Individuals with body dysmorphic disorder (BDD) suffer from unpleasant, repetitive thoughts about imagined defects in appearance which are difficult to control.

The purpose of this study was to test for deficits in cognitive inhibition in BDD.

To test for deficits in cognitive inhibition in BDD, we applied a negative priming paradigm. Specifically, we explored whether BDD patients exhibit greater deficits in cognitive inhibition when lexical targets are threatening than when they are non-threatening.

Surprisingly, BDD patients exhibited deficits in cognitive inhibition only for non-threatening but not for threatening information.

Although BDD patients often describe their negative thoughts about their appearance as distressing, they may experience them as valid and thus may not try to control them.

This study assessed the changes in the isoprenoid pathway and its metabolites in seizure disorder (ILAE classification – I generalized – idiopathic generalized epilepsy with age-related onset – epilepsy with generalized tonic clonic seizures on awakening) and the metabolic cascade produced by isoprenoid pathway dysregulation.

The following parameters were assessed in seizure disorder: isoprenoid pathway metabolites, tyrosine and tryptophan catabolites, glycoconjugates metabolism and red blood cell (RBC) membrane composition.

There was elevation in plasma HMG-CoA reductase activity, serum digoxin and dolichol and a reduction in RBC membrane Na-K+ ATPase activity, serum magnesium and ubiquinone levels. Serum tryptophan, serotonin, strychnine, nicotine and quinolinic acid were elevated while tyrosine, dopamine, morphine and norepinephrine were decreased. The total serum glycosaminoglycans and glycosaminoglycan fractions (except dermatan sulfate), the activity of glycosaminoglycans (GAG) degrading enzymes and glycohydrolases, carbohydrate residues of glycoproteins and serum glycolipids were elevated. Total serum cholesterol, LDL cholesterol and free fatty acids were increased while HDL cholesterol and triglycerides were unaltered. The concentration of membrane hexose, fucose, cholesterol and phospholipids in the RBC membrane decreased significantly but the total RBC membrane GAG was unaltered.

Epileptogenesis could be due to a dysfunctional isoprenoidal pathway and paroxysmal hypothalamic digoxin hypersecretion.

Cryotherapy has a long tradition in somatic medicine. Yet we know very little about its impact on psyche and mood disturbances in particular. Therefore there is a real need for scientific investigations into this problem.

The study reported here was an initial approach to whole-body cryotherapy (WBCT) as a potential treatment modality for depression and was expected to provide rough data helping to design a future project with extended methodology, larger sample groups and longer follow-up.

Twenty-three patients aged 37–70 years gave informed consent to participate in the study. Ten WBCT procedures (160 s, −150°C) were applied within 2 weeks. Participants were recruited from depressed day hospital patients. Antidepressive medication was not ceased. Symptoms were rated at the beginning and end of this intervention using the 21-item Hamilton Depression Rating Scale (HDRS). Changes in scores were analyzed in the group of patients for every item separately as well as for the sum of all items for each patient.

Almost for each individual HDRS item, the overall score for all patients together was significantly lower after WBCT. This means that all symptoms, except for day–night mood fluctuations, were presumably positively influenced by cryotherapy. The HDRS sum-score for each patient after WBCT was lower than that of the baseline and reached statistical significance in a paired samples t-test. Every patient was therefore considerably relieved after WBCT.

It appears that WBCT helps in alleviating depression symptoms. Should this be confirmed in the extended study we are currently implementing, WBCT may become an auxiliary treatment in depression.

Identification of schizophrenia, a common neuropsychiatric disorder, is based on clinical examination. An easily measurable peripheral marker, which may enable a more rapid and more accurate diagnosis, is not available. A possible candidate is the D3 dopamine receptor on lymphocytes.

The D3 receptor is investigated for its clinical significance as a marker for diagnosing schizophrenia.

From eight schizophrenic patients and eight controls lymphocyte RNA was isolated. A semiquantitative reverse transcription–polymerase chain reaction (RT-PCR) was carried out and the intensities of the specific D3 dopamine receptor bands of patients and controls were compared.

No difference could be seen between the intensities of the bands from patients and controls.

An aberrant D3 dopamine receptor mRNA expression in lymphocytes of schizophrenics could not be demonstrated. This might be caused by down-regulation of D3 receptor production by antipsychotic drug treatment. At present, the D3 receptor seems to have no diagnostic value in schizophrenia.

Research findings on the relationship between cognitive functioning and psychiatric symptoms in schizophrenia have yielded inconsistent results. Although several models were postulated linking cognition and symptoms, the most recent studies point in the direction of cognition and symptoms being relatively independent disease processes.

The hypothesis that cognitive decline and psychiatric symptoms are independent disease processes was tested.

The relationship between cognitive functioning and clinical symptoms was examined in a large sample of 100 schizophrenia patients.

The hypothesis was largely confirmed.

No convincing evidence was found that symptoms and cognition were related.

Alterations of the immune–neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticoids (GCs) when under stress.

A total of 21 CFS patients and 20 healthy age- and gender-matched controls underwent a standardized psychosocial stress test (Trier Social Stress Test, TSST). Salivary and plasma cortisol levels were measured repeatedly following exposure to the stressor. GC sensitivity was assessed in vitro by dexamethasone inhibition of lipopolysaccharide-stimulated production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNC-α).

Cortisol responses following the TSST did not differ significantly between CFS patients and healthy controls. GC sensitivity differed significantly between CFS patients and healthy controls, with CFS patients showing a greater sensitivity towards GCs (TNF-α: F1/39 = 7.32, P = 0.01; IL-6: F1/39 = 9.73, P = 0.004).

Consistent with recent evidence, CFS patients are characterized by an enhanced sensitivity to glucocorticoids. The implications for secondary processes, such as the regulatory influence of glucocorticoids on immune processes, are discussed.

Mood disorders are related to considerable morbidity and mortality, and although there is little doubt that they are brain-based disorders, their neural correlates still remain elusive. A neuro-anatomic model of mood regulation comprising the prefrontal cortex, amygdala-hippocampus complex, thalamus, basal ganglia, and connections among these areas has been proposed.

We reviewed the evidence for regional brain abnormalities in bipolar disorder, and attempted to integrate available findings into a comprehensive pathophysiological model of illness.

A computerized Medline Ovid search was conducted for the period 1966–2002, and complemented by a manual search of bibliographical references from recent reviews. Articles meeting specified criteria were included.

Hyperintense lesions in cortical and subcortical regions are the most consistently reported and widely studied structural abnormalities. Smaller prefrontal cortical volume is a common finding in bipolar disorder and unipolar depression. Enlarged amygdala (in bipolar disorder) and smaller hippocampus (in unipolar depression) have been reported by several groups. Decreased volumes (in unipolar depression) and increased or unaltered volumes (in bipolar disorder) of striatal structures have been reported.

Bipolar and unipolar mood disorders are associated with detectable structural brain abnormalities. The histopathology underlying such anatomical changes remains to be elucidated. To reach more definitive conclusions about neuroanatomical changes that take place during the course of mood disorders, prospective longitudinal studies are needed. Also, integration with functional imaging is necessary in order to elucidate the relevance of identified structural abnormalities.

The present epidemiological study investigates sex- and age-adjusted 4-week, 12-month, and lifetime prevalence rates of somatoform disorders in in-patients with musculoskeletal and cardiovascular diseases in comparison with prevalence rates of these disorders in the general population in Germany.

Prevalence rates were calculated from two samples, one from rehabilitation in-patients with musculoskeletal (n = 187) or cardiovascular (n = 116) diseases, and one from a large sample of the German National Health Interview and Examination Survey – Mental Health Supplement (GHS-MHS; n = 3889). The prevalence rates were based on the M-CIDI, an interview for the assessment of mental disorders.

The adjusted prevalence rates of any mental disorder in both clinical samples are higher compared with rates of the general population (e.g. lifetime musculoskeletal, 59.3%; cardiovascular, 56.2%; general population, 47.9%). Prevalence rates of patients with cardiovascular (e.g. 12.2%) and musculoskeletal (21.5%) diseases do not indicate an increased prevalence of somatoform disorders compared with the general population (18.2%).

The results confirm that patients with chronic somatic diseases have increased prevalence rates of mental disorders. However, these increased prevalence rates go primarily back to affective and anxiety disorders and not to somatoform disorders. The diagnostic criteria for somatoform disorders and the question algorithm of the M-CIDI are probably responsible for potential underestimation of somatoform disorders in patients with chronic somatic diseases.

With the increased accessibility of the CT scanner, psychiatrists managing schizophrenia and first-episode psychosis have incorporated this imaging technique into their diagnostic work-up. This practice has been reinforced by published criteria for CT scanning in psychiatric patients suggesting that cranial CT should be used as a screening tool to exclude intracranial pathology in all patients with a first presentation of schizophrenia or first psychotic episode.

This study reviews the performance of these criteria.

This consisted of a 3-year retrospective case-note audit, using published criteria, of all male in-patients with an established diagnosis of schizophrenia who had a cranial CT during the review period.

The efficacy of the published criteria is not supported. In addition, non-specific abnormalities on cranial CT are related to duration of illness and not age in this sample.

There is a need to establish new and clinically meaningful approaches for the use of cranial CT and similar technologies in clinical psychiatry. Cranial CT performs poorly as a universal screening tool in this population. The decision to use such imaging techniques should be made on a case-by-case basis using all available clinical evidence.

Diencephalic tumours are usually presented with the sign and symptoms of increased intracranial pressure, endocrinological changes and visual disturbances. Psychiatric manifestation of such rare tumours is not well known.

To investigate the challenges and benefits of psychiatric evaluation on the diagnosis of diencephalic tumours and to emphasize the presence of psychosis as an initial phenomenon.

Two cases who presented with the characteristic symptoms of psychosis and diagnosed diencephalic tumour are reported. A detailed radiological examination confirmed such diagnosis in both cases and surgical treatment was done.

First, all patients who presented with a history of unexplained behaviour change must be evaluated by psychiatrists to exclude an organic pathology. Secondly, until the diagnosis of diencephalic tumour is confirmed, the surgical management must be performed.

We reviewed the neurochemical brain imaging literature in bipolar disorder to synthesize the findings and provide directions for future research.

Relevant articles were retrieved by computerized Medline Ovid search (up to and including 2002) and complemented by bibliographic manual searches of reviews known to the authors.

PET and SPECT studies in bipolar disorder have identified changes in various aspects of dopaminergic and serotonergic neurotransmission. Ligands for other neurotransmitters are actively being pursued. Spectroscopy studies have utilized a number of MRS-sensitive nuclei to chemically ‘biopsy’ the brain of patients with bipolar disorder. Few consistent findings are emerging, however, the majority of nuclei that can be measured are not directly related to the pathophysiology of the disorder.

Brain imaging has the potential to unravel the neurochemical underpinnings of bipolar disorder, however, there is a continuing need for clinical, technical and methodological sophistication.

Capgras syndrome (CS), the most common type of delusional misidentification syndrome, is the delusional belief that significant people in the patient's life have been replaced by identical doubles. Capgras syndrome is thought to be a rare syndrome which commonly occurs in a psychotic context.

The objective of this study was to estimate the 5-year prevalence rate of CS in a university hospital in-patient setting and determine associated etiological and sociodemographic factors.

All patient files and medical records were reviewed in detail for the presence of Capgras syndrome. The sociodemographic variables, clinical manifestations, and psychiatric and medical diagnoses of patients who fulfilled clinical criteria for Capgras syndrome were recorded for statistical evaluation.

The retrospective evaluation of patient files in 920 cases admitted to our psychiatric in-patient unit over 5 years revealed that 12 patients fulfilled the criteria for Capgras syndrome. The crude prevalence of Capgras syndrome in this population during 5-year period was 1.3% (1.8% for females, 0.9% for males). Schizophrenia (50%) was the most common psychiatric diagnosis in these patients. Only two patients presented with an organic etiology underlying Capgras syndrome.

The results of this study indicate that Capgras syndrome is not a rare syndrome, and commonly occurs during the course of either functional or organic psychotic illness. Age seems to be an important predicting factor for the etiology of psychosis underlying Capgras syndrome.