One week after Sir William Gull read his seminal report on anorexia nervosa to the Clinical Society of London, a brief account was published (Anonymous, 1873). In Paris, Charles Lasègue, editor of Archives Générales de Médecine read the report and printed an immediate editorial riposte, parts of which will be quoted in this communication.

Pagophagia, or the excessive consumption of ice or iced drinks, is popularly regarded as a novel manifestation of pica, which has emerged, predominantly in the USA, over the last 30 years. However, a sampling of historical sources reveals that not only are there warnings in the writings of both Hippocrates and Aristotle concerning the dangers of excessive intake of cold or iced water, but a series of medical works, from the sixteenth century on, incorporate discussion and illustrative case histories about the detrimental effect of immoderate usage of cold water, ice and snow, frequently in the context of disordered eating.

Eight patients with endogenous depression who had received no antidepressant treatment for the previous year were treated with the noradrenaline (NA) uptake inhibitor, desipramine (DMI). Pre-treatment plasma melatonin concentrations were normal. After one day of DMI treatment plasma melatonin concentrations were increased but the response was impaired compared to normal subjects. The acute effect of DMI on plasma melatonin persisted after six weeks of treatment. These findings question the hypothesis that beta adrenoceptors are supersensitive in depression and that antidepressant drugs act by down-regulating these receptors.

Utilizing a wide range of eighteenth- and nineteenth-century biographical sources, the eating pathology of Dr Samuel Johnson is illustrated and examined. His presenting symptoms are considered in the light of modern criteria for eating disorders and current research on bulimia nervosa and rumination disorder.

The history of psychiatric journals is outlined from their inception in the late eighteenth century. In the development of psychological medicine they serve as intellectual markers of the complex relations between institutional psychiatry, neurology, the psychosocial sciences and the psychotherapeutic movement. Their current status is briefly discussed.

Regional cerebral blood flow (rCBF) during a word fluency task was compared in twenty-five male, right-handed, medicated schizophrenic patients and twenty-five age-matched male, right-handed healthy volunteers, using 99mtechnetium-HMPAO multidetector single-photon emission tomography. Increased rCBF in caudate and thalamus was found in patients, probably secondary to neuroleptic medication. Patients showed decreased rCBF in left frontal cortical regions and increased rCBF in left posterior cortical regions, compared to controls. Patterns of left-sided frontal rCBF dominance in controls were reversed in patients, as were normal patterns of right-sided parietal rCBF dominance. Negative symptom score correlated inversely with mesial frontal rCBF, particularly on the left.

Several authors have reported attenuated adrenocorticotropin hormone (ACTH) responses to corticotropin releasing factor (CRF) administration in melancholic patients as compared with healthy controls. In order to explore the integrity of the hypothalamic–pituitary–adrenal (HPA)-axis in melancholics, we examined the following parameters in 98 subjects: the ACTH; β-endorphin; and cortisol responses to ovine CRF (oCRF) (100 μg/i.v.); and the postdexamethasone cortisol values. We found significant lower CRF-induced ACTH responses in melancholic patients as opposed to healthy controls and minor depressives, while major depressives occupied an intermediate position. The psychopathological correlates of the blunted CRF-induced ACTH responses were feelings of worthlessness, self-reproach, or excessive guilt. The CRF-stimulated β-endorphin and cortisol response did not differ between the study samples. Higher baseline plasma cortisol was associated with attenuated CRF-induced ACTH responses, but these effects were not pertinent to melancholia. There were no relationships between the disordered oCRF test results, and postdexamethasone cortisol values, age, body size, sex and severity of illness. The diagnostic power of the oCRF and the dexamethasone suppression test for melancholia is enhanced when both test results are combined.

Urinary excretion of neopterins and biopterins was measured in 23 patients with severe depression before and after receiving electroconvulsive therapy (ECT) and 26 healthy control subjects. Patients with psychotic depression and those responding to ECT had neopterin:biopterin (N:B) ratio significantly higher than controls before commencing ECT and positive therapeutic response was associated with reduction of N:B ratio towards control values. As a raised N:B ratio implies failure to convert neopterin to biopterin it is possible that reduced availability of tetrahydrobiopterin, the essential cofactor for the formation of noradrenaline, serotonin and dopamine, may exert rate limiting control over the synthesis of monoamines implicated in the pathogenesis of depressive disorders. The N:B ratio may be a marker for certain depressive subtypes and response to ECT.

Smooth pursuit eye movements to a sinusoidally moving target were recorded using the electro-oculogram in 49 subjects with bipolar disorder, 19 with major depressive disorder and 61 with definite schizophrenia, and compared with 145 normal controls. The signals were analysed in the frequency domain to yield a signal to noise ratio that is known to relate to accuracy of smooth pursuit. Smooth pursuit was found to be significantly poorer in schizophrenics than in bipolars, major depressed or controls. Eye-tracking performance was independent of the effects of neuroleptics, tricyclic antidepressants or lithium, and was not altered by the severity of depression in the affective psychoses. There was a small, but significant worsening of smooth pursuit with age in controls and schizophrenics, but this did not account for the group differences. The results support the view that among the major psychoses eye-tracking dysfunction is specific to schizophrenia.