Nightmares are frightening dreams awakening the dreamer. In psychiatry they are often considered as an indication of psychopathology or even as a feature of schizophrenia. Assumptions are made that nightmares occur more often in psychiatric patients than in the normal population and that they are accompanied by an elevated anxiety level in the daytime. From a psychophysiological point of view nightmares possibly are derailed attemps of problem solving, of overcoming frightening experiences. In this review the importance of nightmares as symptom in psychiatry is assessed. It appears that they are no indication of an elevated anxiety level in the day-time or of psychopathology in general, and they are no criterium for the diagnosis of schizophrenia either.

A magnetoencephalogram (MEG) is the registration of the magnetic field in points near the head. Because MEG's are weak fields, they have to be measured by means of superconducting sensors. The electric active population of neurons can be computed from the distribution of the magnetic field at a certain instant of time. This is called the inverse problem. In order to solve this probem, both the generators and the head have to be modelled. Usually, a patch of active neurons is modelled as a current dipole. Commonly, the head is described by three compartments, representing the brain, the skull and the scalp. The compartments may have the shape of spheres or they may have a realistic shape. Integration of EEG and MEG with MRI leads to a technique for functional imaging of the brain with a time resolution of one millisecond and a spatial resolution of one centimetre. Clinical applications are the non-invasive localization of an epileptic focus or the presurgical mapping of the sensorimotor cortex.

Norharman is a ß-carboline, possibly of endogenous origin, although cigarette smoking and food are sources too. In brain specific binding sites have been demonstrated. In higher doses norharman binds to benzodiazepine receptors and has MAO-B inhibitory activity. From animal experiments it can be concluded that norharman induces sedation and muscle relaxation. A role in psychosis is unclear, a role in the pathogenesis in anxiety is possible, but has to be further substantiated. As current research suggests, norharman may be an important factor in addiction and withdrawal.

Since the introduction of the monoamine oxydase inhibitors and the first tricyclic antidepressant (TCA) imipramine in the late fifties, the treatment of depressive disorders has been changed dramatically. Althought a great variety of antidepressants such as TCA's, selective serotoninte-re-uptake inhibitors (SSRI's) mianserin, trazodone, mirtazapine, moclobemide and venlafaxine has become available, the exact mode of action is not revealed as yet, and classification should be done according to the interference of antidepressants with central monoaminergic processes.

As to the potential of causing interactions, special attention has to be given to the SSRI's because of their interference with the CYP450 isozyme system. Therapeutic monotoring is recommended for the TCA's. The choiseforan antidepressant should be based on various factors like symptomatology and severity of the depression, potential interactions and somatic and/or psychiatric comorbidity.

Extensive clinical research has demonstrated that TCA's are the most effective for major depression with melancholia (vital depression) and depressive disorders in the elderly.

In de neurologische praktijk is het diagnostisch gebruik van EEG-onderzoek drastisch verminderd ten bate van radiologische beeldvorming. In de klinische psychiatrie bestaan twee grote indicatiegebieden voor klinisch-neurofysiologisch onderzoek: de evaluatie van organische psychosyndromen en van stoornissen met episodisch of paroxysmaal karakter. Mits het een overlappingsgebied met de neurologie betreft, merkt men hier dezelfde trend.

The research on anxiety disorders of the department of psychiatry of the Vrije Universiteit is briefly reviewed. Studies have included comparisons between pharmacotherapy and cognitive behaviour therapy and combination treatments of panic disorder and of obsessive-compulsive disorder. Also, the hyperventilation model of panic disorder could be rejected as a result of an ambulatory monitoring study. Provocation studies with adrenalin in panic disorder have shown less support for a psychological model of panic than expected. Recommendations for future research include studies on anxiety in the very young and in the elderly, studies on comorbidity in anxiety, especially with alcoholism and depression and the development of treatment manuals for general practice. The issue is raised whether investing in neuroimaging studies will critically advance our knowledge in the near future.

Research investigating the neurobiological underpinnings of anxiety disorder have mainly been focused on dysfunction of the GABA, noradrenergic and serotonergic (5-HT) neuronal systems. Just recently, in both animal and human studies, evidence has been found for a possible role of the cholecystokinin (CCK) neuronal system in the pathogenesis of anxiety disorder.

Behaviorally, animal studies revealed anxiogenic-like properties for the ‘central’ CCKB receptor agonists, while CCKB receptor antagonists displayed intrinsic anxiolytic properties. Similarly, in man, CCKB receptor agonists, like pentagastrin and CCK4, were found to be able to elicited panic attacks in both panic disorder (PD) patients and healthy volunteers. These effects appear due to stimulation of the CCKB receptor. In addition, clinically effective panicolytic agents reduce the sensitivity to CCK4 in PD patients. Taken together, these findings may suggest a role for CCK in the neurobiology of PD. On the other hand, there is circumstantial evidence for involvement of several other neuronal systems, such as the serotonergic, noradrenergic and GABA-ergic system, in the regulation of anxiety. Interestingly, evidence has been found for an interaction between CCK and 5-HT and that this interaction plays a role in the mediation of anxiety.

This presentation will critically discuss the evidence for the role of the CCKB receptor in anxiety and in addition, will focus on the putative evidence that the role of CCK in anxiety is mediated by its interaction with the serotonergic neuronal system.

In this review the results are discussed on the prediction of response to pharmacotherapy in panic disorder (PD) and social phobia (SP). From the literature it appears that in PD variables indicative of illness severity are predictors of non-response. In our own studies we found that non-responders to pharmacotherapy in PD are characterised by a higher score on the Blood-Injury subscale of the Fear Questionnaire, a higher plasma MHPG and a higher heart rate. In SP non-responders to pharmacotherapy were also characterised by a higher heart rate. They also appeared to have a higher blood pressure. Furthermore non-responders to pharmacotherapy in SP had higher scores on several psychometric scales, indicative of illness severity.

Patients with panic disorder (PD) report a transient feeling of anxiety upon inhalation of CO2 enriched air. They rate this experience as similar to symptoms of a panic attack. This hypersensitivity has been proposed as an experimental disease model. This paper examines the validity of single breath inhalation of 35% CO2 as a model for PD.