It remains a mystery as to how genetic and environmental factors cause schizophrenia.

To develop a pathophysiological model of schizophrenia that has greater explanatory power than existing hypotheses of the disorder.

Published findings on schizophrenia are integrated with more recent data from human and animal studies of striatal and cerebellar functions.

The analysis shows that during phylo- and ontogenesis two primarily motor-control mechanisms are applied at the intentional (limbic) level of functioning to organize emotional and cognitive behavior: one for initiating and dosing (drive) and the other for the representational guidance (guidance) of both movements and intentions. The intentional drive and guidance mechanisms are organized through a ventral, respectively, a dorsal cortical–subcortical circuitry.

A deficient implementation of these mechanisms at the limbic domain manifests itself as schizophrenia, whereby the heterogeneity in symptomatology is explained by the extent of the remaining cerebral activity and by the degree of indirect activation of these systems. In general, activation manifests itself as positive symptomatology and the absence of such activation as negative symptomatology. The model provides a more comprehensive explanation for existing clinical and epidemiological data than do the current alternatives. It is compatible with the major prevailing views on the illness, such as the theories that regard this as a progressive neurodevelopmental, or a connectivity disorder, or one resulting from a deficient cerebral lateralization, or an interrupted cortico–thalamo–cerebello–cortical circuitry. The model fits with recent theories in evolutionary psychology and evolutionary psychiatry.

Unexplained medical symptoms are common in children. They constitute the main feature of somatoform disorders of childhood (i.e. pain disorders, conversion disorder and chronic fatigue syndrome or neurasthenia).

To describe assessment and treatment strategies for severe somatoform disorders of childhood.

Review of recommendations for clinical practice and clinical trials.

A number of specific techniques have been described. Clinical accounts indicate that many children benefit and can recover. There is some empirical evidence supporting the beneficial effects of techniques such as family cognitive-behavioural therapy and relaxation technique for the less severe disorders.

Existing helpful clinical guidelines require empiric validation.

Personality disorder, mental retardation and aggression are frequently encountered therapeutic problems in epilepsy patients.

This paper gives an overview of symptomatology and treatment of personality disorder, interictal aggression and mental retardation in epilepsy.

Literature review supplemented by clinical experience.

Personality changes in patients with epilepsy are often symptoms of an organic psychosyndrome. Aggression is not more frequent among epilepsy patients than in the general population, but if it does happen it is often more severe. There is a need for controlled treatment studies. A treatment strategy is suggested. In the mentally retarded, diagnostic instruments should be used to overcome diagnostic difficulties.

Prevalence studies based on DSM-IV personality disorder, conducted in the community, are needed, as well as systematic research on diagnosis and treatment of personality disorder in epilepsy patients. Randomized controlled trials (RCTs) considering the effectiveness and adverse effects of antidepressants and neuroleptics in epileptic patients with mental retardation are seriously needed. In the meantime, the Expert Consensus Guideline Series on Treatment of Psychiatric and Behavioural Problems in Mental Retardation is useful. The use of neuroleptics for the treatment of aggressive or destructive behaviour in nonpsychotic mentally retarded patients remains controversial.

To explore the relation between Parkinson's disease (PD) and depression from a conceptual point of view.

Discussion of the relevant literature on the conceptual, phenomenological and therapeutical aspects of depression in Parkinson's disease.

Both semantic confusion and an erroneous belief in the mind-body distinction have contributed to some common misunderstandings of the nosology and etiology of depression in Parkinson's disease.

The consequences of a different, integrated, neuropsychiatric approach for both diagnosis and treatment are discussed.

To evaluate the tolerability and efficacy of risperidone in childhood autistic disorder.

A multicenter, open-label, dose-titration study involving seven autistic children (mean age 7.6 years) receiving risperidone for 4 weeks.

Mean dose was 0.01 mg/kg/day on day 1, 0.019 mg/kg/day on day 7 (range 0.01–0.041 mg/kg/day) and 0.035 mg/kg/day on day 28 (range 0.014–0.064 mg/kg/day). Over the 4-week period, the Ritvo–Freeman Real Life Rating Scale total score measuring autistic behavior was significantly decreased (P = 0.019), as was the affectual reactions subscale (P = 0.029). Aberrant Behavior Checklist total score was significantly improved (P < 0.001), as were all subscales except inappropriate speech. Visual Analog Scale for individual target symptoms was significantly decreased (P = 0.001), and Clinical Global Impression severity of illness score was significantly improved (P = 0.006). The incidence of adverse effects was low, and no extrapyramidal symptoms were observed. No significant changes or clinically relevant abnormalities occurred in laboratory tests, vital signs or electrocardiograms. Plasma concentrations of the drug were similar to those in adult patients.

These favorable results suggest that larger controlled trials of risperidone should be performed in autistic or mentally retarded patients with behavioral disturbances.