Somatization has been defined in a number of ways. Despite their differences, these definitions have one element in common, namely the presence of somatic symptoms that cannot be explained (adequately) by organic findings.

The primary objectives of the dissertation were to gain a better insight into the concept of somatization, and to study (prospectively) the relationship between neuroticism and alexithymia, two personality traits that have been shown to be related to somatization, the affective state dimensions positive and negative affect (or psychological distress) and medically unexplained symptoms.

A selective review was conducted regarding conceptual and methodological issues related to somatization. A total number of 318 patients, presenting to their primary care physician with medically unexplained symptoms, participated in the prospective study. Both at baseline and at 6-month follow-up a number of measures were filled out with respect to somatization, neuroticism, alexithymia, negative and positive affect, anxiety and depression.

The concept of somatization was clarified, thereby making use of the distinction between presenting and functional somatization. The personality traits neuroticism and alexithymia were found to have an indirect influence on symptom reports. Both the cross-sectional and follow-up data pointed to the importance of positive and negative affect as determinants of (changes in) number of symptoms (over time). Negative affect, together with the alexithymia dimension measuring difficulty identifying feelings, predicted symptom persistence.

The theoretical as well as therapeutic implications of the present paper may give an impetus to new research in the domain of somatization.

Intense and rapidly changing mood states are a major feature of borderline personality disorder (BPD), which is thought to arise from affective vulnerability.

There have been only a few studies investigating affective processing in BPD, and particularly neither psychophysiological nor neurofunctional correlates of abnormal emotional processing have been identified so far.

Studies are reported using psychophysiological or functional neuroimaging methodology.

The psychophysiological study did not indicate a general emotional hyperresponsiveness in BPD. Low autonomic arousal seemed to reflect dissociative states in borderline subjects experiencing intense emotions. In the functional magnetic resonance imaging study enhanced amygdala activation was found in BPD, and it is suggested to reflect the intense and slowly subsiding emotions commonly observed in response to even low-level stressors.

Implications for psychotherapy are discussed.

The aim of the present study was to examine the effects of age and gender on depressive classification and phenomenology in unipolar depressed in-patients.

The authors have assessed 14 items relevant to depressive symptomatology from the Structured Clinical Interview for DSM-III (SCID) and the Hamilton Depression Rating Scale (HDRS) in 180 depressed in-patients.

Melancholia was significantly more prominent in older depressed patients (≥ 55 years), whereas minor depression (i.e. adjustment disorder with depressed mood and dysthymic disorder) in younger (< 55 years) depressed subjects. Older depressed subjects exhibited significantly more anorexia/weight loss, non-reactivity, depressed mood, loss of interest, early morning awakening, loss of energy, somatic anxiety, loss of insight, psychotic symptoms and retardation than younger depressed people. Male depressed subjects showed significantly more loss of interest, suicidal ideation and agitation than their female counterparts. Psychomotor disorders, a distinct quality of mood and early morning awakening were characteristics of older depressed males, while diurnal variation occurred more frequently in older depressed females.

It is concluded that increasing age in unipolar depression may be accompanied by an increase in severity of illness, increased frequency of some melancholic symptoms, particularly in men and a higher frequency of major depression in women and of melancholia in men.

It has been established that thyrotropin-releasing hormone (TRH) affects several aspects of immunoreactivity, e.g. production of proinflammatory cytokines. It has been shown that TRH enhances the therapeutic efficiency of classical tricyclic antidepressants. Proinflammatory cytokines may play a role in the etiology of depression, whereas the therapeutic efficacy of antidepressants may be related to their negative immunoregulatory effects.

In order to verify the hypothesis that TRH-induced increase of therapeutic efficiency of classical tricyclic antidepressants results from synergistic inhibitory effects of these agents on the secretion of proinflammatory cytokines, we determine the effect of imipramine or fluoxetine with and without TRH on the production of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) by stimulated human whole blood cells.

Diluted whole blood of 17 volunteers was incubated with imipramine or fluoxetine (both in doses of 10−5 M) with or without TRH (in a dose of 10−5 M). The supernatants were collected 24 h later for the assay of TNF-α and after 72 h for the assays of IFN-γ and IL-10. The three cytokines were assayed by ELISA methods.

A significant decrease in production of IFN-γ was observed in cells stimulated with mitogens and co-incubated with imipramine or fluoxetine and TRH. Under the same conditions, TRH alone did not change the production of these cytokines, whereas imipramine alone significantly decreases IFN-γ production, and fluoxetine alone significantly decreases IFN-γ and TNF-α production.

Although a significant decrease in IFN-γ production was observed after joint application of TRH and antidepressants, our data did not support the above-mentioned hypothesis. Indeed, we did not observe synergistic inhibitory effects of these agents on the secretion of proinflammatory cytokines.

In the present paper the association of stress-induced cortisol with memory impairment is discussed

An experiment is described in which an attempt is made to block stress-induced cortisol by lowering 5-HT neurotransmission by means of acute tryptophan depletion (ATD). Forty-five healthy control subjects participated in the experiment.

Stress-induced peak cortisol and immediate memory performance were negatively associated. ATD tended to block stress-induced cortisol response. ATD also blocked the association between peak cortisol response and memory impairment.

Stress-induced cortisol and its association with memory impairment is mediated at least partially by serotonin.

Interictal affective disorders are common in patients with epilepsy and there is a need for evidence-based treatment guidelines.

This paper gives an overview of research concerning treatment of interictal affective disorders and interictal anxiety disorders in epilepsy.

Literature review supplemented by clinical experience.

Interictal psychiatric disorder can be characterized as intermittent pleomorphic psychopathology. The most common manifestations are interictal dysphoric disorder (IDD) and depression. There is a lack of randomized control trials (RCTs) concerning effectiveness and side-effects of antidepressants in epilepsy patients.

Treatment implications of the concept of IDD and other interictal disorders are an optimized dosage of anti-epileptics in combination with antidepressants. This coincides with recent guidelines concerning combinations of psychotropic medication, such as for depression and bipolar disorder, in general psychiatry. Systematic research involving the DSM-IV categories of generalized anxiety disorder, panic disorder and agoraphobia and depression is not yet available. Prevalence and treatment of interictal anxiety disorders and depressive disorder in epilepsy should be the subject of further research, in order to enable development of evidence-based treatment guidelines for these disorders in epilepsy patients.

Chronic fatigue syndrome (CFS) is a complex syndrome with a psychiatric comorbidity of 70–80%. A psychiatric interview is necessary in order to exclude psychiatric illness and to identify psychiatric comorbidity. Studies have demonstrated that in general medical practice and in the non-psychiatric specialist practice, physicians tend to underdiagnose psychopathology in patients with CFS. There are many questions unanswered about the treatment of CFS

Typical issues for the psychiatric practice are reviewed: psychiatric comorbidity, dysregulation of the PHA-axis and the treatment of CFS.

Depression, somatization, sleeping disorders and anxiety disorders are the most important psychopathological symptoms found in CFS patients. CFS should not be regarded as a masked (somatoform) depression. Although the results from neuroendocrinological studies assessing the hypothalamic–pituitary–adrenal axis (HPA-axis) are inconsistent, they suggest that there is a subgroup of CFS patients suffering from a discrete dysregulation of the HPA-axis resulting in basal hypocortisolaemia. These findings, however, do not reveal a causal relationship. Antidepressants do not seem to have a positive influence on the symptom of fatigue, but appear to be beneficial in alleviating the symptoms of depression and social functioning. Cognitive behaviour therapy and graded exercise show a significant improvement on fatigue and other symptoms and are the only treatments available for CFS patients.

This article describes an exploratory study of MMPI-2 administration to 20 patients with Korsakoff's disease, all admitted to the Korsakoff unit of a major psychiatric hospital in the Netherlands.

We compared their MMPI-2 basic profiles with those of an inpatient alcohol-dependent non-Korsakoff group. Attention was also given to content scales and some selected supplementary scales. Furthermore, we explored the differences between MMPI-2 profiles of Korsakoff patients with and without insight into oneself and one's disease.

Compared with both the Dutch norms and the scale means of the non-Korsakoff alcoholics, Korsakoff patients showed an extraordinary flat profile. Illness insight appeared to be related to the levels of the various scales.

The results show the potential usefulness of the MMPI-2 in the differential diagnosis of chronic alcoholism and Korsakoff's disease.

Knowledge on fundamental aspects of the influence of ‘stress’ on animal and human organisms is accumulating. In clinical situations, however, psychiatrists still do not use apropriate instruments to recognize and handle the impact of daily life stress. DSM-IV is insufficient in this respect.

A different approach is sketched for clinicians to be able to integrate knowledge from research more effectively.

Application of a ‘broad’ biological view may reveal the significance of interpretation, emotion, impulse and reaction as stages of a ‘mental tract’, which is involved in processing the input of stressful situations.

This may lead to a more rational ‘targeting’ of pharmacological and psychotherapeutic strategies in clinical practice.

A re-orientation of clinical psychiatry from mere classification towards a ‘broad’ biological approach may pave the way for a more rational and purposeful application of research findings to therapy.

Here we propose a stress model with disease-specific aspects and aspecific factors. The latter are subdivided into load (perception, psychic defence mechanisms), strain (psychophysiological responses) and stress sensu strictu (biological and behavioural compensation). Insufficiently compensated strain will result in being sick and precipitation of a specific disease according to one's predisposition. In the clinical practice, multiconditionality requires a multidimensional analysis, the the five-axial DSM-system being designed especially for this purpose. Multidisciplinary treatment is then organized accordingly, i.e. Axis I: case management, medication; Axis II, (focal) psychotherapy; Axis III, somatic specialists; Axis IV, social worker; Axis V, psychotherapy for coping deficits.

To test the efficacy of this multimethodical approach.

In a 1-year prospective study of 257 admissions in a department of psychiatry in a general hospital, the General Health Questionnaire (30 items) was filled out at admission, discharge and first polyclinical visit post-discharge.

The 213 evaluable questionnaires at admission did not show differences (17–18.9) between the four groups, mood disorders (62%), alcoholism (17%), psychoses (15%) and anxiety disorders (6%). At discharge all four groups had reached the cut-off value for ‘not-sick’ (< 6), this remaining so at follow-up; the three measurements differed significantly throughout the patient groups. Hospitalization was definitely 28.2 days shorter than the Dutch mean of 42 days.

Working to the proposed clinical model for multiconditionalty is effective on intensity and duration of disorders, sustained improvement is attained.

It remains a mystery as to how genetic and environmental factors cause schizophrenia.

To develop a pathophysiological model of schizophrenia that has greater explanatory power than existing hypotheses of the disorder.

Published findings on schizophrenia are integrated with more recent data from human and animal studies of striatal and cerebellar functions.

The analysis shows that during phylo- and ontogenesis two primarily motor-control mechanisms are applied at the intentional (limbic) level of functioning to organize emotional and cognitive behavior: one for initiating and dosing (drive) and the other for the representational guidance (guidance) of both movements and intentions. The intentional drive and guidance mechanisms are organized through a ventral, respectively, a dorsal cortical–subcortical circuitry.

A deficient implementation of these mechanisms at the limbic domain manifests itself as schizophrenia, whereby the heterogeneity in symptomatology is explained by the extent of the remaining cerebral activity and by the degree of indirect activation of these systems. In general, activation manifests itself as positive symptomatology and the absence of such activation as negative symptomatology. The model provides a more comprehensive explanation for existing clinical and epidemiological data than do the current alternatives. It is compatible with the major prevailing views on the illness, such as the theories that regard this as a progressive neurodevelopmental, or a connectivity disorder, or one resulting from a deficient cerebral lateralization, or an interrupted cortico–thalamo–cerebello–cortical circuitry. The model fits with recent theories in evolutionary psychology and evolutionary psychiatry.