Melatonin is a hormone secreted by the pineal gland mainly during the night. The discovery that this melatonin secretion decreases under the influence of bright light, gave rise to the use of light therapy in some affective disorders. The literature on the relationship between melatonin secretion and mood is reviewed concerning seasonal affective disorder, non-seasonal affective disorder and premenstrual syndrome. Light therapy could reduce an abnormal high melatonin secretion back to normal proportions. None of the affective disorders, however, is accompanied by an unusual high melatonin level. Nevertheless, light therapy as well as other therapies that suppress melatonin have a therapeutic effect. This is not the case with the administration of melatonin. Mood is not affected by extra melatonin in seasonal affective disorder but it is in both other affective disorders. Melatonin plays a part in the pathogenesis of the affective disorders but it is not yet clear which one.

Since some years it has become evident that objective disturbances can be found in patients suffering from personality disorders. Research findings from earlier date already demonstrated low levels of 5-hydroxyindoleacetic acid in the cerebrospinal fluid, especially in patients with personality disorders, under exclusion of depressive features. Furthermore, data have been collected on the correlation between a hyposerotonergic state and disturbances in aggression and impulse control in a variety of syndromes such as automutilation, bulimia nervosa, suicide attempts and various states of drug abuse.

However, psychopharmacological research in personality disorders is rare and to date mainly patients with borderline and schizotypical personality disorders have been studied. It is quite remarkable for this area to find more review articles than original contributions based on the results of clinical trials. A great variety of recommendations for pharmacotherapy in these patients exists in literature, among which treatment with carbamazepine, lithium, low-dose neuroleptics, tricyclic antidepressants and serotonin uptake inhibitors. In this article we will analyze the research methodology and the results of clinical trials forming the base for pharmacotherapeutic treatment recommendations.

Only the results of well-controlled studies will be reviewed.

Risperidone (Risperdal®) is a recently developed antipsychotic drug with the combination of serotonin-5HT2A-and dopamine-D2-antagonism (SDA). In patients with schizophrenia, risperidone reduces positive symptoms at least equally effective as haloperidol, however, risperidone has a reduced propensity for the induction of extrapyramidal symptoms.

In addition, available evidence indicates that risperidone may be an effective treatment for negative symptoms. The optimum daily dose range is between 4 and 8 mgfor most patients. In this review article, risperidone is compared with some other (classical and atypical) neuroleptics. In addition, the pharmacological and pharmacokinetic properties of risperidone are reviewed.

Memory complaints and altered states of consciousness with automatic behaviour of narcoleptic patients indicate cognitive dysfunctioning. Although more problems arise while performing attention tasks than memory tasks, the neuropsychological test inquiry doesn't indicate one particular neuropsychological function as consistently impaired. They often perform well because they compensate impaired wakefulness by an increased willingness to respond. Neurophysiological research indicates that the sometimes occurring cognitive dysfunction is associated with a waxing and waning between wakefulness and sleep. The increased psychopathology is partly a reflection of, partly a reaction to the symptoms. The impact of hypersomnia on psychosocial functioning is more important than that of epilepsy in epileptics. In severe cases smoking and driving should better be dissuaded.