[Resources, Childhood Trauma and Psychopathology in a Psychiatric Inpatient Sample]. / Ressourcen, Kindheitstraumata und Psychopathologie bei stationär psychiatrischen Patienten.

Childhood trauma can have a negative impact on the development of personal and social resources in later adulthood. This is problematic, because resources can be a protective factor against the development of psychiatric disorders and are potentially beneficial for therapy outcomes. The current study considered the association between childhood trauma and resources as well as the impact of these 2 factors on psychopathology and symptom reduction in a psychiatric in-patient sample. We anticipated negative relationships between resources and the extent of childhood traumatization as well as resources and psychiatric symptoms. We also expected a positive association between trauma and symptoms. Furthermore, we assumed that higher current resources would be associated with a higher symptom reduction and more severe traumatization in childhood with a lower reduction of symptoms. These hypotheses were tested with correlation and regression analysis in a sample of n=93 patients with depressive and posttraumatic symptomatology in a psychiatric clinic in Offenburg. As expected, we found negative associations between resources and childhood trauma as well as resources and symptoms. However, contrary to our predictions, we could only find a significant association between childhood traumatization and posttraumatic, but not depressive symptoms. Also, there was no significant association between resources or childhood trauma and therapy outcome. The reported associations are relevant concerning the prevention of psychiatric disorders and thus have multiple implications for the development and use of preventive and therapeutic interventions.

Theory of mind deficits in chronically depressed patients.

BACKGROUND: Poor theory of mind (ToM) performance has been found in patients with mood disorders, but it has not been examined in the subgroup of chronic depression where ToM deficits may be even more persistent than in acute depressive episodes. The aim of this study was to compare the ToM performance of chronically depressed patients with a healthy control group and to clarify the relation of ToM to other cognitive functions. METHODS: ToM performance was assessed in 30 chronically depressed patients and 30 matched healthy controls by two cartoon picture story tests. In addition, logical memory, alertness, and executive functioning were evaluated. RESULTS: Chronically depressed patients were markedly impaired in all ToM- and neuropsychological tasks compared to healthy controls. Performance in the different ToM tests was significantly correlated with at least one other cognitive variable. After controlling for logical memory and working memory, no ToM tasks predicted being a patient. CONCLUSIONS: Patients with chronic depression present significant deficits in "reading" social interactions, which may be associated with general cognitive impairments.

Efficacy of quetiapine monotherapy in rapid-cycling bipolar disorder in comparison with sodium valproate.

BACKGROUND: Rapid-cycling bipolar disorder is often characterized by a lack of response to psychopharmacological treatment, and a standard therapy has not been developed yet. The aim of this study was to examine the long-term efficacy and safety of a monotherapy with quetiapine or sodium valproate (VPA) in patients with rapid-cycling bipolar disorder. METHODS: This open-label, randomized, parallel group monotherapy pilot study was conducted at 3 German centers. A sample of 38 remitted or partly remitted patients with bipolar disorder and rapid cycling (quetiapine n = 22; VPA n = 16) were treated with quetiapine or VPA (flexible dose design) for 12 months. RESULTS: Forty-one percent of the patients with quetiapine and 50% with VPA completed the trial. On the basis of ITT-LOCF, Life Chart Method data showed that patients being treated with quetiapine had significantly less moderate to severe depressive days than patients on VPA (mean +/- SD, 11.7 +/- 16.9 days vs 27.7 +/- 24.9 days; P = 0.04) while they did not differ in the number of days with manic or hypomanic symptoms. Furthermore, according to the Clinical Global Impression Scale, bipolar version, the responder rates tended to be higher for quetiapine than for VPA. There were no differences found evaluating the Hamilton Depression Rating Scale, the Montgomery-Asberg Depression Scale, and the Young Mania Rating Scale. The incidence of adverse events, especially of orthostatic dysregulation, sedation, and weight gain, was significantly higher in the quetiapine group. CONCLUSIONS: In this study, quetiapine was more effective than VPA on the number of depressive days and similar to VPA in the treatment of manic symptoms. Quetiapine was associated with a greater incidence of side effects, particularly orthostatic dysregulation, sedation, and weight gain.

Stress, personality and depressive symptoms in a 6.5 year follow-up of subjects at familial risk for affective disorders and controls.

BACKGROUND: The aim of the study was to identify risk factors in subjects at risk for depressive disorders and controls. METHODS: In a 6.5 year follow-up study we examined the effects of personality (neuroticism, frustration intolerance, rigidity, melancholic type), adverse life events and chronic difficulties on depressive symptoms in 89 high-risk subjects (HRS, siblings and children of patients suffering from an affective disorder), without any mental illness at wave 1 (T1), and 49 controls without any personal and family history of psychiatric disorder at T1. To this end, regression analysis and path analysis using a structural equation model (only for HRS) were performed. RESULTS: Risk factors for depressive symptoms at wave 2 (T2) in HRS comprised acute adverse life events, frustration intolerance (T1) and depressive symptoms (T1). Risk factors for depressive symptoms in controls included chronic difficulties, neuroticism and rigidity. HRS had less stressful life events and the same risk for chronic difficulties, but perceived adverse events as more stressful. LIMITATION: The sample size of the control group is too small for identifying slight effects. CONCLUSION: Our results indicate that the impact on the emergence of depressive symptoms of various risk factors is different in high-risk subjects and controls. High-risk subjects are more sensitive to the depressogenic effects of acute stress and thus avoid potential stressful changes in their life to a higher extent. On the other hand, the influence of persistent factors such as personality traits (neuroticism, rigidity) and chronic difficulties on subsequent depressive symptoms was less pronounced in HRS as compared to controls.

Spectroscopic findings in attention-deficit/hyperactivity disorder: review and meta-analysis.

OBJECTIVES: The last decade has seen an increasing interest in the method of magnet resonance spectroscopy (MRS) since this is the only research tool that allows a non-invasive in vivo assessment of neurochemical aspects of ADHD without employing ionising radiation. In this paper we review published MRS results with respect to childhood, adolescence and adult ADHD. METHOD: We searched the Medline (Pub Med) database using the key words ADHD, attention-deficit/hyperactivity disorder, magnet resonance spectroscopy, MRS and spectroscopy. Citations of identified articles were also searched for relevant studies. Meta-analyses were performed for the measured metabolites and regions of assessment. RESULTS: Sixteen studies could be identified that used MRS to investigate the neurobiology of ADHD. Two regions could be identified as the focus of spectroscopic investigations--the frontal lobe including anterior cingulate cortex and parts of prefrontal cortex and the basal ganglia, mostly striatum, alongside the fronto-striato-thalamo-frontal circuits. As for metabolites, in the majority of studies the ratios to creatine and not absolute concentrations of metabolites were estimated. Choline compounds, N-acetyl-aspartate and glutamate/glutamine (to creatine ratios) could be identified as being altered in several studies in ADHD. The meta-analysis showed increased choline compounds in several researched regions. DISCUSSION: MRS is a promising tool for the non-invasive in vivo assessment of the cerebral neurochemistry in ADHD. More regions of interest (ROI) like amygdala, hippocampus, thalamus and cerebellum should be assessed in future studies. Further methodological improvements of MRS are desirable in order to assess the absolute metabolite concentration of several ROIs at the same time. Such developments will open novel perspectives in spectroscopic investigations of ADHD.

Sodium-myo-inositol co-transporter (SMIT-1) mRNA is increased in neutrophils of patients with bipolar 1 disorder and down-regulated under treatment with mood stabilizers.

Recent in-vitro data indicate that depletion of neural cells of myo-inositol by virtue of down-regulation of the high-affinity sodium-myo-inositol co-transporter (SMIT) may be a common mechanism of action of the mood stabilizers lithium, valproate and carbamazepine. The authors sought to investigate whether or not down-regulation of SMIT also occurs in vivo in bipolar patients. Expression of SMIT mRNA was measured in neutrophils of bipolar patients either unmedicated or treated with lithium salts or valproate and in neutrophils of unmedicated, matched healthy controls using quantitative real-time PCR. The content of SMIT mRNA was significantly reduced in neutrophils of lithium-treated bipolar patients compared to controls and to untreated bipolar patients. Untreated bipolar I patients but not bipolar II patients exhibited a significantly higher expression of SMIT mRNA than controls. Neutrophils of bipolar I patients treated with valproate exhibited a significantly lower expression of SMIT mRNA than untreated bipolar I patients but did not differ from controls. These results suggest that lithium and valproate down-regulate SMIT mRNA in vivo in patients. In addition the data provide first evidence that up-regulation of SMIT might be associated with an increased risk for bipolar I disorder.