Abnormal premorbid personality has long been considered to be an important feature of patients who develop schizophrenia, or schizophrenic-like psychoses late in life. Schizoid and paranoid personality traits in particular are repeatedly reported to have preceded the development of psychosis by many years. Such personality abnormalities have been viewed as part of a schizophrenic spectrum disorder, causally invoked in the aetiology of psychosis, or even regarded as an adaptive protection of vulnerable individuals against psychotic breakdown. An ICD-10 diagnosable personality disorder, however, is seen in only about 50% of patients who develop a paranoid psychosis late in life. The premorbid personality abnormalities encountered in late-onset paranoid states and delusional disorder are different from those reported in schizophrenia and there appears to be a genetic basis for these differences. The role of such personality disturbance in the aetiology of psychosis is controversial but probably only minor.

The role of the neuropeptide cholecystokinin in schizophrenia has been widely explored because of its modulating action on midbrain dopamine neurons. The recent discovery of more specific receptor subtype cholecystokinin antagonists should be considered as potential treatment for schizophrenia with fewer side effects. This paper reviews cholecystokinin/dopamine interactions in animal and human studies. Clinical trials with cholecystokinin agonists and antagonists in schizophrenia are updated.

In order to evaluate the validity of the Montgomery and Asberg Depression Rating Scale (MADRS) in a Black African context, the MADRS construction study was replicated in Benin (West Africa) following the same initial procedure. Ninety-two Beninese French-speaking, major depressed out-patients were rated with the French version of the CPRS and were administered 75 mg/day clomipramine for 4 weeks. Forty-nine patients were rated at the end of the period. A list of items with a frequency higher than 70% was pre-selected from this data in strict accordance with the Montgomery and Asberg procedure; the ten items most sensitive to change Were then extracted from this list. The new scale shared eight of the ten MADRS items. Only pessimistic and suicidal thoughts, perhaps culture-bound, were absent and replaced in the new list by reported muscular tension and reduced sexual interest. None of the classic African symptoms involving somatic complaints or persecution ideas were selected by the procedure. The interest of using a shortened version of the MADRS, limited to the common eight items, is discussed.

Serotonin uptake by platelets was determined in 11 patients suffering from carcinoma of the pancreas, eleven patients hospitalized for chronic physical disease, 19 patients suffering from major depression unipolar type, and 19 healthy volunteers. The Vmax values of serotonin uptake were significantly lower in patients suffering from carcinoma of the pancreas (F = 18.6, df = 28, Ρ < 0.001) and chronic physical disease (F = 21.3, df = 28, Ρ < 0.0001) than in healthy volunteers. The Vmax values of the depressed patients were also significantly lower (F = 4.27, df = 36, Ρ < 0.05) than those in the control group. No difference was found between the carcinomatous and the chronically ill patients. Km values of serotonin uptake by platelets were significantly decreased in both groups of patients with organic disease (F = 5.91, df = 28, Ρ < 0.025; F = 4.44, df = 28, Ρ < 0.045 respectively) as compared to the control group, but were similar in the depressed and the control groups (F = 0.42, df = 20, P = 0.52). Since the patients with chronic disease were chronically medicated, the decreased serotonin uptake may not be disease-dependent but rather associated with medication. However, the carcinomatous patients were drug-free and in this group the decreased uptake and serotonin transporter hypersensitivity may have been disease-dependent. These results suggest the involvement of the presynaptic serotonergic system in the susceptibility of pancreatic carcinomatous patients to prodromal depression.

The cognitive effects of bromocriptine (10 mg/day) in chronic neuroleptic-treated schizophrenic patients were studied in a 4-month trial. Ten neuropsychological variables were used for the evaluations. Nine patients and seven controls completed the study. They were tested three times: before the beginning of the study, and after 2 and 4 months of treatment. The results showed that treated patients globally performed significantly better than the controls (P < 0.05), and that the digit symbol substitution test was significantly improved (P < 0.03). The WAIS performance score was also significantly improved (P < 0.02). The picture arrangement test was improved, but did not reach significance (P < 0.07). Verbal tests were not improved. It therefore appears that addition of a D2 dopamine agonist in neuroleptic-treated patients can improve some of their cognitive functions. Two explanations can be proposed: i) bromocriptine decreases neuroleptic-induced motor side effects or ii) has an effect on a putative hypodopaminergic function in schizophrenia.

The natural history of alcoholism is still a matter of debate. Very few studies have addressed the issue of the post-treatment course longitudinally. We present the results of a long-term follow-up study in ninety-six alcohol dependent patients who were treated in a combined in-patient and out-patient treatment programme. Two, five and ten years after the initial treatment in 1976, they were re-investigated. Ninety-four percent of the patients could be located ten years after treatment. Fifty-one percent were abstinent, 22% were deceased, 14% of the patients’ drinking was unchanged and 7% had improved. This outcome is discussed and compared with the results of other long-term studies.

CT findings in 17 patients and MRI in one patient with post partum psychiatric disorder (PPPD; psychosis: n = 17, depressive neurosis: n = 1) were compared with randomly selected CT scans in non-PPPD patients matched for age and sex. In the PPPD group, 13 examinations (controls: 8) revealed one or several abnormal findings such as sulcal widening, ventricular enlargement and asymmetry. There was a higher prevalence of abnormal CT/MRI findings in the PPPD group (trend, P < 0.1).