Z. Spiric

Is there a biological difference between trauma-related depression and PTSD? DST says ‘NO’

The use of the low-dose dexamethasone suppression test (DST) as a potentially discriminative marker between post-traumatic stress disorder (PTSD) and depression is still under discussion. In order to compare the influence of these psychopathologies on the DST results, we examined suppression in war-traumatized subjects with one or both of these disorders, as well as in healthy controls. Based on our previous findings, we hypothesized that subjects with any disorder would exhibit higher dexamethasone suppression than healthy controls due to traumatic experiences. This study was a part of a broader project in which simultaneous psychological and biological investigations were carried out in hospital conditions on 399 male participants: 57 with PTSD, 28 with depression, 76 with PTSD+depression, and 238 healthy controls. Cortisol was measured in blood samples taken at 0900 h before and after administering 0.5mg of dexamethasone (at 2300 h). Group means ± standard deviation of cortisol suppression were: 79.4±18.5 in the PTSD group, 80.8±11.6 in the depression group, 77.5±24.6 in the group with PTSD+depression, and 66.8±34.6 in healthy controls. The first three groups suppressed significantly more than the fourth. When the number of traumas was introduced as a covariate, the differences disappeared. The hypothesis was confirmed: in respect to DST, the examined trauma-related psychopathologies showed the same pattern: hypersuppression, due to multiple traumatic experiences.

Posttraumatic and depressive symptoms in β-endorphin dynamics

A disturbed beta-endorphin system can be a part of the post-traumatic stress disorder (PTSD) and depression allostasis. Study subjects (N=392) included those with PTSD and/or (stress-induced) depression, and healthy controls with and without traumas. The aim of the study was to examine the network of relations centered around plasma beta-endorphin. The network included anxiety (as a personality trait), traumatic events, pain, aggressiveness, depressive symptoms, and three clusters of PTSD symptoms: intrusions, avoidance, and hyperarousal. Beta-endorphin was represented by individual mean from 13 time points (BEmean), reflecting the total amount of the peripherally secreted hormone, and the coefficient of variation (BEvar), calculated as the ratio of standard deviation to the mean, reflecting the hormone׳s dynamics. BEvar correlated with all other variables, BEmean had no correlations. Structural equation modeling (SEM) was used to examine all interrelations (including their directions) of BEvar and the state/trait variables in the context of their entirety. The model revealed that hyperarousal and anxiety were the only direct agents of peripheral beta-endorphin fluctuations, mediating the effects of other variables. Traumatic events and intrusions act on BEvar via hyperarousal, while depressive symptoms, avoidance, and pain act via anxiety. Hyperarousal should be emphasized as the main agent not only because its effect on BEvar is larger than that of anxiety, but also because it increases anxiety itself (via avoidance and pain). All influences on BEvar are positive and they indicate long-term (sensitizing) effects (as opposed to direct stimulation, for example, by acute pain, anger, etc.). Relations apart from beta-endorphin are also discussed.

Executive Function in Treatment-Resistant Depression Before and After Electroconvulsive Therapy

Abstract Objectives: The aim of this study was to examine executive functions (EF) in patients with treatment-resistant depression (TRD) before and after bitemporal electroconvulsive therapy (ECT) and to evaluate possible associations between the depression severity and executive tasks performances. Methods: Patients (n = 29), treated with bitemporal ECT, underwent assessment at three time points: baseline, immediately after ECT course and 1 month later. The Stockings of Cambridge (SOC, CANTAB) was used to assess EF: (1) number of problems solved in minimum moves (SOC-P), (2) initial thinking time (SOC-I) and (3) subsequent thinking time (SOC-T). Results: The scores on the Hamilton Depression Rating Scale and the Clinical Global Impression scale were significantly reduced over time, with no negative effects on the EF. Among SOC subtests, only SOC-I improved over time, which was significantly correlated with the depressive symptoms reduction. SOC-T and SOC-P remained unchanged and did not correlate with mood. Interestingly, the patients with more lifetime psychiatric hospitalisations and more ECT applications were more likely to drop-out and to have longer SOC-T while performing the test. Conclusions: Our results support the view that ECT does not produce long-lasting EF deficits, nor exacerbates the pre-existing ones. The improvement of the EF performances during and after the ECT-induced alleviation of mood symptoms in TRD is based mostly on the reduction of time needed to plan the problem solution.

Atypical case of Wilson's disease with psychotic onset, low 24 hour urine copper and the absence of Kayser-Fleischer rings.

INTRODUCTION Wilsons disease is typically manifested in two clinical forms, neurological and hepatic and in rare cases it starts with psychiatric symptoms exclusively. We presented a rare atypical case of Wilsons disease with psy- chotic onset. CASE REPORT A 22-year-old male patient was initially presented with predominant signs and symptoms of psychiatric disorder and then later with the development of neurological signs and symptoms. Neuroimaging, detected metal deposits in central nervous system (CNS) but not in peripheral organs, while serum analysis excluded pantothenate-kinase associated neurodegeneration and aceruloplasminemia. In favor of the diagnosis of Wilsons disease there were reduced concentrations of copper and ceruloplasmin concentrations and metal deposits in CNS, but other pathognomonic signs and symptoms were absent: increased copper in urine, Kayser-Fleischer rings in Descemets corneal membrane and deposits of copper in liver. Introduction of penicillamine treatment resulted in improvement in mental and general health of the patient. Molecular genetic analysis definitely confirmed the diagnosis of Wilsons disease. CONCLUSION Wilsons disease can remain undetected for a long period of time if masked with dominant or exclusive psychiatric symptoms. If clear clinical symptoms and signs, and unambiguous laboratory findings are not present, it is necessary to perform molecular genetic analysis to confirm the definitive diagnosis.

Is Electroconvulsive Therapy Improving Executive Functions in Unipolar Depression Patients

In an acute episode of unipolar depression, patients show lower performance on the tests which make substantial demands on executive functions. Several studies documented that the impairment sometimes remains even in remitted patient, partially due to the antidepressant side effects or ECT. The aim of the present study was to evaluate executive functions in subjects who underwent ECT for therapy-resistant depression. Methods A course of bilateral ECT (mean number of applications 8.8+/-3.2) was applied to 22 patients (age 46.3±9.8; males 45.8%;IQ 97.2±11.6) with baseline HAMD 28.5±3.6, DASS 95±15, MMSE 29.1±1,1, who were tested by Sockings of Cambridge (SOC) tests (Cambridge Automated Neuropsychological Test Battery)at baseline (T0), immediately after ECT (T1) and one month later (T2). ECT was delivered with a modern square-wave machine with EEG and ECG monitoring. Modified treatment was performed in all cases. Results The intensity of depressive symptoms (HAMD and DASS) was significantly reduced at T1 and T2in comparison to baseline (p Conclusion ECT reduced depression without impairing executive function. As it is less likely that improvement in mean thinking time on SOC is directly associated with ECT, we suggest that improved execution is rather due to the decreased individual sensitivity to negative feedback during performing the task.