Preliminary new data support the enhancement of ‘everyday’ creativity among those persons with bipolar disorders who manifest milder rather than more severe mood elevations, and among certain individuals who are likely to carry bipolar liability but themselves show no clinical mood elevations – in this case, unipolar depressives with a family history of bipolar disorder, when compared with depressives lacking this history. Creativity was assessed using the lifetime creativity scales (Richards el al, 1988). Underlying mechanisms may be multifactorial and complex. Results suggest that both personal and family history should be considered when making predictions concerning creativity and affective disorders.

Late-onset schizophrenia remains an understudied area. Neuroimaging techniques, which have been widely employed in the study of earlier-onset schizophrenic patients, have only recently been applied to patients with a later onset of illness. This paper reviews current knowledge about brain abnormalities in late-onset schizophrenia, and attempts an integration of the findings with clinical, genetic and epidemiological factors which pertain in such disorders. Suggestions are made for future research regarding this group of patients.

In 55 chronic schizophrenics, the occurrence of infectious diseases during their mothers’ pregnancies was investigated. Different psychiatric diagnostic systems were compared. Infections were reported by the mothers of familial and sporadic DSM III-R schizophrenics in equal proportion. However, applying Leonhard's classification, the frequency of infections was found to be significantly increased in ‘systematic’ schizophrenia (mainly exogenously induced in the view of Leonhard) compared to ‘unsystematic’ schizophrenia (mainly genetically determined according to Leonhard's findings). Most of the infections occurred during the second trimester (nine out of 13). Thus, in the ‘systematic’ forms of schizophrenia (low genetic loading), maternal infections in this crucial period of neurodevelopmenl would appear to be important causative factors in the cytoarchitectural deviance delected in the central nervous system of schizophrenics.

In a survey of the suicide trends in Italy between 1959 and 1988, a slight increase was recorded both among males (+ 19%) and females (+ 10%). Geographically, the regions with the highest suicide rate are the Northern ones (up to twice the national average). The age groups with the highest suicide risk are those over 74 years. Gender distribution differences show that among females over the age of 65, the suicide rate rose by 70% between 1974 and 1989, versus 77% for males of the same age. Between 1978 and 1989, the suicide rate among people in search of a first job rose by 25%; among the employed it rose by 37%, while among people in search of a new job it rose by 594%. The highest specific suicide rale was recorded among the divorced (32.4 × 100000), while ihe level of education with the highest suicide rate is the secondary school (9 × 100000). Suicide methods include hanging (30%), jumping (22.4%) and firearms (11.5%).

We have attempted to evaluate quantitative changes in the mental health delivery system in Greece, dictated by a fiveyear program to reform psychiatric care. By the end of the program, a number of psychiatric units in general hospitals, as well as community mental health centres, had been created, while the number of beds in psychiatric hospitals have been significantly reduced. Mental health services have become more accessible to the population, and served more patients. However, not all the objectives of the program have been met. Only about half of the initially proposed number of beds in the psychiatric units in general hospitals have been actually developed. The catchment area, a basic pre-requisite of the program, has not been put into effect. Finally, the noticeable trend towards a restriction of the role of psychiatric hospitals did not coincide with the development of adequate new services.

The monoamine hypothesis of depression and its direct derivation, the receptor theory, have constituted for several years a frame of reference for researchers working in the field of biological psychiatry. Although most of the data are derived from animal findings and must be considered inconclusive in view of various controversies, some guidelines may be identified: these would suggest that changes in postsynaptic beta-adrenoreceptors, presynaptic alpha 2-adrenoreceptors, as well as in type 2 serotonin receptors and dopaminergic autoreceptors may be involved in the mode of action of antidepressant drugs and, consequently, in the pathophysiology of depression. Nowadays, any attempt to correlate depression with the dysfunction of a single neurotransmitter or receptor is no longer tenable, since it is clear that depression is a heterogeneous disorder which involves abnormalities in the interactive relationships between neurotransmitters and receptors. If, on the one hand, this new model has opened up new fields of research and has led to the investigation of new systems, eg the GABAergic and GABA B receptors, on the other hand, it has been strongly limited by the lack of research tools and reliable peripheral CNS models for in vivo studies. A possible approach to this unresolved dilemma may be provided by molecular biology techniques, which have permitted the identification of the genes and sequencing of the primary structure of several membrane receptors. It is now established that receptors may be grouped into four superfamilies; in depression, there exists compelling evidence of alterations mainly in receptors belonging to the G-protein-coupled family: it is plausible that depression may be related to a disorder of the G-protein-coupled receptor superfamily. Such an hypothesis would represent an attempt to unify the different receptor abnormalities found in depression or following antidepressant treatments, and to shift from the monoamine paradigm to a new heuristic model. In addition, it would accommodate the various dysfunctions likely to be encountered and would open up new theoretical perspectives in the treatment of depression.

Norway was the first European country to be introduced to the American diagnostic system DSM III. In this paper the author presents some of the main results of the Norwegian studies of the DSM III personality disorders with particular emphasis on validity, comorbidity and treatment.

The prognostic significance of an index episode of affective disorder with delusions was assessed in a longitudinal study of a cohort of adolescent psychiatric inpatients (n = 43). Part I of a study has been reported in a previous article. Initial assessmentdata (anamnestic variables, clinical assessment) did not discriminate between onset of affective disorder and schizophrenia. Part II of the study provides a longitudinal perspective of the cohort's diagnostic and life adjustment: diagnoses of schizophrenia increased, schizophreniform disorders disappeared, affective disorders were stable and a schizo-affective category emerged. Patients in the schizophrenic category had severely impaired life adjustment, while the level of functioning in unipolar and bipolar patients was consistently satisfactory. Compared to the initial diagnosis, the cohort showed a tendency to develop into schizophrenia. It is too early to affirm that every adolescent with delusional symptoms at onset will later develop schizophrenia, however, this risk appears real.

This study presents the clinical and demographic characteristics of a sample of 131 patients, who met DSM III-R criteria for obsessive-compulsive disorder (OCD). Our aim was to compare our epidemiological data with non-European research, and to investigate the relationship between OCD symptoms and other clinical features, ie other Axis I concomitant disturbances, personality disorders (Axis II) and family history. Furthermore, we evaluated the age at onset distribution according to sex, family history and presence/absence of a comorbid diagnosis of mood disorder, by means of survival analysis.

Brain alterations have been sought since the beginning of the century to explain the ‘dementia’ of dementia præcox. Kraepelin suggested in 1913 that it might have its internal origins in early childhood, while Southard (1915) considered likely a congenital or early acquired basis for the development of the disease. Afterwards, degenerative processes were described for decades until neurodevelopmental theories emerged recently (Lewis, 1988).

Using pneumoencephalography, Jacobi and Winkler (1927) first reported that some patients with schizophrenia presented enlarged ventricles. Johnstone et al (1976, 1978), in CT-scan studies, observed an increase in mean lateral ventricular size in a group of institutionalized schizophrenic patients. This finding has been replicated by other studies (Weinberger et al, 1983) but challenged by others (Gluck et al, 1980; Jernigan et al, 1982).

Serum-antibodies against an organ specific CNS antigen as well as against serotonin and gangliosides (Gm 1) were analysed by ELISA in 34 patients with schizophrenia, ten patients with schizoaffective psychosis and 13 patients with major depressive disorder. Sixty-two patients with various rheumatic disorders and 32 blood donors were included in the study as controls. Sixty-two percent of the 13 patients with major depressive disorder had antibodies to serotonin and 69% to gangliosides, whereas antibody positive sera was only found in 38% of the 34 patients with schizophrenia. The same antibodies were found in only 6% (antibodies to serotonin) and 13% (antibodies to gangliosides) of the 32 blood donors and in a similar frequency in patients with schizoaffective psychosis. Organ specific antibodies to CNS-antigen could not be detected in the psychiatric patient group at any significant level. It is speculated that auto-immune reactions towards a serotonin receptor may be involved in the etiopathogenesis of major depressive disorder.

Alcoholic and psychiatric family history were investigated in two groups of alcoholics, recruited differently, and controls. Alcoholics with or without a family history of alcoholism (AFH + and AFH − ) were compared with regard to professional qualifications, personal psychiatric history, age at onset and reasons given for becoming alcoholic. The results can be summarized as follows: the family ‘aggregate’ of alcoholism found was independent of the recruitment. This was not the case for personal psychiatric history for which a gradient was found in the two alcoholic groups. Rates of alcoholism were higher in both the first and second degree relatives. Alcoholics with AFH+ and AFH− differed significantly with regard to inducement by profession, and tended to differ as to age of onset.

As a pre-test validity study, a French version of the 28-item general health questionnaire was carried out on 158 general psychiatric patients, without any selection on diagnosis. These patients were concomitantly assessed by psychiatrists with a list of DSM III-R criteria for affective and anxiety disorders. Internal consistency of the questionnaire proved to be excellent. Principal component analysis provided a 4-factor solution, including a ‘depressive’ factor, close to that originally proposed by Goldberg and Hilllier (1979), but with some differences in the loading of insomnia. Although there were some differences in case distribution between the centres, this study confirms internal validity of the GHQ-28 as a screening instrument for psychiatric research.

The paper describes the construction and validation of a brief self-rating scale for social integration in the elderly: the 17-item Social Integration and Independence Questionnaire (SIIQ). The questionnaire was tested on a sample of 160 individuals over the age of 65. Principle component analysis elicited four factors accounting for 48.8% of the cumulative variance: ‘Independence’, ‘Social Integration’, ‘Familial’ and ‘Depression’ (20.7, 10.6, 9.0 and 8.4% of the cumulative variance). The four factors measure the adjustment of elderly people in the community.

Chronic Hallucinatory Psychosis (CHP) is typically a French disease entity initially described by G Ballet (1911) and whose diagnostic criteria were established by Pull (1987). This diagnosis is not used in English and German literature. The aim of this study was to investigate the relationship between Pull's criteria for CHP and the criteria for schizophrenia defined by 14 different diagnostic systems and schizoaffective disorders. Seventy-two non-affective psychotic patients (34 men, 38 women), aged 20 to 84, in exacerbated or stabilized phase, were interviewed by the same investigator (SD). The patient distribution between the diagnoses in the different diagnostic systems was carried out using a computerized 208-item checklist. The main results indicated that the definite CHP diagnosis was significantly related to the Catego S + (C = 0.52; P < 0.01), New-Haven, (C = 0.40; P < 0.05) and Schneider (C = 0.54; P < 0.001) systems for schizophrenia and with the depressive-schizoaffective disorder (C =0.39; P < 0.05) in the RDC system. The probable CHP diagnosis was significantly linked with the same systems and with the probable RDC (C = 0.39; P < 0.05) for schizophrenia. These results emphasize that in 13 out of the 14 diagnostic systems, schizophrenic and schizoaffective disorders overlapped with CHP in the French diagnostic system. Among these systems, four schizophrenic diagnoses were significantly linked to CHP. In contrast, the Bleuler system for schizophrenia was not related to CHP at all.

Social skill training is aimed at not only preventing rehospitalization of chronic psychiatric patients by maintaining them in the community, but also to help patients have a good quality of life. We address the question of how social skill training could improve the quality of life of chronic mentally ill patients. A theoretical model, including environmental as well as individual considerations, indicates which psychological factors could be both targets of social skill training interventions and determinatives of patients subjective quality of life. The clinical and research implications of this theoretical model are discussed.

Schizophrenic patients seem to react sensitively to expressed affect. Expressed emotion research has shown the negative impact of specific family communication styles on the course of illness. Further studies have discussed its relation to gender. This study examines the dyadic aspects of the therapist-patient relationship, the interaction between therapist's ratings and patient's psychopathology, and the predictive value concerning the course of illness. Results show a significant association with gender. Male therapists were inclined to reduce their therapeutic commitment when being confronted with patients who suffered from disturbances Of ego-function, attention, or perception. Female therapists felt rejected by patients with delusions and with formal thought disorders, but perceived themselves as competent when dealing with anergic patients. Furthermore, patients with a less favorable course of illness at the 2-year follow-up could be discriminated by the quality of the therapist-patient relationship at the end of the primary therapeutic intervention.

Lateral gaze aversions which follow reflective or thought provoking questions are called conjugated lateral eye movements (CLEMs). This response was studied in 20 schizophrenic patients, 20 depressive patients and 20 healthy controls. Frontal and parietal EEG measures were recorded simultaneously with the question/answer task. There were no differences in CLEMs among the 3 groups. Schizophrenic and depressive patients demonstrated a significantly reduced EEG-power on the left and an increased power on the right in comparison with healthy controls. This may point to a functional interhemispheric ‘disconnection’ in patients. Comparative correlations revealed EEG-power increase during the occurrence of contralateral CLEMs in the whole 10 min task.

To prove the hypothesis of a common defect in the central nervous system and immune system in patients with major depression, we examined the inhibition of phytohemagglutinin (PHA)-induced lymphocyte proliferation by in vitro and in vivo administration of glucocorticoids in 20 patients with major depression. The patients were divided into two groups according to the results of the dexamethasone suppression test (DST). Six patients showed cortisol non-suppression. They had significantly higher baseline plasma cortisol levels in comparison with cortisol suppressors. The lymphocytes from cortisol non-suppressors were significantly stronger inhibited by in vitro administration of glucocorticoids compared to the lymphocytes from cortisol suppressors. However, there were no significant differences of lymphocyte inhibition by in vivo administration of glucocorticoids between both patient groups. From our results we conclude that cortisol non-suppressors reveal impaired down-regulation of glucocorticoid receptors of lymphocytes. Furthermore, the effect of glucocorticoids on lymphocyte reactivity may reflect the effects on brain structures in patients with major depression.