Systematic and detailed psychopathological examination of 400 consecutive primary major depressives failed to confirm common clinical stereotypes which ascribe greater somatisation, hypochondriasis, agitation, psychotic tendencies, and chronicity to old age. Those above 65 were more likely to suffer from single episodes of depression that were often precipitated, whereas subjects whose illness began earlier were more likely to express depression as part of a recurrent unipolar or bipolar disorder, with higher rates of affective temperamental pathology and familial affective illness. The acute clinical picture was relatively uniform in older and younger depressives and, taken together with the other findings, tends to favour a spectrum model of primary mood disorders.

In the preceding translation we tried to provide a literal rendering of the complete original article, changing it only for purposes of clarity or comprehensibility. We now offer our own judgements of the content of the article. We have made them short because we believe most of the problems with the article by Smulevitch will be readily evident to anyone who normally has access to the British Journal of Psychiatry, and who may compare our original article (Merskey & Shafran, 1986) with the content of the Smulevitch one.

Discriminant function analyses were performed on plasma concentrations of prolactin, growth hormone, Cortisol, TSH, and the neurophysins measured over 17 hours in 70 newly admitted drug-free psychiatric patients and 35 control subjects. The hormone data distinguished between patients with different classes of drug-free psychosis (26 schizophrenic, 12 with manic disorder, 10 with major depressive disorder, psychotic subtype, 9 with schizoaffective mania (SAM)). Higher plasma Cortisol and lower TSH concentrations separated eight of nine SAM patients from all others.

It is widely accepted that depression shows a tendency to run in families. This is partly due to genetic influences — and the subject has been covered in recent reviews. This article, therefore, does not aim to recapitulate the genetic evidence but rather aims to elucidate the mode of transmission, to achieve an understanding of relevant gene-environment co-actions and interactions, and to describe attempts to identify and localise major genes.

Various irregularities in serotonin (5-HT) function have been postulated as causes of affective disorders. Serotonin has been related to many of the major symptoms of depression, e.g. mood, appetite, sleep, activity, and cognitive dysfunction. Interference with 5-HT synthesis or storage has been shown to induce depression in vulnerable individuals. Decreased levels of 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid, decreased plasma tryptophan, low tryptophan neutral amino acid ratio, abnormalities in serotonergic function indicated by neuroendocrine challenge tests and various platelet measures, have been reported in depressed patients. Concentrations of 5-HIAA, the major metabolite of 5-HT in plasma, were found to be significantly negatively correlated with severity of depression as measured by the Hamilton Rating Scale for Depression score and specific depressive symptoms, despite the fact that plasma 5-HIAA is largely peripheral in origin. Blood platelets, which have been suggested as models for serotonergic nerve terminals, have a significantly decreased number of 5-HT uptake sites and 3H-imipramine binding sites in depressed patients. Antidepressant drugs may act, in part, by enhancing serotonergic activity. The serotonergic deficit may occur at any of several levels: diminished availability of precursor, impaired activity of tryptophan hydroxylase, abnormalities in 5-HT release or uptake, 5-HT receptor abnormalities or interactions with other neurotransmitters.

Gastrointestinal permeability was assessed by means of absorption of 51Cr-labelled EDTA in 24 patients with schizophrenia (12 in relapse and 12 in remission). The results were compared with those for patients with coeliac disease and those for normal controls. Significant differences between the schizophrenic patients and the normal controls were not established. The results for the schizophrenic patients in remission were no different from those for the patients in relapse, and there was no evidence from the study of an effect on gastrointestinal permeability of either anticholinergic or antidepressant medication. It is concluded that schizophrenia is, at least in the majority of cases, unrelated to coeliac disease.

In a consecutive sample of 208 male prisoners interviewed on the tenth day (T1) after entry, high levels of psychiatric symptoms as measured by the GHQ were recorded. These GHQ scores were strongly correlated with perceived worries and concerns of the prisoners (‘cognitive stress’). After 60 days of detention (T2), a significant fall in GHQ scores was observed, and they were still correlated with cognitive stress. A significant negative correlation between cognitive stress at T1 and GHQ scores at T2 was observed. The relationship between potential vulnerability factors (life experiences, social network, personality factors) and GHQ scores was not strong at either T1 or T2. Psychiatric symptoms are common during the early phase of imprisonment but are not durable.

By concentrating on the apparently uncharacteristic stages in the course of schizophrenia, Huber has drawn attention to subjectively basic symptoms (Huber, 1980, 1983; Huber et al, 1979). He has shown in his long-term follow-up investigations of schizophrenic outpatients that uncharacteristic (basic) stages (see below) prevail in the long term when compared with periods of relapse. His new typology of psychopathological outcome underlined these uncharacteristic (purely asthemic) types of remission (“reiner Defekt” — Huber 1957a, 1961, 1966).

To paraphrase Kant, theory without data is mere intellectual play, but data without theory are blind. “Mediating Processes in Schizophrenia” is a topic demanding theory as well as data. Although the topic may seem limited in scope, it actually probes the causes of schizophrenia. The causes involved in ‘mediating processes’, however, are not the usually considered primary or distal causes of schizophrenia, such as genetics or early environment. Instead they are the more proximal causes – mechanisms that are closer to illness onset, exacerbation, or improvement. It is amazing how little attention is paid to this kind of cause.

A clinical assessment was made of 145 long-term users of hospital and social-services day psychiatric facilities, and 84 consented to laboratory pathological screening. We recorded data on relevant medical care where that was being provided. Based on clinical assessment, 59 patients (41%) were judged to have medical problems potentially requiring care. Based on pathological screening 39 (44% of those assessed) had unmet needs, and this rating was associated with poor compliance with attendance and treatment plans. Altogether, 12 patients had important unmet needs, mainly for detailed medical investigation, although none required immediate hospital admission. Long-term patients should be medically reassessed and supervised at appropriate intervals.

An assessment of 106 long-stay psychogeriatric in-patients in an East London borough was made using the CAPE and supplementary items in order to obtain a comprehensive picture of their needs; 51 long-stay residents in the care of local authority social services provided a comparison. Patients in hospital were found to be more disturbed, more disabled and more dependent than residents in local authority care.

Depression is a very common condition, and most depressed patients in many countries are treated by their General Practitioners. It is a frequent cause of suicide – one of the major causes of death in young adults – and is the disorder most commonly associated with deliberate self-poisoning, a large percentage of suicides being due to poisoning with drugs that are only available on prescription. Self-poisoning with older tricyclic antidepressants (TCAs) poses major clinical management problems, since the majority of patients who overdose with these agents do not reach hospital alive. Though there is no convincing evidence that any one antidepressant is more effective than others or more rapid in onset of therapeutic action, antidepressants do differ substantially in their side-effect profiles and in their toxicity in overdosage, those introduced before 1970 being relatively more toxic. Since suicide rates have been reduced by limiting the availability of toxic substances such as barbiturates and harmful domestic gas, restricting the use of older antidepressants in favour of newer, safer compounds for depressed patients being treated in general practice would also seem to be advisable.

One hundred and ten consecutive new patients presenting with major affective disorders were divided into five categories according to pattern of presentation: recurrent manic disorder, recurrent depressive disorder, bipolar disorder, single episodes of manic disorder, and single episodes of major depressive disorder. Manic patients predominated, and recurrent manic disorder was much more frequent than either recurrent depressive or bipolar disorder. The manic and bipolar patients were younger. Females predominanted in all five groups of patients. The two manic groups were less likely to be married, but this was probably a reflection of their younger age. No differences were demonstrated with regard to educational status or occupation. There were no significant differences with regard to sibship position, family size, or polygamous/monogamous parents. Manic patients were more likely to have suffered permanent separation from one or both parents before the age of 12 years. A relatively low proportion of the patients had a positive history of mental disorder among first- or second-degree relatives. Manic and bipolar patients tended to present in hospital relatively early in their illness.

In a study of children adopted at an early age, discrimination between hereditary and family dynamic factors is possible. The biological parents have given the child their genetic characteristics and sometimes the very early environment, while the adoptive parents have provided the more permanent family environment and rearing. The major goal of the Finnish adoptive family study was to re-assess the genetic contributions to schizophrenia and to provide further measures of the adoptive family rearing environment. In other words, we were interested in the joint effects of genetic and family environmental variables and in their possible contribution to both the psychopathology and the healthy functioning of adoptees during their development. This approach paid attention to the possibility that a healthy, possibly protective, rearing family environment may reduce the genetic risk. During the course of the study, we also considered whether the direction of the effects between genetic and family environmental factors can be clarified through a prospective, longitudinal study of the adoptees at risk.

Two hundred and four subjects, 22–35 years old, were selected from a surburban part of Khartoum. They were assessed using the Self-Rating Questionnaire, the Eysenck Personality Inventory, and a Sudanese rating scale of anxiety and depression. Socio-economic information was collected. A psychiatric interview and a medical examination were carried out. It was found that 40.3% had at least one psychiatric symptom, and 16.6% received clinical diagnoses according to DSM-III. The most common diagnoses were depressive illness (neurotic and endogenous) (8.4%) and generalised anxiety (3.4%). Alcohol abuse was very rare (0.4%). There was no sex difference.

An individual's responses to Goldberg's 30-item General Health Questionnaire are usually represented as a single score which provides a measure of the number of psychiatric symptoms reported. No account is taken of the nature of the symptoms. Factor analyses of the GHQ-30 were undertaken in ten randomly selected samples of 600 adults each, and also on 12 age-sex groupings covering the age range 18–98. The results indicate an impressive degree of consistency of the factor structure, and the identification of five distinct factors corresponding to anxiety, feelings of incompetence, depression, difficulty in coping, and social dysfunction.

The functional roles of monaminergic transmitters in depression have been widely studied during the past decade. Data from that research suggest that lower levels of the 5-HT metabolite, 5-HIAA, in the cerebrospinal fluid; 5-HT uptake in human platelets; and platelets [3H]-imipramine binding sites occur in depressed patients. In recent years several potent and selective 5-HT uptake inhibitors have become available for clinical studies. The first shown to have antidepressant effects, zimelidine, was followed by similar compounds such as femoxetine, fluvoxamine, Citalopram, indalpine, fluoxetine, paroxetine, and sertraline. The effectiveness of serotonin inhibitors in treating other disorders, such as obsessive–compulsive disorder, anxiety, and panic disorder, has also been demonstrated. This review reports the data from clinical studies with these agents. The 5-HT uptake inhibitors are devoid of anticholinergic properties and have not produced weight gain or sedative side-effects, but may have another profile of side-effects. Headache, nausea, and vomiting have been reported, however.

Eleven patients with major depression and 12 control subjects were administered corticotropin-releasing hormone (CRH), aqueous arginine vasopressin (AVP), and insulin hypoglycaemia (IH) to test for differences in hypothalamic–pituitary–adrenal (HPA) axis function. Patients with major depression demonstrated lower ACTH responses to CRH when compared with controls, and a trend toward such after administration of AVP. Despite lower ACTH responses in patients with depression, there were no differences in Cortisol responses to these stimuli. In the CRH and AVP tests, there was no correlation between the basal Cortisol and ACTH responses in either controls or patients, but in the IH test there was a negative correlation between these responses for both groups. The ACTH responses to CRH and AVP were positively correlated in controls and patients. Cortisol responses to all three provocative stimuli were positively correlated in both subject groups. These findings are consistent with the hypothesis that hypothalamic or supra-hypothalamic overactivity may be involved in the development of HPA-axis abnormalities in patients with depression.

In a prospective, longitudinal study of high-risk offspring of schizophrenic mothers, of several dimensions of pre-morbid behaviour ‘peculiarity’ predicted subsequent schizophrenia or schizotypy. Peculiarity/eccentricity may represent a subtle marker of the schizophrenic genotype. ‘Pre-schizophrenics', as compared with ‘pre-schizotypes', were characterised by affective dyscontrol, reflected in less introverted and more disturbed behaviour.