We studied the effects of pentagastrin, an analogue of the cholecystokinin tetrapeptide (CCK4), in 15 patients with panic disorder and 15 healthy controls. Three different intravenous dosages of pentagastrin (0.1, 0.3 and 0.6 μ/kg) and placebo (saline) were investigated. Subjects were randomly allocated to two of the four dosage groups and tested on two separate occasions, one week apart, using a double-blind incomplete block design. A total of 59 intravenous injections were carried out. The panic rate with pentagastrin, irrespective of the dosage, was 55% (12/22) for patients and 5% (1/22) for controls. None of the subjects panicked with saline. The frequency of panic attacks between the three pentagastrin doses in patients was not different. One control subject had a panic-like attack at the highest dose of pentagastrin. These findings concur with previous studies on the panicogenic effect of CCK4 and pentagastrin and suggest a greater sensitivity for CCK agonists in patients suffering from panic disorder than in healthy controls.

In biological psychiatry, the biopsychosocial model is broadly supported. This does not mean a rejection of materialism, but of reductionism. Psychological (and social) psychiatry is deemed to be a necessary supplement to biological psychiatry.

This is one of the lessons made avalaible by Freud. In addition, there are other lessons to be taken from his work. From his view on the mind-body relationship a useful strategy for theory construction can be abstracted:

1. specify the relevant (neuro)physiologiocal mechanims,

2. specify the relevant mental mechanisms,

3. look for that output of the neurophysiological mechanisms that can also serve as the input of the mental mechanisms, and conversely. Especially the third directive will be of use for adherents of the biopsychosocial model.

We may also learn from Freud's mistakes. He rightly used his interactionistic but non-dualistic arguments for the vindication of a relatively autonomous psychological psychiatry. However, he wrongly delayed biological-psychiatric tasks to an indefinite future.

Systemic lupus erythematosus (SLE) is an autoimmune disease with a large variety of clinical signs. Delirium, affective disorders, psychoses, anxiety disorders, personality changes or combinations oftheforementioned are the mental disorders frequently encountered with SLE. There are only few indications for an obvious pathogenic mechanism responsible for the mental disorders occurring with SLE. It seems that the psychopathology in SLE largely is reactive in its nature and as such related to the presence of a serious disease. Psychotic features are possibly an exception because they may be related to pathological changes in the brain of the SLE patient. The administration of corticosteroids is not responsible for the psychiatric syndromes observed in SLE.

Research on the phenomenon of self-injurious behaviour (SIB) has been very limited despite the relative high prevalence of this type of disorder. The relative lack of knowledge of psychopathology in this field and the methodological problems in performing research projects may have contributed to the limitations in the interest for this area. Recently, research into biological aspects of the etiopathogenesis of SIB has yielded results that might open new vistas for a rational and effective pharmacotherapeutical approach. In this concise review the psychiatric, neurological, biological, pharmacological and methodological aspects of SIB in mental retardation will be mentioned.