In 1904 and 1906, Heymans reported the results of two prospective questionnaire surveys on déjà vu experiences and depersonalization in a sample of mainly students. Déjà vu experiences appeared to be more frequent than episodes of depersonalization. Emotional sensitivity, unstable mood fluctuations, apathetic episodes and irregular working rhythm emerged as predisposing personality traits. With the exception of the working rhythm, these traits were more prominent among the respondents with episodes of depersonalization than among those with déjà vu experiences. Heymans inferred that these findings supported his hypothesis that déjà vu experiences and depersonalization both resulted from the diminishing or disappearance of a sense of familiarity due to a momentary reduction of psychological energy. A re-analysis of Heymans' data partly confirmed his findings and conclusions as to the predisposing factors. The authors conclude that his studies and his hypothesis have been hitherto undervalued and would deserve more attention.

It would be unwise to hazard a diagnosis for those attacks of illness to which Van Gogh was subject and which he dreaded. Karl Jaspers (1922) believed it might be possible to speak of schizophrenia, but few people today would retain this diagnosis as there is no indication of it in either the paintings or in the copious writings. Psychomotor epilepsy has, more recently and with greater plausibility, been proposed while certain symptoms are suggestive of attacks of vertigo of labyrinthine origin. The outbursts of anger, the anxiety attacks contribute to a clinical picture indisputably exacerbated by absinthe abuse. And there were frequent periods of dysphoria and depression. But who would dare to pin any of the classical labels of melancholia on Van Gogh?

Sixty years ago the distinguished epidemiologist Joseph Goldberger, following his outstanding achievements in clarifying the causes of pellagra, was offered a large research grant to investigate schizophrenia. He responded to the proposal by studying the available evidence concerning the schizophrenic syndrome and then politely declined to take up the challenge. ‘In five or more years’, he wrote, ‘I could probably find out nothing. Much work will be needed on the physiology of the central nervous system and on many collateral problems before dementia praecox can be understood’ (Parsons, 1943).

A meta-analysis was carried out on 53 cases of dementia praecox (DP) and 134 cases of manic-depressive insanity (MDI) originally diagnosed by Kraepelin or his collaborators in Munich in 1908. The original case material was coded in terms of Present State Examination syndromes and analysed statistically for internal consistency and discrimination between the two diagnostic entities. Kraepelin's DP and MDI were found to define homogeneous groups of disorders which could be clearly distinguished from one another. A CATEGO re-classification of the cases revealed an 80·2% concordance rate between Kraepelin's diagnoses and ICD-9. Cluster analysis of the original data reproduced closely Kraepelin's dichotomous classification of the psychoses but suggested that DP was a narrower concept than schizophrenia today, while MDI was a composite group including both ‘typical’ manic-depressive illnesses and schizoaffective disorders.

We report the results of a collaborative linkage study using 12 polymorphic markers (9 loci) from the long arm of chromosome 11, and 24 families multiply affected with schizophrenia and other closely related disorders. This region is of interest because several families have been reported in which balanced translocations involving 11q apparently co-segregate with psychotic illness. In addition, the dopamine D2 receptor, porphobilinogen deaminase, and tyrosinase genes map within the region studied and may be aetiologically involved in schizophrenia. We have primarily analysed genotypic data by the LOD score method using a range of single gene models. In order to minimize error due to mis-specification of genetic parameters we have analysed data from markers at candidate gene loci by the non-parametric extended sib-pair method in addition to the LOD score method. Our results suggest that most of the region can be excluded from containing a gene of major effect in the aetiology of this disease.

Sir Aubrey Lewis studied 61 depressives in considerable detail, principally cross-sectionally but also by reviewing progress. He concluded that he could find no qualitative distinctions between the depressed patients and thus established himself as a strong and influential advocate of the unitary view of depression (i.e. that depression varies dimensionally, not categorically). Subsequently, Kiloh & Garside (proponents of the binary view of two depressive ‘types’) coded the Lewis data and undertook a principal components analysis. They claimed success in distinguishing ‘endogenous’ and ‘neurotic’ depressive types within Lewis' sample. In this paper we re-analyse the data set using both a latent class categorical approach and mixture analyses. We suggest that any demonstration of sub-types was limited by relative homogeneity of the sample (in that up to 80% had probable or possible psychotic conditions), and by Lewis rating a number of important features (e.g. delusions) dimensionally rather than categorically. Nevertheless, we identify one categorical class (essentially an agitated psychotic depressive condition) and a residual (presumably heterogeneous) class. The presence of those two classes was supported by demonstrating bimodality in composite scores derived from the fourteen differentiating clinical features (and not evident when all clinical features were considered), and formally confirmed by mixture analyses. Membership of the categorical class was determined principally by psychotic features (delusions and hallucinations) and by objectively-judged psychomotor disturbance, and we consider the nature of that ‘class’. Lewis' data set is unusual (in having self-report and observationally rated data), and historically important in demonstrating that conclusions may depend on the choice of variables examined and analytical approaches.

A brief historical outline is provided of the concept of specificity in biology and medicine. The advent of scientifically based therapeutics, and especially clinical pharmacology, has directed increasing attention to the role of non-specific factors in the field of mental disorders. The actions and effects of placebos are discussed in relation to the specific/non-specific dichotomy with particular reference to both pharmacological and psychological modes of treatment.

Schizophrenic subjects (N = 30) performed less well than controls (N = 30) on neuropsychological tests sensitive to frontal and temporal lobe impairment and showed prolonged latency of the P300 event-related potential. Relatives of schizophrenic probands were also tested. Relatives with an abnormal P300 had a similar range of neuropsychological deficits as were found in the schizophrenic group and relatives with a normal P300 response performed as well as the normal control group. The results suggest that neurophysiological and neuropsychological testing of relatives may help to clarify the mode of inheritance of schizophrenia in some families.