Der WHO Wellbeing Index (WHO-5) als Depressivitätsmaß

Der WHO-5 erfasst mit fünf Items psychisches Wohlbefinden, er dient auch als Screeninginstrument zur Erfassung depressiver Symptomatik. Wenige Studien untersuchten diesen Validitätsaspekt jedoch im klinischen Kontext. Ziel der vorliegenden Studie war es, die Messinvarianz des WHO-5 zwischen depressiven und nicht-depressiven Stichproben sowie Art und Spezifität des Zusammenhangs mit Skalen zur Erfassung der Depressionsschwere zu überprüfen. Insgesamt 414 Personen füllten den WHO-5 und das BDI-II aus. Aktuell erfüllten 207 Personen die DSM-IV-Kriterien einer Major Depression (SKID-I). Eine Teilstichprobe erhielt zusätzlich das Beck-Anxiety-Inventory (BAI) und wurde auf der Hamilton-Depression-Rating-Scale (HAM-D) und der Hamilton- Anxiety-Rating-Scale (HAM-A) durch trainierte Rater eingeschätzt. Der WHO-5 wies hohe Messinvarianz bezüglich des Vorliegens/Nichtvorliegens einer Major Depression auf. Er zeigte hohe negative Zusammenhänge mit selbst- und fremdeingeschätzter Depressivität (BDI-II, HAM-D), insbesondere bei milderer und moderater Symptomschwere und auch nach Kontrolle gleichzeitig bestehender Angstsymptomatik. Diese Ergebnisse unterstützen die Verwendung des WHO-5 als Depressionsmaß, zumindest im Bereich milder und mittlerer Depressionsschwere.

Prolonged inflammation following critical illness may impair long-term survival: a hypothesis with potential therapeutic implications

Despite successful intensive care a substantial portion of critically ill patients dies after discharge from the intensive care unit or hospital. Observational studies investigating long-term survival of critically ill patients reported that most deaths occur during the first months or year after discharge. Only limited data on the causes of impaired quality of life and post-intensive care unit deaths exist in the current literature. In this manuscript we hypothesize that the acute inflammatory response which characteristically accompanies critical illness is ensued by a prolonged imbalance or activation of the immune system. Such a chronic low-grade inflammatory response to critical illness may be sub-clinical and persist for a variable period of time after discharge from the intensive care unit and hospital. Chronic inflammation is a well-recognized risk factor for long-term morbidity and mortality, particularly from cardiovascular causes, and may thus partly contribute to the impaired quality of life as well as increased morbidity and mortality following intensive care unit and hospital discharge of critically ill patients. Assuming that critical illness is indeed followed by a prolonged inflammatory response, important implications for treatment would arise. An interesting and potentially beneficial therapy could be the administration of immune-modulating drugs during the time after intensive care unit or hospital discharge until chronic inflammation has subsided. Statins are well-investigated and effective drugs to attenuate chronic inflammation and could potentially also improve long-term outcome of critically ill patients after intensive care unit or hospital discharge. Future studies evaluating the course of inflammation during and after critical illness as well as its response to statin therapy are required.

Reduction in rat phosphatidylethanolamine binding protein-1 (PEBP1) after chronic corticosterone treatment may be paralleled by cognitive impairment: a first study

Chronic stress is associated with hippocampal atrophy and cognitive dysfunction. This study investigates how long-lasting administration of corticosterone as a mimic of experimentally induced stress affects psychometric performance and the expression of the phosphatidylethanolamine binding protein (PEBP1) in the adult hippocampus of one-year-old male rats. Psychometric investigations were conducted in rats before and after corticosterone treatment using a holeboard test system. Rats were randomly attributed to 2 groups (n = 7) for daily subcutaneous injection of either 26.8 mg/kg body weight corticosterone or sesame oil (vehicle control). Treatment was continued for 60 days, followed by cognitive retesting in the holeboard system. For protein analysis, the hippocampal proteome was separated by 2D electrophoresis (2DE) followed by image processing, statistical analysis, protein identification via peptide mass fingerprinting and gel matching and subsequent functional network mapping and molecular pathway analysis. Differential expression of PEBP1 was additionally quantified by Western blot analysis. Results show that chronic corticosterone significantly decreased rat hippocampal PEBP1 expression and induced a working and reference memory dysfunction. From this, we derive the preliminary hypothesis that PEBP1 may be a novel molecular mediator influencing cognitive integrity during chronic corticosterone exposure in rat hippocampus.

Pushing forward in embodied cognition: May we mouse the mathematical mind?

Freely available software has popularized “mousetracking” to study cognitive processing; this involves the on-line recording of cursor positions while participants move a computer mouse to indicate their choice. Movement trajectories of the cursor can then be reconstructed off-line to assess the efficiency of responding in time and across space. Here we focus on the process of selecting among alternative numerical responses. Several studies have recently measured the mathematical mind with cursor movements while people decided about number magnitude or parity, computed sums or differences, or simply located numbers on a number line. After some general methodological considerations about mouse tracking we discuss several conceptual concerns that become particularly evident when “mousing” the mathematical mind.