Plasma melatonin was used to determine overall beta‐adrenergic transmission through pineal neuro‐effector junctions during desmethylimipramine (DMI) treatment in 10 normal subjects. Changes in plasma melatonin indicated that an initial increase in noradrenaline (NA) transmission produced by DMI was counteracted by adaptive changes which restored transmission to normal by the third week of treatment. A 'rebound' increase in NA transmission was seen on DMI withdrawal. The results suggest that the adaptive changes which occur in NA synapses during DMI treatment do not, as has been proposed, decrease NA transmission below normal levels, but instead restore homeostasis in the presence of the drug.

A distinction is made(British Medical Journal, 1978; Munro, 1980) between an excessive preoccupation with minor bodily defect, dysmorphophobia, and monosymptomatic psychosis in which a delusion of bodily change may be the sole symptom of an underlying schizophrenic or depressive illness. Hay (1981) has argued for careful distinction between the over-valued idea of dysmorphophobia and the delusion of depressive or schizophrenic illness. But in the absence of any features suggesting psychosis, scrutiny of the abnormal belief in isolation may fail to detect which sort it is. Riding and Munro (1975) hold the distinction to depend upon assessment of the abnormal belief as being of ‘neurotic’ versus ‘delusional’ intensity and of the degree of personality involvement. Andreasen and Bardach (1977) have proposed formal diagnostic criteria incorporating similar features: the dysmorphophobic symptom of excessive concern with appearance, the desire for surgery or underlying presence of personality disorder, and the absence of psychotic symptomatology. However, judgements of ‘neurotic’ versus ‘delusional’ intensity, of absence of psychotic symptomatology and of personality involvement may be particularly difficult against a background of developing personality and in adolescence the problem may be further compounded by the cumulative and recursive effects upon personality development of psychological disturbance.

It is claimed that the dexamethasone suppression test (DST) can be used in the diagnosis of depression, on the grounds that a positive test occurs in about half of patients with depressive illness but in few patients with other diagnoses. It is also variously claimed that a positive test is associated with particular types or features of depressive illness, that it is an index of severity, and thatitcan be used to predictoutcome. Many of these claims appear in the literature, fail to be reproduced by others, but nevertheless become incorporated into a persistent body of unsubstan tiated professional folk lore. The aim of this paper is to evaluate these claims, and to establish what use the test does have in the diagnosis and management of a depressive illness. (1) Method that either 3 @tg/l00ml or 4 @tg/100 ml gave the best discrimination. Plasma cortisol assay methods have been reviewed in detail by Meltzer & Fang (1983); they concluded that results from CPBA and RIAâ€"the two commonest methodsâ€"are not necessarily com parable, as different RIA methods may over-or underestimate cortisol levels, as measured by CPBA. They suggest that any study on the DST should show that the cortisol assay method used is sensitive in the concentration range of interest, and that it is accurate by comparison with a reference method. Studies reviewed here have used criterion values of between 4 and 6 @ig/l00 ml; one author (Sachar et a!, 1980) has used 3 @ig/100 ml. The risk with a lower value is that more false positives will be collected, and with a higher value that fewer depressed patients will be identified. However, because of variations in the accuracy of plasma cortisol assay methods, it may be appropriate for a cutoff point other than 5 @tg/l00ml to be used in some studies. et al (l981a), in their standardisation paper, found that a level above 5 @tg/l00 ml provided the best separation between depressed and non-depressed patients. They used a competitive protein binding assay (CPBA) for plasma cortisol, while Stokes et al (1984), who used a radioimmunoassay (RIA), found 363

SynopsisRadioligand binding to intact platelets was carried out in antidepressant-free patients and the 1 mg dexamethasone suppression test (DST) was performed. There were no differences in binding characteristics between patients and controls for either [H]yohimbine or [H]imipramine. There were no differences in binding between patients classified as endogenous using the Newcastle Scale, compared with non-endogenous patients, and no difference between DST suppressors and non-suppressors. The severity of depression did not affect binding values. After 4–6 weeks antidepressant treatment [H]yohimbine binding was significantly reduced but [H]imipramine binding was unaffected.

No abstract

The plasma prolactin (PRL) response to haloperidol 2 or 4 mg i.m. was studied in 18 schizophrenic men during their routine treatment with neuroleptic drugs. A substantial rise of the PRL level above the treatment baseline occurred in all but four of the 20 tests showing that the PRL elevation induced by treatment was not maximal. The challenge was ineffective only in patients receiving very high daily doses of medication. The increment was inversely correlated to the daily dose of medication but unrelated to plasma haloperidol concentrations during the test. Chronic schizophrenics who were receiving long term treatment and had low basal PRL levels did not show tolerance to the prolactin stimulating effect of haloperidol. That prolactin rose during the test in patients who had improved during their current treatment indicates that the degree of dopamine receptor blockade required for therapeutic effects is below that which produces a maximal PRL response.

No abstract

Anterior pituitary response to TRH 200 micrograms i.v. was studied in ten chronic schizophrenic patients during long-term neuroleptic treatment. Nine patients had normal prolactin (PRL) response as compared with controls but in one the response was blunted; one patient had an exaggerated response. Prolactin increment was higher following TRH than haloperidol challenge. No growth hormone (GH) response to TRH was found and TSH responses were comparable to controls.