Affective disorders cluster in patients with cardiac diseases, in particular in coronary artery disease (CAD) which has become one of the most prevalent chronic disorders in the western world. Affective dysregulation has been recognized as a major riskfactor for cardiac death in patients with CAD. Therefore treatment of affective dysregulation is important from both the psychiatric and cardiac perspective. An evidence based treatment algorithm for affective disorders is as yet not available. In this paper a possible etiological model for the relationship between affective and cardiac dysregulation is proposed, based on the stress-diathesis model.

Since the introduction of a separate axis in DSM-III (1980), the validity of the categorical nature of the classification of personality disorders has been seriously questioned. Subsequently, a number of multidimensional alternatives have been proposed based on statistical procedures or theoretical considerations. At the same time, the study of the neurobiological underpinnings of personality and personality disorders has created a better understanding of etiological and pathogenetic processes responsible for these chronic disorders. The findings of these studies corroborate some of the major findings of statistical studies regarding the nature of the frequent comorbidity of axis II disorders. In the discussion, a mixed, two-tier diagnostic model is proposed to serve both scientific and clinical aims without the disadvantages of an exclusive choice for either categorical or dimensional approaches to the classification of personality pathology.

Antipsychotic drugs are effective in psychoses, whatever the etiology of the disorder. The positive symptoms tend to respond more readily. The need for developing new drugs arises from the refractoriness of the negative symptoms, the 10-25% of the patients that are treatment-resistant and the problems of short-, and long-term extrapyramidal side-effects. Thus far, six drugs, differing from the classical antipsychotics, have been licensedfor use: olanzepine, risperidone and quetiapine; the longest registration exists for sulpiride and clozapine while the most recent one is for amisulpride. This review starts with a brief introduction to symptomatology, and takes differences with the classical drugs in pharmacology, pharmacokinetics, clinical aspects and side-effects into consideration. Clozapine, risperidone and sulpiride may be considered for clinical use in refractory patients; these three, olanzapine and amisulpride when extrapyramidal side-effects cause a clinical problem. Amisulpride and sulpiride have a dual therapeutic acion: On negative symptoms at low dose, on positive symptomen at high doses.

Given the diagnostic ambiguity of physically unexplained complaints we wanted to study whether the clinically and symptomatically characterized groups, all of them defined according to DSM-III-R criteria, could be reclassified using selected empirical and theoretical variables of operationally defined parameters.

Patients with conversion (N = 75), somatization or undifferentiated somatoform disorders (N = 74) and major depression (N = 70) according to DSM-III-R underwent multidimensional work-up including psychopathological, personality-psychological, illness, behavioral and coping assessment. The clinically characterized groups should be statistically reclassified by discriminant analytic techniques.

The existing diagnostic categories according to DSM-III-R could be widely confirmed by the statistical reconstitution of the clinical groups. Conversion, somatization and depressive disorder presented as distinct clinical categories.

A classification relying widely on symptoms still seems to be too superficial and does not represent the complexity of these patients. Thus, the modern classification systems with their purely phenomenological criteria should be added with further dimensions.

Many genetic disorders are caused by mutations in single genes (monogenic diseases), and the inheritance pattern of these diseases follows simple rules. If a mutation in both copies of the gene on both chromosome homologues is necessary to cause the disease, the inheritance pattern is recessive, and a patient is the offspring of two clinically unaffected carriers. However, if a mutation in a single homologue is sufficient, the inheritance pattern is dominant and the disease is transmitted from generation to generation. Monogenic diseases are responsible for only a small fraction of all patients with genetic diseases. Many common diseases, including cancer, heart disease, diabetes and several psychiatric diseases, are the results of a complex interaction between genetic and environmental factors. However, these diseases can have important genetic components and can therefore still be considered genetic diseases. The identification of genes involved in complex genetic diseases can be very important for the understanding and treatment of these diseases. Over the last 15 years, much progress has been made in the identification of genes responsible for monogenic diseases, but the identification of genes involved in complex diseases has been more difficult, and at this moment little is known about the genes involved in most common diseases.

Immunotherapy with interferon-alfa has become standard therapy in selected patients with viral hepatitis and chronic myelogenous leukemia. In addition, it is used in a variety of other diseases, both as standard therapy and in clinical trials. Its use is expected to expand in the following decade. Interferon can cause (severe) neuropsychiatric side effects. These side effects are discussed. Adequate management of these side effects is important, as is close collaboration between the oncologist and the psychiatrist. The cornerstone of management is patient education: this prevents interruption of therapy by patients who were not warned for neuropsychiatric side effects. Furthermore, patients should report in case of rapidly arising mood disorders. Interferon-alfa induced mood disorder is reported to be treatable. Three case descriptions illustrate this, but also illustrate some limits to successful treatment.

Behavioural genetics is the study of the hereditary influence on behaviour, and can therefore be regarded as the intersection between behavioural sciences and genetics. As with most other fields of research it is difficult to exactly pinpoint when behavioural genetics started. In fact, one might say that the notion behavioural traits can be inherited may have appeared in human thought as early at 8000 BC, when the domestication of the dog began.

The scientific era of behavioural genetics is generally considered to start with Charles Darwin. In his famous book On the Origin of Species by Means of natural Selection, or the Preservation of favoured Races in the Struggle for Life, published in 1859 (and sold out the first day), he devoted an entire chapter on instinctive behavioural patterns. Some years later, in his book The Descent of Man and Selection in Relation to Sex, he clearly stated that the difference between the mind of a human being and the mind of an animal ‘is certainly one of degree and not of kind’. Moreover he gave considerable thought that mental powers (and insanity) are heritable aspects.

The different forms of antidepressive continuation therapy, used in the Netherlands, to prevent relapse after electroconvulsive therapy, were examined by sending a questionaire to all ECT centers. Common practice is in agreement with the results of current research. However, recent studies suggest that pharmacological continuation therapy is less usefull to prevent relapse when pharmacotherapeutic resistance has been proven in the past. In these cases ECT-continuation therapy might bring a solution. On the effect of ECT-continuation therapy are few valid research results available.

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.

Most forms of behaviour whether normal or abnormal, show a tendency to run in families. However, these can range from symptoms of dementia and movement disorder caused by the comparatively rare autosomal dominant Huntington's disease to common everyday aspects of behaviour such as religious persuasion or career choice. Normal behaviours and most common disorders do not show simple mendelian inheritance but instead have more complex patterns of transmission involving either major genes with incomplete penetrance, multiple genes of small effect, or a combination of the two. In addition, common complex phenotypes usually involve the combination of genetic and environmental factors. Therefore once family studies have shown that a disorder or trait is familial the next stage is to perform twin studies and, if possible adoption studies to investigate whether this results from shared genes, shared environment or a combination of the two.

Positron emission tomography is one of the most important techniques of functional imaging in psychiatry. This paper gives a synopsis of the findings in mood disorders: determination of brain glucose metabolism, cerebral blood flow and receptor studies. Investigation in a resting state as well as after activation are discussed.

Although findings are somewhat discrepant hypometabolism, and/or hypoperfusion, most often in frontal and limbic areas are frequently described. Further research is needed, and standardization of the methodology would be most wellcome.

A fundamental issue in the neurobiology of adaptation disorders is how the hormones of the hypothalamic-pituitary-adrenal (HPA) axis protect the brain from such disorders, and how in a different context these very same stress hormones may enhance vulnerability. This contribution focuses on the corticosteroids which exert through two distinct nuclear receptor types control over gene networks underlying stress system activity in brain. The mineralocorticoid receptor mediates the pro-active mode of corticosteroid action involved in maintenance of basal stress system activity. The glucocorticoid receptor mediates the reactive feedback mode aimed to facilitate recovery from stress-induced disturbance. The balance between these pro-active and reactive modes of control is thought to be of critical importance for homeostasis, and thus for control of hormone-responsive genes which enhance vulnerability to stress-related affective and neurodegenerative disorders.

The alterations in the inflammatory response system (IRS) appear to be quite different between OCD and anorexia nervosa and are also different from the changes observed in major depression. In anorexia nervosa, there is some evidence for increased production of monocytic cytokines, i.e. tumor necrosis factor-α (TNFα) and interleukin-6 (IL-6), and decreased production of Th-1 like cytokines, i.e. IL-2 and IFNγ. In the same patients there are also signs of immunosuppression, e.g. lowered numbers of CD4 and CD8 T cells and increased production of transforming growth factor-beta (TGFβ). The increased production of monocytic cytokines may be the consequence of the hyponutritional status of those patients. The diminished production of the Th-1 like cytokines may be the consequence of at least four different factors: 1) the deficiency in nutritional factors; 2) neuroendocrine disorders, such as increased Cortisol production; 3) the increased TGFβ production; and 4) lower serum dipeptidyl peptidase activity. In OCD no consistent or specific alterations in the IRS are observed. There is no evidence that IRS activation may play a role in the pathophysiology of OCD and anorexia nervosa.