The demonstration that an endocrine disorder can precipitate a specific mental illness would be an important step towards the development of much needed animal models of affective disorder. To this end we have sought and found evidence for a causal connection between Cushings syndrome and the apprearance of a depressive illness (Kelly et al, 1980 and 1983). Whether or not hyperthyroidism can cause a manic depressive illness is at present uncertain. Reported values for the incidence of depression in hyperthyroidism vary from 1–20 per cent (Bursten, 1961; Clower et al, 1969; Dunlap and Moersch, 1935; Johnson, 1928; Katzenelbogen and Luton, 1935; Kleinschmidt et al, 1956; Lidz and Whitehorn, 1949) and these are similar to estimates of the incidence of depression in a general population (Watts et al, 1964; Shepherd et al, 1966; Crombie, 1974; Brown and Harris, 1978). Similarly estimates of the incidence of hyperthyroidism in depressed patients are around 1 per cent (Bursten, 1961; Bluestone, 1957; Martin, 1963) which is also similar to the incidence of hyperthyroidism in the general population (Tunbridge et al, 1975). Finally in a population of patients with recurrent manic depressive illness, the eight observed episodes of hyperthyroidism striking during normal health were not apparently followed by any mental disturbance (Checkley, 1978). We now report upon a patient in whom two episodes of mania coincided with two episodes of hyperthyroidism and discuss the possibility that the two illnesses were related to each other.

A treatment trial comparing cognitive therapy and pharmacotherapy, alone and in combination, in depressed out-patients, indicated that outcome on cognitive variables was similar to outcome on mood and severity measures, pharmacotherapy being less effective than cognitive therapy or the combined treatment in a hospital and a general practice sample. While combined treatment was superior to cognitive therapy in the hospital outpatients, the two treatments were equivalent in the general practice. Significant effects were obtained on measures of views of self, the world and the future, whose validity was demonstrated. The pattern of change through treatment showed the same order of progress for responders, while non-responders to cognitive therapy tended to do worst. The specificity of treatment effect is discussed.

A young man aged 23 made contact and asked to talk about an adverse drug reaction. He had been puzzled and frightened by what had happened to him and although he was a very experienced drug-user he had not fully realized that a drug could cause such consequences—he had feared that he was going mad. He came along not as ‘a patient’ but because he believed that he had something to tell which might add to medical insights.

A four-year follow-up of clinically selected hyperactive boys with and without associated conduct disorder investigated their outcome during early adolescence and was taken from a structured behavioural interview and standard psychological testing.

Boys originally diagnosed as “purely” hyperactive continued to be inattentive and impulsive at follow-up, but showed very few aggressive and antisocial behaviours. Hyperactive boys who had earlier been undersocialized and aggressive continued to have problems with attention and impulsivity, were reported to be aggressive, noncompliant, egocentric, exhibiting antisocial behaviours and using alcohol. These findings suggest that antisocial and delinquent behaviour often reported in follow-up studies of hyperactive boys may be linked to childhood aggression and unsocialized behaviour, rather than the syndrome of hyperactivity.

A case of tuberculous Addison's disease presenting with psychosis, profound hyponatraemia, and detectable plasma antidiuretic hormone is reported. Clinical and biochemical improvement after corticosteroid replacement was followed by relapse with further psychosis and inappropriate antidiuretic hormone secretion: both were promptly reversed by demethylchlortetracycline. The association of psychological symptoms with Addison's disease, the role of anti-diuretic hormone secretion in Addison's disease, and the inter-relationship between Addison's disease, psychosis and anti-diuretic hormone secretion are discussed.

Goldstone and Sarbin proposed that auditory hallucinations occur because imagery in a non-preferred sensory mode is more easily misinterpreted as having an external origin. This led to the hypothesis that auditory hallucinators would show less preference for auditory than for visual imagery. Our results suggest that this is true. We also compared the vividness of internally-generated auditory imagery with that of visual imagery, independently of preference, to see whether vividness was impaired in the non-preferred mode in hallucinators. The evidence suggested that this was not the case, but we did find a significantly deficient capacity for creating vivid images of either kind in process patients (i.e. those with poor premorbid status) compared with reactive (good premorbid) patients, regardless of any history of hallucinations. The withdrawal of external attention which characterizes process patients might also be expected to impair their ability to confirm or disconfirm the external origin of an auditory stimulus. We predicted therefore that process hallucinators would be particularly incompetent in spatial location of sounds: our experimental results confirmed this to be the case.

The authors conducted a preliminary trial of a 5-day course of diphenoxylate in the treatment of out-patients with methadone withdrawal symptoms. Diphenoxylate provided substantial relief from detoxification symptoms with no drug-associated adverse effects.

Prolactin, Cortisol, growth hormone and TSH serum levels (before and 15 minutes after treatment) were measured in 62 patients with endogenous depression randomly allocated to real or pseudo-ECT. Prolactin increased significantly more in those receiving real ECT than in those receiving pseudo-ECT, but the size of this effect had diminished by the time of the last (8th) treatment in the trial. Cortisol secretion was also significantly increased following the first treatment by real ECT, but this increase was of significantly smaller size in patients with delusions. Tolerance to the effects of ECT on Cortisol secretion was not observed. No effects of ECT on growth hormone or TSH secretion were detected, and no clear evidence was obtained that endocrine responses can be used as a predictor of response to ECT.

Psychological deterioration, defect state and psychological deficit are all terms introduced this century to replace Kraepelin's idea of dementia praecox. They all express the notion that schizophrenics have some global impairment in psychological functioning, which is different from the presenile dementias or recognised causes of cerebral dysfunction. At the beginning of the century it was generally regarded as organic in nature. In the 1960s the social revolution in psychiatry encouraged the view that the deterioration was psychosocial, the effect of institutionalisation. There has been a recent trend to revive the organic formulation.

The five articles which follow examine the idea from different points of view. They were commissioned because correspondence to the editor indicated that the issue was topical and controversial. It is hoped that they may be the first of a series of multi-author contributions on topical issues.

Manfred Bleuler presents his view that deterioration is not a progressive condition, but one of several outcomes, and even then liable to remission. Luc Ciompi discusses the relationship between organic and psychosocial factors in its cause, and concludes that it is the result of an interaction between the two. Tim Crow gives a clear account of the organic model. David Abrahamson draws attention to some methodological issues, which have led to a false clinical impression, and wrongly overemphasised the extent of deterioration. Digby Tantam analyses the complex effect of drug treatment.

There has been attention drawn recently to those parents who deliberately harm their children in relatively unusual ways such as poisoning (Rogers et al, 1976; Lorber et al, 1980; Kempe and Heifer, 1980). Prognosis has been poor, with a high mortality rate for the children unless removed, and parental denial precluding any form of family rehabilitation.

Pemoline is a central nervous system stimulant, with pharmacological effects resembling amphetamine and methylphenidate in increasing central dopamine transmission (Fuxe et al, 1970; Sheel-Kurge, 1971).

A case of childhood bipolar disorder, manic type, is presented in which electroconvulsive therapy was used for the acute manic episode. The pharmacological complications which led to this choice of treatment and the computerized tomography finding of ventricular enlargement, are discussed.

Two cases are described where auditory hallucinations persisted, in spite of medication, in two schizophrenic patients, one with acute onset and one with a severe chronic illness. The hallucinations were treated successfully by methods derived from Green's theory that auditory hallucinations are represented in the non-dominant hemisphere.

Naylor's recent hypothesis that vanadium ‘poisoning’ could be a factor in the severity of manic-depressive illness drew attention to the normal and even essential presence of vanadium in the diet, and in human living tissues. The whole brain may contain only about 45 micrograms of vanadium (Underwood, 1977; 1979), as against 500 micrograms of manganese, 130 μgm selenium, and less than 20 μgm molybdenum—others of the 12 or so essential metals required in traces. We might take copper as the principle trace metal—an important component of over 50 enzymes, including monoamine oxidase and dopamine β-hydroxylase—with a total in the whole man of about 100 mg. In contrast, metals like potassium (140 gm), magnesium (35 gm), iron and zinc (3–4 gm) are not present in traces but in gram quantities. Lithium, present naturally in the body in extremely minute amounts, is raised in therapy to occupy a borderline position in the scale, rather more than copper, less than zinc.

Very few patients with ulcerative colitis are likely to be referred or to refer themselves for psychotherapy for their condition. Recently I was asked by a gastro-enterologist to see Caroline, a young woman in her early thirties, who had ulcerative colitis, with a view to her discussing having psychotherapy. This was because she had caused him and a social worker in this hospital to be concerned about her emotional state.

As scientific technologies become more sophisticated, clinicians may come to think that they must devolve into passive recipients rather than contributors to the advances in basic knowledge. This perception and accompanying modesty towards the neurosciences, however, is an error. The intellectual trade between clinician and bench scientist has always been bi-directional and nowhere is this more clearly evident than in recent interactions between psychiatry and neuroscience.

Regular, long term haemodialysis is a standard treatment of patients in chronic renal failure. Its psychiatric implications have been dealt with in a number of studies, most of which concentrate on purely psychological or social aspects, for example patients' perception of and response to illness (Pritchard, 1974), the relevance to outcome of basic personality (Kaplan De-Nour and Czaczkes, 1976), or the impact on the family of dialysis carried out at home (Farmer et al, 1979). There are two distinct psychiatric syndromes of importance which can be clinically recognized.