Until the last decade there was considerable confusion about the nosology of childhood psychoses. As Kanner (1958) has pointed out, certain psychodynamically orientated writers (Szurek, 1956; Beres, 1956) have eschewed the important operation of differential diagnosis. This has led to the notion of ‘equality of schizophrenias' (Darr and Worden, 1951) and thus to the idea of a single psychosis of childhood. The controversy over this approach has now waned in the face of empirical evidence from aetiological, phenomenological and follow-up studies, and many authors have stressed the importance of age of onset in their typologies or in their attempts at a more comprehensive classification (Kanner and Lesser, 1958; Mahler et al., 1949, 1952; Bender, 1947, 1959; Anthony, 1958, 1962, and Eisenberg, 1967). As this is also central to the present study it merits examination in greater detail.

This paper analyses the clinical picture in 80 children referred to the Park Hospital, Oxford, or to the Newcastle department of child psychiatry, and admitted for intensive assessment of their psychosis. All were seen by two psychiatrists and nearly three quarters of them in Oxford. The diagnostic criteria, and the differentiation by age of onset into infantile psychosis (I.P.) and late onset psychosis (L.O.P.) were discussed in the previous paper (Kolvin, I).

The first paper of this sequence discussed the division of childhood psychoses into those with onset before the age of 3 (infantile psychoses, I.P.) and those with onset after the age of 5 (late onset psychoses, L.O.P.). The second paper described in detail the clinical phenomena in 80 psychotic children so classified at Oxford or Newcastle (see Table I), and showed that this division corresponded to clear-cut distinctions in the clinical pictures. The I.P. group showed gaze avoidance, abnormal pre-occupations, self-isolating patterns of behaviour, echolalia, overactivity. The L.O.P. group showed hallucinations and thought disorder. With these two groups clearly established we now look to see whether anything in their family and background also distinguishes them.

It is a common assumption in child psychiatry that the personality and attitudes of parents exert a fundamental influence on the developing child. This hypothesis merits careful examination. The authors were particularly interested in testing it in relation to aberrant personalities and undeniable psychiatric disorder in childhood. Theoretically there are two main methodological steps;

1. (i) The proving of a correlation between parental and childhood variables. The present paper concentrates on this step.

2. (ii) experimental or other studies to demon strate causal relationships between these variables.

A series of recent papers (Creak, 1961, 1963; Rutter, 1966; Brown, 1963; Lotter, 1967; Schain and Yannet, 1960) have provided evidence of degrees of cerebral dysfunction in infantile autism (Kanner, 1943) and other infantile psychoses. They have demonstrated that groups of cases of infantile psychoses satisfying broadly similar diagnostic criteria have in their backgrounds a variable frequency of cerebral insult and abnormal discharge in the EEC The diagnostic criteria in such series are of crucial importance. Imprecision and vagueness hamper comparisons between series. In childhood psychoses some investigators have excluded those cases in which there was any history or clinical evidence of organic features in an attempt to obtain a ‘pure’ group. This technique, while valid in delineating a syndrome, is handicapping to subsequent etiological study. For these reasons the present authors have used only age of onset and behavioural features as their ascertainment criteria it was a behavioural rather than an aetiological diagnosis.

This is the sixth and final paper of a series studying various symptomatic, physical and social aspects of a sample of 47 cases of infantile psychosis (I.P.) and 33 cases of late onset psychosis (L.O.P.). They were seen at the Park Hospital for Children, Oxford, and the Newcastle Child Psychiatry Unit.

Child psychiatrists are much exercised at the present time about the classification of clinical syndromes occurring in children (Rutter et al., 1969). Perhaps surprisingly, there is less difficulty in the case of such relatively rare conditions as childhood psychoses, the psychoneuroses or even the syndromes associated with neurological dysfunction than there is in the categorization of the common behaviour disorders.

Various abnormalities have been demonstrated in schizophrenic patients in response to injected insulin. Thomas et al. (22), Harris (8), Freeman et al. (7), Mayer-Gross (10), and Braceland et al. (4) have shown a delayed or decreased response of blood glucose to insulin in schizophrenic patients. Meduna and McCulloch (11) observed that those schizophrenic patients who suffered from confusion and clouding of the sensorium particularly displayed a delayed or decreased response to injected insulin as well as a urinary hyperglycaemic factor and decreased tolerance to oral and intravenous glucose. Subsequent studies by Mueller (12, 13) demonstrated a rise or lack of fall in the plasma free fatty acids (FFA) following the administration of insulin intramuscularly or intravenously in chronic schizophrenic patients. Van Sickle et al. (23) confirmed these findings of insulin resistance in chronic schizophrenia and noted that this low FFA response was neither related to an abnormal release of, nor response to, epinephrine.

Kasanin (10) seems to have been the first author to use the term 'schizo-affective psychosis'. He drew attention to Lange's observations of catatonic features in mania, and to Claude's concept of 'schizomanie’. The case records of his young and acutely ill patients make one wonder, however, whether Kasanin had been sufficiently ready to recognize mixed manic-depressive states. Arising from the study of more prolonged illnesses, the Kleist-Leonhard school attempted to construct a number of sub-categories of schizophrenia in order to accommodate ‘cycloid’ cases. In this country, the term 'schizo-affective’ is at the present time in bad odour. Aubrey Lewis (11), employing very searching criteria, discovered schizophrenic symptoms in 23 of his 61 patients with affective psychoses, but derived them from hereditary and personality factors. Both Batchelor (2) and Mayer-Gross, Slater, and Roth (13), while admitting the occasional co-existence of manic-depressive and schizophrenic psychoses largely ascribed to mixed inheritance, have indicated that the schizo-affective label could be avoided by a more rigorous diagnostic approach and follow-up. These were employed recently by Clayton et al. (6), and of 39 schizo-affective patients 33 were re-assessed after at least one year; only 13 were still ill; and although 5 of them continued to show some schizophrenic symptoms, the authors interpreted their findings to indicate that schizophrenic deterioration was not a usual result of schizo-affective illness. Moreover, the family histories suggested a very strong relationship with ordinary affective illnesses rather than with schizophrenia or schizo-affective psychoses. These workers did not, therefore, confirm the claims of others (e.g. those arising from Mitsuda's (14) twin studies) to the effect that atypical psychoses were in a genetically different category from schizophrenia and manic-depression. The concept of 'schizo-affective’ has been devastatingly criticized by Foulds and Caine (7) on logical grounds.

There have been numerous psychotherapeutic approaches (e.g., total push, community therapy, token economy, buddy system, etc.) advocated for hospitalized chronic schizophrenics. Although these programs have had relative success in producing improvement in at least some of these patients, it remains to be demonstrated whether this improvement is due to the specific nature of these programs or to certain non-specific factors, such as attention and/or structure, common to all psychotherapeutic interactions.

According to a recent theory, schizophrenia is confined to people with a particular genetic predisposition and the disorder arises from a specific breakdown in the central part of the system that controls growth (Burch 1964, 1968). We call diseases of this general class autoaggressive. Their pathogenesis has two distinctive phases: initiation and development. Initiation, which is a purely random process, entails a form of spontaneous somatic gene mutation in growth-control stem cells.

There is good evidence that genetic factors are necessary, though by no means sufficient, for the development of schizophrenia. Several studies have compared the incidence of schizophrenia in identical and in fraternal twin pairs: these studies are discussed, for example, in the Medical Research Council Annual Report 1965–66 (pp. 54–61), where Essen-Möller's (1963) cumulative figures are quoted: Identical (MZ) pairs: 69 per cent concordant for schizophrenia (both schizophrenic) (194/280 pairs). Fraternal (DZ) pairs: 13 per cent concordant for schizophrenia (both schizophrenic) (59/448 pairs).

Evidence from a detailed investigation and review of the literature on monozygotic twins discordant for schizophrenia indicates that the schizophrenic index case was lighter in weight at birth than his co-twin (Stabenau and Pollin, 1967). Lane and Albee (1966) reported that schizophrenic singletons were significantly lighter in birth weight than their sibs.

The decarboxylation of 3, 4-dihydroxyphenyl-alanine (Dopa) to dopamine has been shown previously in animal and human tissues in both in vitro and in vivo studies (Sourkes, 1966; Vogel et al., 1970). However, very little information is available as to whether or not the decarboxylation of Dopa occurs in human red blood cells (RBC). In the present experiment we demonstrated this change in RBC from normals and from schizophrenics. An ionization chamber method was used for an instantaneous and continuous measurement of 14CO2 production from DL-dopa-carboxyl-14C by RBC in vitro.

The experience and meaning of grief differs with the progression of self-awareness of the experiencer in his ontogenetic evolution from utter dependence to differentiated integration. Autonomy, achieved by very few adults, carries with it the connotation of transcendence over mere obedience and conformity to the canons of society. This is different from deviance in two important respects. Deviance is a movement in a horizontal direction away from cultural dominance, and therefore could manifest itself in antisocial activities. Autonomy, being a movement in a vertical direction, is supra-cultural and non-conformist rather than antisocial. All this has a great deal to do with existential grief, the experience of which can change according to the level of ontology of the experiencer. The following operational definitions are needed to treat the subject of ontological grief in a meaningful manner.

The available evidence suggests that adolescent drug addicts are likely to have an underlying personality disorder, to come from broken homes, and to have parents who are alcoholic, antisocial or mentally ill (Nylander, 1964; Chein, 1965; Rosenberg, 1969a and b). Assuming that a background of family instability is related to deviant behaviour—including the abuse of drugs—it seems probable that some of the siblings of young addicts, who grew up in similar circumstances, would also become the subjects of psychiatric disorder.

Weintraub and Aronson have described a method for the study of Psychological Defence Mechanisms through verbal behaviour analysis in psychiatric patients and controls (Weintraub and Aronson, 1962, 1964, 1965 and 1967). In this study we have re-tested their method on a group of middle-aged English depressed patients and matched surgical controls.

As a recent review of the literature makes clear (Savage, 1970), there is very little available evidence on the performance of elderly psychiatric patients on tests of extraversion and neuroticism. The aim of this study is to present some normative data on the Maudsley Personality Inventory (Eysenck, 1959) for elderly subjects and to compare this with the results obtained from younger samples.