Despite his acknowledged pre-eminence among British psychiatrists of the 19th century, Henry Maudsley (1835–1918) remains a ‘shadowy figure’, a name known through the Hospital and annual lecture funded by his beneficence. Apart from the homage paid by Sir Aubrey Lewis in 1951, there has been no recent attempt at any biography nor any critical reappraisal of Maudsley's life and work. On the basis of reviewing his role in the Medico-Psychological Association (MPA), his rather pessimistic and degenerationist philosophy, his undoubted wealth and his ‘hypercritical nature’, it is possible to define an alternative view of his significance and influence.

‘…comical, almost pitiable at times, is the ludicrous display of vanity by men of great eminence…they leave behind them carefully preserved letters and elaborate memoirs of what they thought and felt’. (Maudsley, 1918)

Psychiatry still lives in a Kraepelinian world and scholarship on the work of Kraepelin has consequently been unhistorical. Selective exegesis of the various editions of his textbook has led to a rigid view of his contribution. However, Kraepelin lived and wrote during an important period of European intellectual history and his work can only be understood against this background. This paper analyses the development of his views in terms of the ‘Research Programme’ he planned early in his life and whose objective was the creation of a stable description and classification of the psychoses. This Kraepelin eventually achieved by longitudinally studying patient cohorts in terms of methodological criteria such as illness course and incurability. In the event, this methodology allowed him to identify by correlation ‘clinical pictures’ that both represented the ‘essence’ of the disease and provided a taxonomic criterion. Although avowedly atheoretical, Kraepelin thus managed to construct (influenced by Kahlbaum and Wundt) an empirical support for his Kantian categorization of the psychoses. A discussion of the cultural variables that moulded these ideas is included.

It is well known that the end of the nineteenth century represented a ‘golden age’ of hysteria and hypnosis research under Jean-Martin Charcot in Paris, but the extent to which metals and magnets figured in this strange and provocative world has been very incompletely told. This paper offers itself as a first corrective to this neglect. In 1876 a certain elderly physician and mesmerist, Victor Burq, asked the Parisian Société de Biologie formally to establish the validity of his so-called ‘metallotherapy’ (later ‘metalloscopy’) treatment for hysteria. The paper argues that Charcot's participation in the investigation of Burq's work – undertaken in conjunction with two other leading French neurologists, Amédée Dumontpallier and Jules Bernard Luys – served as a major catalyst in arousing the great neurologist's interest in hypnosis in the first place, and was subsequently responsible for several of his key beliefs about the underlying physiological link between hypnosis and hysteria. It is also shown how these early metalloscopy studies – and especially the discovery by Charcot and his colleagues of so-called metalloscopic ‘transfer’ – opened the door to the rise of a neo-mesmeric, and increasingly occult, branch of hypnosis research in French psychiatry, which has to date, in the secondary literature, gone almost wholly unremarked.

Trosse's account of his life has been described as one of the strangest pieces of realism in the English language. It gives a detailed description of the author's personal experience of three episodes of psychotic disorder during the years 1656–7. The disorder has been considered an early instance of schizophrenia, but evidence is presented here to suggest that a more plausible diagnosis was alcoholic psychosis and affective disorder.

The development of knowledge about the mechanism of action of tricyclic and the so-called ‘atypical’ antidepressants (AD) is reviewed. The discovery of clinically active antidepressants with little or no effect on noradrenaline or serotonin uptake has disproved the widely accepted concept that inhibition of monoamine uptake is a prerequisite for antidepressant activity. Another serious objection to this hypothesis is that blockade of monoamine uptake occurs in a matter of minutes after administration while 2–3 weeks of repeated treatment are necessary for the clinical AD effect. Nevertheless, the effect of repeated treatment with AD is compatible with the hypothesis that changes in central monoamine transmission are involved in the clinical activity of these drugs. Major changes in monoamine function after repeated treatment with AD include: desensitization and reduced density of noradrenaline receptors coupled to the adenylcyclase system, opposite changes in the sensitivity of α1 (increased) and α2-adrenoreceptors (decreased), down regulation of serotonin2 receptors and complex changes in the behavioural and electrophysiological responsiveness to serotonin agonists, subsensitivity of presynaptic dopamine receptors and enhanced activity of the mesolimbic dopamine system, decreased and increased density of GABA-A and GABA-B receptors respectively and down regulation of [3H]benzodiazepine binding.

It remains to be clarified whether some of these changes have larger roles than others or whether they all contribute to the AD activity. An important role of dopamine in the activity of AD drugs is suggested by findings in the forced swimming test, whereas both catecholamines seem to be involved in the attenuation of escape deficit provoked by inescapable shock (learned helplessness). No clear evidence for a role of serotonin (with the possible exception of serotonin1A receptors) or GABA has been obtained in these experimental models of depression. The general validity of these findings obviously rests on the assumption that these models represent significant aspects of human depression.

Nine physically healthy, adult autistic men, with normal or near normal intelligence, and 13 healthy male controls were examined in a CT brain scan study. CT scans were analysed with a fully automated computer-assisted program, and regional brain radiodensities were measured with careful attention to artefacts. Autistic patients revealed significantly larger third, but not lateral, ventricular size and significantly lower mean caudate, but equivalent mean frontal and thalamic, radiodensities compared to controls. The sizes of the Sylvian fissures and interhemispheric fissure were equivalent between groups. The findings are consistent with selective subcortical abnormalities in autism.

Regional cerebral blood flow, oxygen consumption and glucose consumption were measured by positron emission tomography in six young autistic men. No significant differences were found between patients and normal controls for any of the physiological variables. The results do not substantiate the previous finding of glucose hypermetabolism in autism; the likely reasons for the variance in findings are discussed.

This paper surveys the measures taken against mental patients in Germany during the National Socialist regime. It covers the eugenic sterilization programme, the killing of handicapped children, the so called Action T4 (the killing of adult psychiatric patients) and the second phase of Action T4 after its official termination, i.e. between 1941 and 1945. The possible social and political causes of these measures, and the attitude of German psychiatrists to them are discussed. In particular, attention is drawn to a prevalent fear of national degeneration, to social Darwinism, and the ideas of Binding & Hoche on ‘permission for the extermination of worthless life’.