-time residential care (usually mental sub-normality hospitals) at follow-up, and only 5 per cent. to 17 per cent. could be said to be well adjusted. Similar findings have been reported in the other published studies (reviewed in Rutter, 1966a). Kanner and Eisenberg have described the course of the characteristics of aloneness or autism shown by all or nearly all children with infantile psychosis (Kanner, 1943; Kanner and Eisenberg, 1955; Eisenberg and Kanner, 1956). Although some psychotic children emerge from their solitude to a greater or lesser extent, a lack of social perceptiveness usually remains even in adolescence or early adult life.

The World Health Organization collaborative study on “Psychological Problems in General Health Care” investigated the form, frequency, course and outcome of common psychological problems in primary care settings at 15 international sites. The research employed a two-stage case-finding procedure. GHQ–12 was administered to 25 916 adults who consulted health-care services. The second-stage assessment (n=5438) consisted of the Composite International Diagnostic Interview (GDI), the Social Disability Schedule, and questionnaires. Possible cases or borderline cases of mental disorder, and a sample of known cases, were followed up at three months and one year. Using standard diagnostic algorithms (ICD–10), prevalence rates were calculated for current disorder (one-month) and lifetime experience disorder. Well-defined psychological problems are frequent in all the general health-care settings examined (median 24.0%). Among the most common were depression, anxiety, alcohol misuse, somatoform disorders, and neurasthenia. Nine per cent of patients suffered from a “subthreshold condition” that did not meet diagnostic criteria but had clinically significant symptoms and functional impairment. The most common co-occurrence was depression and anxiety. Comorbidity increases the likelihood of recognition of mental disorders in general health care, and the likelihood of receiving treatment.

The number of deaths in a large series of suicide attempters followed up after their attempts was 3.3 times greater than expected. Suicide or probable suicide occurred in 2.8% by the end of the eighth year of follow-up, the rate of suicidal deaths being 26.9 times the expected rate. The highest risk of suicide was during the first 3 years, especially in the first 6 months, following an attempt. Factors identified at the time of the attempts which were associated with suicide risk included: being male, advancing age (females only), psychiatric disorder (especially schizophrenia), long-term use of hypnotics, poor physical health, and repeat attempts. Recent disruption of a relationship with a partner and major rows rarely preceded the attempts of those who later killed themselves. Factors predicting long-term risk of suicide also predicted short-term risk. There were more than double the expected number of deaths from natural causes, the excess being greatest in females. Markedly high death rates were found for endocrine, circulatory and respiratory diseases, and accidents.

Out of 253 patients fulfilling criteria for a first episode of schizophrenic illness, 120 entered a randomised placebo-controlled trial of maintenance neuroleptic medication on discharge; they were followed to relapse or loss to follow-up, for two years or to the end of the study. Of those on active medication, 46% relapsed, as did 62% of those on placebo; the most important determinant of relapse was duration of illness prior to starting neuroleptic medication. This finding might be because extended duration of symptoms before admission is more likely to be present in illnesses which in any case will have poor prognosis, or because susceptibility to relapse is reduced by early institution of treatment. The study provides no data on which a decision between these alternative explanations can be based.

The ability to recognise fear is impaired in people with damage to the amygdala and, interestingly, in adult psychopathy. Here we confirm that deficits in recognising fear exist in children with psychopathic traits. We show for the first time that, as with patients with amygdala damage, this deficit can be temporarily corrected by simply asking them to focus on the eyes of other people. These data support models of psychopathy that emphasise specific dysfunction of the amygdala and suggest an innovative approach for intervening early in the development of psychopathy.

Accounts of the major DMSs are given using theoretical models of the functional components underlying recognition of familiar people. Thus, Capgras' syndrome is suggested to involve impairment of processes that can support ‘covert’ recognition of familiar faces in prosopagnosia. It therefore forms a potential ‘mirror image’ of the impairments underlying prosopagnosia, and earlier attempts to link the two conditions directly are questioned. Frégoli syndrome and intermetamorphosis are explained as defects at different stages of an information-processing chain. Not only are these accounts consistent with the association of different DMSs with different brain injuries, but they also offer both suggestions for new inquiries and predictions about possible preserved and impaired abilities.