Oncogenes are genes whose expression has been associated with malignant transformation of cells in tissue culture and with neoplastic change in vivo (Bishop, 1987). Much of the current understanding of their nature and action has stemmed from work, over the past 20 years, on tumour viruses (Temin, 1971; Rapp, 1983). One group of tumour viruses, the retroviruses, are unique in possessing an enzyme, reverse transcriptase, which transcribes to the cell DNA a copy of the viral RNA genome (Marks, 1987). After the discovery of viral oncogenes, such DNA copies were used as probes in hybridisation studies (Stehelin et al, 1976; Frankel & Fischinger, 1976). These probes, capable of annealing to complementary DNA sequences, revealed the existence of the latter in normal, unaffected cells (Willecke & Schäfer, 1984). These sequences, called cellular or proto-oncogenes, exist in a wide range of eukaryotic organisms, from yeast to man.

The 1980s witnessed the honeymoon between American psychiatry and an enigmatic and mysterious drug complication called neuroleptic malignant syndrome (NMS). I fear that the 1990s are witnessing the same in British psychiatry. Gone is the era when case reports in British literature described the syndrome without identifying it by name (Allan & White, 1972; Moyes, 1973), ostensibly owing to lack of awareness. Probably, no one had bothered to read the original description in the French-language literature (Delay et al, 1960). The pendulum has now swung to the other extreme. Every known drug-related complication is being labelled NMS. In the US, Addonizio et al (1986) suggested a ridiculously high incidence figure of 12.2%. The same trend for overdiagnosis is seen in the recent case report by Dalkin & Lee (1990). The authors of this case report seem to have forgotten that NMS is an idiosyncratic adverse drug reaction which is dose-independent. There is no reason to label every neuroleptic overdose as NMS on grounds of raised creatine phosphokinase (CPK) level.

The diagnostic concept and classification of chronic depressions has long been a matter of controversy. Kraepelin (1921) considered chronic depression to be a ‘rudiment’ of fully developed manic-depressive insanity, and this view was shared by Slater & Roth (1969), who cited occasional dramatic improvement in patients with neurasthenic disorder when they received convulsive therapy.

An exploratory factor analysis of the HAD was carried out in 568 cancer patients. Two distinct, but correlated, factors emerged which corresponded to the questionnaire's anxiety and depression subscales. The factor structure proved stable when subsamples of the total sample were investigated. The internal consistency of the two subscales was also high. These results provide support for the use of the separate subscales of the HAD in studies of emotional disturbance in cancer patients.

A 40-year-old man suffered both a short-term memory defect and bipolar mood disorder. It is postulated that both conditions are due to progressive cerebral sarcoidosis affecting the limbic system. The need for early detection and treatment is emphasised.

Fifty patients with UC and 50 matched controls with urolithiasis were interviewed with the SADS (lifetime version) and completed the SCL–90. According to information given during the SADS, there was a history of psychiatric disturbance in 11 UC patients (22%) and 8 controls (16%). At the time of the interview a psychiatric disturbance was present in 31 UC patients (62%) and four controls (8%), the most frequent diagnoses in the former being minor depression and generalised anxiety disorder. Patients with UC scored significantly higher than the controls on all the different SCL–90 subscales.

Among 307 adults with OCD, early onset (age 5–15 years) was more common in men and later onset (age 26–35 years) in women. Early onset was associated with more checking, and late onset with more washing. More women than men had a history of treated depression; 12% of the women but none of the men had a history of anorexia. More women than men were married. Gender-divergent features may reflect differential aetiological factors. Our sample resembled others in the literature in its slight overall female preponderance, low rate of marriage and low fertility, onset mainly before age 35 years, chronicity, and common present and past depression.

Sixty-three relatives of 52 schizophrenics living at home were offered a package of treatments by professionals working in an everyday NHS setting: educational seminars, relatives' groups, and family meetings. Thirty-two relatives refused intervention. Of the 31 relatives who agreed, 14 attended neither the educational seminars nor the relatives' groups. Seventeen relatives had a mean of ten treatment sessions, but there was little change in their level of expressed emotion after intervention. The number of patients who relapsed was the same in the 18 months before and after intervention, although the total number of relapses fell after intervention.

British Journal of Psychiatry (1991), 158, 110–113

“To isolate and quantify possible determinants of any increased prevalence of depressive disorders in women we studied a select group of men and women, initially similar in terms of a number of putative social determinants of depression, and reviewed the sample five years later when social role diversity was anticipated. We used the Diagnostic Interview Schedule (DIS) to generate DSM–III and RDC diagnoses to estimate lifetime depressive disorders, and established (via corroborative reports) the likely accuracy of those data. Despite lifetime depression being a relatively common experience, no significant sex differences in depressive episodes were demonstrated, suggesting the possible irrelevance of biological factors in determining any sex difference. As there was not major social role divergence over the five year study, we interpret the lack of a sex difference as a consequence, and suggest that findings support the view that social factors are of key relevance in determining any female preponderance in depression described in general population studies.”

Eighteen long-stay patients from an old county asylum moved into hospital hostels. After 12–24 months, there were significant reductions in overall symptoms, as rated by the CPRS and the Krawiecka scale, as well as in deviant but not general behaviour, rated by the REHAB scale. Six later moved to live in supported accommodation. All relatives and patients who expressed an opinion to an independent assessor were satisfied with their present accommodation or wished to move to more independent living.

“In a prospective, randomised, controlled trial to determine whether comprehensive lifestyle changes affect coronary atherosclerosis after 1 year, 28 patients were assigned to an experimental group (low-fat vegetarian diet, stopping smoking, stress management training, and moderate exercise) and 20 to a usual-care control group. 195 coronary artery lesions were analysed by quantitative coronary angiography. The average percentage diameter stenosis regressed from 40.0 (SD 16.9)% to 37.8 (16.5)% in the experimental group yet progressed from 42.7 (15.5)% to 46.1 (18.5)% in the control group. When only lesions greater than 50% stenosed were analysed, the average percentage diameter stenosis regressed from 61.1 (8.8)% to 55.8 (11.0)% in the experimental group and progressed from 61.7 (9.5)% to 64.4 (16.3)% in the control group. Overall, 82% of experimental-group patients had an average change towards regression. Comprehensive lifestyle changes may be able to bring about regression of even severe coronary atherosclerosis after only 1 year, without use of lipid-lowering drugs.”

In a cohort of five patients from the Middle East with the Gilles de la Tourette syndrome, family history of a tic disorder or the Gilles de la Tourette syndrome was positive in three cases. In one of these there was a multiply affected pedigree spanning six generations. The phenomenology of the syndrome is the same as that described in Western reports. The familial pattern of inheritance and cross-cultural similarity emphasise the biological factors in the aetiology of the syndrome.

Five consecutive cases of the NMS are presented, in all of which a catatonic state preceded the onset of the condition. Catatonia would appear to represent a highly significant risk factor for the NMS and a possible causal link between the two disorders is suggested.