In this review the most important hypotheses for the occurrence of the clinical picture of hepatic encephalopathy are discussed. As possible pathogenetic mechanisms are raised: dysfunction of the serotonergic system due to an increased tryptophan uptake in the brain, an elevated intracerebral ammoniac concentration and glutamine synthesis, and a heightened intracerebral GABA-activity.

The dysregulation of the serotonergic system as a consequence of the increased intracerebral tryptophan uptake is described as one of the most important pathogenetic mechanisms. The elevated intracerebral ammoniac concentration and the elevated intracerebral glutamine synthesis play in this a facilitating role. The similarity in symptomatology of the clinical picture of HE and the serotonergic syndrome support this hypothesis. Due to contradictory research findings the role of the GABA-ergic system and the occurrence of HE remains unclear.

The last two decades have witnessed an upsurge in the interest in anxiety disorders. Much research effort has been dedicated to panic disorder and obsessive compulsive disorder. However, it is only very recently that we have begun to understand some of the basic principles about the psychopharmacology of social phobia. Drug classes so far studied include beta-blockers, non-selective and irreversible MAO-inhibitors (MAOI's) and benzodiazepinen. Beta-blockers appear to be of use in specific social phobias, like public speaking. There is considerable evidence suggesting that MAOI's are effective in reducing both social anxiety as well as social avoidance. A disadvantage of the conventional irreversible MAOI's is their risk for hypertensive crises when combined with dietary tyramine.

So far only a small number of studies with selective MAOI-A inhibitors such as moclobemide and brofaromine have been conducted in social phobia, and the results indicate that both compounds are effective.

Drugs exerting selective and specific actions on certain components of e.g. the serotonergic system can now be studied and it is hoped that the role of serotonin and other neuronal systems in social phobia can be elucidated.

In order to gain more information about selective serotonergic drugs the first double blind placebo-controlled study with fluvoxamine in social phobia is here reported. Preliminary results indicate a reduction of social anxiety.

Finally the role of peptides in the treatment of social phobia is critically reviewed. The MSH/ACTH analog Org 2766 was investigated in patients suffering from social phobia. No anxiolytic effects of this peptide could be observed.

In this review article, based on a literature study, present ideas upon the relation between M. Parkinson and concomittant depression are dicussed. After a short introduction, it is demonstrated that epidemiological studies show that a common pathophysiological basis can be assumed. Briefly pheno-menological aspects are mentioned, whereafter the changes in the different neurotransmittersystems are discussed in greater detail. The ratio of dopaminergic and serotonergic activities in the basal ganglia constitute an important determinant for the severity of motor symptoms in Parkinson's disease. Reduced serotonergic metabolism may be a compensatory mechanism for the reduced dopaminergic activity. At the same time, a reduced serotonergic activity can predispose to a depression. Lower activities in parts of the dopaminergic, serotonergic and noradrenergic systems may each be responsible for part of the affective symptomatology in depressed Parkinson patients.

The parasomnias are important yet badly recognised dysfunctions in clinical psychiatry. The clinical presentation and consequences in adults differ considerably from the often benign dysfunction in childhood. We present a case of incubus in a patient suffering from recurrent unipolar affective psychosis (type mania). The polysomnographic features are discussed and the differentiation from other paroxysmal amnestic conditions is emphasized. Pathophysiology encompasses a Slow Wave Sleep (SWS) arousal disorder probably related to a serotoninergic dysfunction. The relationship withpsychopa-thology is discussed.