Schizophrenia is consistently associated with lower IQ compared to the IQ of control groups, or estimated premorbid IQ. It is not likely that the IQ scores deteriorate during the prodromal phase or first psychotic episode; they are already present before the onset of the prodromal phase and have been detected in childhood.

We investigated cognitive functioning and IQ levels in a group of 36 patients with schizophrenia or other psychotic disorders.

The IQ scores in our sample were lower than average. The IQ showed a relation with attention, memory, speed of information processing and some aspects of executive functioning. However, when IQ scores were corrected for processing speed, they were no longer below average.

These findings are important in considering the value of intelligence levels in schizophrenia. IQ scores should be judged in combination with cognitive functioning and school career to assess a patients capabilities in society. Cognitive functions and other variables might have a considerable influence on IQ scores. This rises the question of whether the low IQ scores are a primary or secondary deficit. Schizophrenia patients may have normal IQs, but could be less capable of making an IQ-test.

For at least 125 years the discussion about the clinical relevance of catatonic symptoms in psychiatry continues. It started from the original description by Kahlbaum and was revived by modern factor analytical studies, that identified the catatonic dimension in about 10% of newly admitted patients.

Over a period of 2 years, four patients with an acute episodic psychosis and prominent catatonic symptoms were examined.

A clinical description is given of the psychopathology and classification is performed according to the various diagnostic instruments.

All patients showed a circular fluctuation of their psychoses, with motor symptoms ranging from the excited to the inhibited pole within one episode. Their clinical pictures also comprised mood swings and anxieties as well as hallucinatory and delusional experiences, whereas the course of disease was characterized by complete recovery without residual symptoms.

The significance of catatonic symptoms is not recognized in the current taxonomies despite the fact that this has major pharmacological treatment implications.

Chronic fatigue syndrome (CFS) is a complex syndrome with a psychiatric comorbidity of 70–80%. A psychiatric interview is necessary in order to exclude psychiatric illness and to identify psychiatric comorbidity. Studies have demonstrated that in general medical practice and in the non-psychiatric specialist practice, physicians tend to underdiagnose psychopathology in patients with CFS. There are many questions unanswered about the treatment of CFS

Typical issues for the psychiatric practice are reviewed: psychiatric comorbidity, dysregulation of the PHA-axis and the treatment of CFS.

Depression, somatization, sleeping disorders and anxiety disorders are the most important psychopathological symptoms found in CFS patients. CFS should not be regarded as a masked (somatoform) depression. Although the results from neuroendocrinological studies assessing the hypothalamic–pituitary–adrenal axis (HPA-axis) are inconsistent, they suggest that there is a subgroup of CFS patients suffering from a discrete dysregulation of the HPA-axis resulting in basal hypocortisolaemia. These findings, however, do not reveal a causal relationship. Antidepressants do not seem to have a positive influence on the symptom of fatigue, but appear to be beneficial in alleviating the symptoms of depression and social functioning. Cognitive behaviour therapy and graded exercise show a significant improvement on fatigue and other symptoms and are the only treatments available for CFS patients.

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.

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.