It is 13 years since Kendell (1976) reviewed the ‘contemporary confusion’ surrounding the classification of depression. Reconsideration of this issue is now timely, especially in light of the development of the new classifications of affective disorder included in DSM–III (American Psychiatric Association, 1980), the revised version, DSM–III–R (American Psychiatric Association, 1987), and the forthcoming ICD–10 (World Health Organization, 1988). Recent activities in neurobiological, genetic and social research also bear importantly on our concepts of the aetiology of depression.

Findings on CT and demographical or clinical data in 80 patients with DSM–III schizophrenia and 45 medical controls were evaluated. Multiple-discriminant analysis showed that the enlargement of the third ventricle and frontal and parietal atrophy could significantly predict the diagnosis of schizophrenia. Widening of Sylvian fissures and parietal atrophy differentiated familial schizophrenics of both horizontal transmission (who had affected siblings) and vertical transmission (who had affected parents or/and offspring) from non-familial patients. Parietal atrophy and a history of birth complications differentiated horizontal from vertical transmission. The CT findings together with some clinical characteristics could differentiate the three subgroups classified by the hereditary form; thus each of these subgroup may belong to a different disease entity, of a different pathophysiology.

The psychopathology and disabilities of a group of institutionalised elderly schizophrenics were compared with those of a group of non-schizophrenic elderly, and with younger schizophrenics reported in a parallel study and in the literature. Elderly schizophrenics showed significantly more psychopathology and disability than the non-schizophrenic elderly; however, they exhibited less psychopathology than younger schizophrenics. Disability among elderly schizophrenics was not correlated with chronicity of institutionalisation or psychopathology. There was a suggestion that disability among elderly schizophrenics may be due to organic deterioration.

Plasma concentrations of prolactin, growth hormone, cortisol, TSH, and the neurophysins were measured over 17 hours in 98 newly admitted psychiatric patients and 35 control subjects. Seventy patients had been free of psychotropic medication for three months. Patients with schizoaffective mania (SAM) differed significantly from control subjects by increased plasma Cortisol concentrations and decreased night-time TSH concentrations. The latter were also significantly lower than in both schizophrenic and manic disorder patients. Plasma Cortisol was increased to a lesser extent in other psychotic subgroups, and increases in prolactin were most marked in the affective psychoses. There was little diagnostic specificity for psychoses other than SAM. Higher Cortisol and prolactin levels may be due to the stimulatory effect of serotonergic pathways, but the neural mechanisms underlying lower night-time TSH levels in SAM are not known. The findings are not consistent with the view (a) that the hormonal changes of the psychoses simply reflect a non-specific response to stress, or (b) that the biological abnormalities of the psychoses can be accounted for by a single continuum of disturbance.

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.

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.

Depression, anxiety and psychomotor performance were assessed in 20 depressed patients during double-blind treatment with amitriptyline or trazodone. There was no difference in onset of antidepressant or anxiolytic action. No decrement or improvement on computerised tasks was found. Dry mouth was significantly more frequent and severe with amitriptyline.

In double-blind sequential study, diazepam was compared with the proven antidepressant moclobemide, in patients with atypical depression. Both agents significantly improved depression ratings over eight weeks of treatment. Diazepam was a significantly better antidepressant than moclobemide at four weeks, although not at eight weeks. All patients ceased diazepam within one year and none reported withdrawal reactions. These data suggest the need to reconsider that benzodiazepines may be antidepressants and to study their possible antidepressant actions.

A longitudinal investigation of psychiatric epidemiology in a general population (the Stirling County study) has indicated that the incidence of depression and anxiety disorders is low relative to prevalence, because these disorders have long durations. In an average year approximately nine adults among 1000 experience a first-ever episode of one of these disorders. Incident cases over the course of a 16-year follow-up were more likely to have had premonitory symptoms than to have been asymptomatic at the beginning of the study. Among the relatively small number of people who exhibited the clearest prodromal manifestations, incidence was 20 per 1000 annually. It might be possible to intervene before such disorders become fully formed and persistent if the precursors are given attention.

The efficacy of lithium prophylaxis in bipolar affective disorder in clinical practice was investigated. Comparison was made between 41 patients who were prescribed prophylactic lithium after two admissions in two years or three admissions in five years and a group of patients who did not receive lithium. The benefits conferred by the prescription of this drug were modest compared with the results from clinical trials.

We have used a novel technique to assess the transport of cations across the erythrocyte membrane in vivo in unmedicated patients suffering an acute manic illness. The results show that erythrocyte cation transport via the sodium-pump enzyme Na+,K+-ATPase is increased in manic patients compared with healthy controls.

We have investigated cation transport in vivo in patients being treated with lithium for bipolar affective illness by studying the disposition of rubidium after an oral load of rubidium chloride. The rate of erythrocyte cation transport was increased in the patients when compared with matched healthy volunteers. However, the rate of in-vivo erythrocyte rubidium accumulation in the euthymic treated patients was significantly lower than in a matched group of unmedicated manic patients. The regulation of specific pathways for cation transport may be altered in individuals predisposed to affective illness.

An analysis of the temporal distribution of 115 in-patient suicides that occurred in two Swiss psychiatric hospitals in the years 1977–86 failed to reveal any statistically significant clustering of suicides. Thus, the modelling effect does not generally play a decisive role in psychiatric in-patient suicide.

All insulin-dependent diabetics between the ages of 16 and 25 years attending the diabetic clinic at the Royal Infirmary, Edinburgh, (152 women and 139 men) were asked to complete the EAT, the EDI, and the GHQ, and to provide a control subject (sibling or close friend) of similar age who would do likewise. Marked differences were found between diabetic women (but not men) and their controls in eating attitudes, in many of the psychological characteristics associated with eating disorders, and in GHQ scores. Although some of the women had classic anorexia nervosa or bulimia, others with abnormal eating attitudes did not fulfil the formal criteria. Overall, diabetics were significantly heavier than controls but the differences in eating attitudes were not eliminated by correcting for overweight. Abnormal scores were associated with high HbA, levels and independently with retinopathy. The weight gain and psychological effects of diabetes are identified as probably of aetiological importance in the abnormal eating attitudes of young diabetic women.

Within a group of hospitals for the mentally handicapped serving the Leicestershire district, a cohort of 215 epileptic patients was identified, who were followed up for four years. The anticonvulsant medication of each patient was reviewed regularly until an optimal balance between seizure control, absence of medication side-effects, and reduction of polypharmacy was attained. After four years 172 patients remained in the study. A significant reduction in polypharmacy was attained overall. Some groups of patients showed a significant reduction in the frequency of seizures, while a small group of patients with frequent seizures remained difficult to control.

The perceived parental rearing practices and attitudes of agoraphobics, social phobics and non-patient normal controls were investigated, employing the EMBU, an inventory for assessing memories of upbringing. Findings obtained previously with out-patients were replicated with in-patients as subjects. Compared with the controls, agoraphobics rated both their parents as having been less emotionally warm but only their mothers as having been rejective. Socially phobic in-patients rated both their parents as having been rejective, as having lacked emotional warmth, and as having been over-protective. Comparisons between agoraphobics and social phobics showed differences in certain aspects of parental rearing, with the socially phobic in-patients assigning ratings more negatively than the agoraphobic group.

The hypothesis of a neurodevelopmental aetiology of manic-depressive psychosis and schizophrenia is based on the relation between onset of puberty and the final regressive events in the central nervous system (elimination of 40% of neuronal synapses), and the discrepancy in body build in the two disorders which is similar to that between early- and late-maturing individuals. The marked rise in manic–depressive psychoses and decline in schizophrenia, particularly the non-paranoid categories, accompanying the decline in mean pubertal age by some four years during the past hundred years are taken as evidence that manic–depressive psychosis affects early maturers and schizophrenia particularly affects late maturers. Gender differences and social differentials accord with this theory. Redundancy of neuronal synapses characterises manic-depressive psychosis, and reduced density of synapses is a characteristic of schizophrenia, whereas ‘normality’, with optimal synaptic density, is in between.

Twenty Asian psychiatric patients suffering from neurotic illness completed the Urdu version of the HAD Scale. The results were compared with the Clinical Interview Schedule. Somatic symptoms were significantly related to various measures of anxiety but not to those of depression. This finding contradicts the previously held view of linking somatic symptoms with the presentation of depression.

An evaluation of 15 patients treated by subcaudate stereotactic tractotomy (SST) for treatment-resistant unipolar affective disorder was made for frequency and severity of recurrence of illness. One-third had died by the time of assessment, but none by suicide. Two-thirds of the sample experienced a reduction in the severity of depressive episodes after the operation; only one-third reported a reduction in frequency of episodes.

Of three siblings in a family, one brother and one sister have both tyrosinase-negative oculocutaneous albinism and a psychotic disorder indistinguishable from schizophrenia. The two disorders may associate within families through genetic linkage or a failure of neurotransmitter homoeostasis.