The prevalence, symptomatology and correlates of anger attacks were studied in 103 depressed French patients, using a French version of the Anger Attacks Questionnaire. The prevalence of anger attacks during the previous month was 46.7%, and the most frequently reported symptoms were feeling of panic (85.1%), tachycardia (83.7%), and feeling out of control (81.3%). The occurrence of anger attacks was significantly associated with intensity of loss of control, and history of panic attacks. There was no significant association with age, gender, severity of depression or anxiety, history of suicidal attempts or mood disorder. Three weeks of treatment with serotoninergic antidepressants induced a significant decrease in anger attack prevalence.

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.

Unequivocal results demonstrating a causal relationship between a disturbance in circadian rhythms and depression have not yet been reported (reviews). However, acute mood changes, such as the antidepressive effect of sleep deprivation, diurnal variations of mood and their interrelationship, are commonly put forward as evidence of the importance of circadian dysregulations in affective disorders. The purpose of the present study is to obtain more insight in the mechanisms underlying these mood changes. The results will be discussed in the context of a recently postulated non-chronobiological explanation.

Earlier studies have suggested that the relationship between diurnal variation of mood and the response to total sleep deprivation (TSD) is clear and unambiguous: improvement of mood during the day prior to TSD (a positive diurnal variation) is followed by a positive response (mood improvement) to TSD, while no improvement or deterioration of mood during the day prior to TSD (a negative diurnal variation) may result in no, or even a negative, TSD response (for references see Van den Hoofdakker). However, these conclusions were based on the results from cross-sectional studies, comparing single TSD effects across individuals. Comparison of sleep deprivation effects within individuals, however, revealed that the course of mood during the day prior to TSD is irrelevant for the TSD response. Accordingly, a favourable response to TSD appeared to be related to the patient's propensity to show diurnal mood variations per se, irrespective of their direction.

Although less undisputed in biological psychiatry than formerly, there are basically still two premisses which underly most hypotheses in biological depression research. These are deeply rooted in the medical way of thinking and have guided the construction of DSM-III. The first is that depressive symptoms and complaints cluster in one or more discrete syndromes, and the second is that these correspond to separate nosological entities, characterized by specific biological derangements and pathogenetic processes. Below a number of issues are raised which cast doubts on the validity of these premisses and on the progress made in pinpointing the derangements looked for.

Serotonin (5-HT) plays an important role in depression and specific 5-HT reuptake blockers appear to be clinically important antidepressants. It is unclear however, which serotonergic mechanism is involved in the antidepressant effect, certainly when regarding the existence of at least seven 5-HT receptor subtypes. By testing different 5-HT ligands in two animal models of depression (forced swimming and DRL72-S test) and comparison with data from literature, evidence is provided for potential antidepressant qualities of 5-HT1A receptor-agonists and 5-HT1C receptor-antagonists. Compounds binding to 5-HT1B, 5-HT2 and 5-HT3 receptors do not have an antidepressant profile. Results of clinical research support the predicted antidepressive effects of 5-HT1A receptor-agonists.

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.

This paper reviews the relationship between cholesterol and psychological functioning. Possibly a relationship exists between the lowering of cholesterol, low serum cholesterol concentration and mood and/or impulse control disorders. This might be associated with a disregulated cerebral serotonin metabolism. These hypotheses are based on (meta-analyses of) epidemiologic research investigating the lowering of cholesterol. One of the findings was an increased mortality due to suicide, homicide and accidents. Much is still unknown about the matters mentioned above. However, recommendations for research and clinical psychiatric practice are formulated.

In this first part of a review on biological psychiatric aspects of obsessive-compulsive disorder (OCD), firstly a short introduction is given about historical, diagnostic and epidemiological issues concerning OCD. Subsequently pharmacologic treatment-studies are discussed. Only serotonin (5-HT) reuptake blockers are proven to be effective. There is accumulating evidence that this therapeutic effect is not due to antidepressant effects. The results of the treatment-studies strongly suggests that 5-HT is involved in OCD. CSF-studies seem to confirm this. Possibly the therapeutic effect is related with adaptive changes of 5-HT receptors. There is evidence that in a subgroup of O CD-patients the dopaminergic system is involved.

Because of the graded nature of adaptational processes, a dimensional diagnostic approach is more adequate than the categorical classification. The broad concept of the serotonin-aggression relationship, irrespective of the diagnostic category, is increasingly questionable and seems to be present in young, white male adults with antisocial personality disorders only. In this group, dopaminergic and neurosteroid-linked mechanisms are important as well.

The narcoleptic syndrome in its most specific way is characterized by a set of clinical symptoms, including cataplexy, irresistable sleep episodes, hypnagogic hallucinations and sleepparalysis; the syndrome has been defined by the association of excessive day-time somnolence and REM-sleep abnormalities. In principle, anamnestic information is sufficient to establish the clinical diagnosis, although neuro-physiological and biochemical data(CSF monoamine metabolites and HLA-typology) are sometimes needed to support the diagnostic procedure. Treatment of excessive daytime somnolence is still primarily based upon CNS stimulants, while treatment of cataplexy and related symptoms rests on antidepressants with a primarily serotonergic mode of action.

Divers sous-types de récepteurs sérotoninergiques de type 5-HT1 ont été mis en évidence. Ils correspondent aux soustypes 5-HT1A (marqué sélectivement par le 8-OH-DPAT), 5-HT1B marqué par le propranolol et certains bêta-antagonistes et présent seulement chez le rat et la souris, absent chez l’homme) et 5-HT1C (marqué par la mésulergine et présent en particulier dans les plexus choroïdes). Un sous-type supplémentaire 5-HT1 non A, non B, non C a été mis en évidence; il est caractérisé par un site de liaison insensible aux concentrations de ligands inhibant sélectivement les sous-types 5-HT1A, 5-HT1B et 5-HT1C, il correspond à un système de transduction adénylcyclasique (activation ou inhibition) et apparaît enfin jouer un rôle important dans la modulation présynaptique de la libération de neurotransmetteurs - non sérotoninergiques - en particulier l’acétylcholine. Ces caractéristiques ont été mises en évidence sur des préparations membranaires de cortex de mammifères par des essais in vitro de liaison de [3H]5-HT, de mesure d’activité adénylcyclasique sur les mêmes préparations et par mesure de libération évoquée de [3H] acétylcholine à partir de préparations synaptosomales de diverses régions cérébrales de rat et de cobaye. Une analyse par autoradiographie quantitative a été réalisée chez l’homme sur des coupes fines de cortex frontal prélevées post-mortem chez des individus normaux et des individus déprimés; les résultats obtenus suggèrent une légère augmentation des sites 5-HT1 non A, non b, non c chez les individus déprimés versus les cerveaux normaux. Les antidépresseurs à faibles concentrations (10 à 100 nM) sont capables d’interagir in vitro avec le fonctionnement de ce récepteur: au niveau du site de reconnaissance en altérant les caractéristiques de liaison de la [3H]5-HT, à celui du système de transduction adénylcyclasique en inhibant l’activation induite par la 5-HT et enfin au niveau de l’effet cellulaire sérotoninergique en réversant partiellement l’effet inhibiteur du trilîuorophénylméthylpipérazine (TFMPP), un agoniste sérotoninergique, sur la libération évoquée d’acétylcholine. Cet effet est observé avec des antidépresseurs inhibiteurs d’uptake de la 5-HT mais aussi avec des inhibiteurs d’uptake de la noradrénaline et non pas avec des benzodiazépines ou des neuroleptiques. Ces résultats suggèrent I’hypothèse selon laquelle le système sérotoninergique fonctionnant à l’aide des récepteurs 5-HT1 non A, non B, non c pourrait réguler la libération de divers autres neurotransmetteurs entraînant par là une régulation du nombre des récepteurs correspondants à ceux-ci. Les antidépresseurs pourraient interagir avec cet effet modulateur sérotoninergique vraisemblablement altéré au cours de pathologies dépressives ou accompagnant celle-ci.