Emotional Intelligence and resilience in mental health professionals caring for patients with serious mental illness

Emotional Intelligence (EI) and resilience may be considered as prerequisites for mental health professionals caring for patients with serious mental illness (SMI), since they are often exposed to severe emotional stress during daily work. Accordingly, this cross-sectional study assessed both EI and resilience and their interrelationship in 61 individuals belonging to an assertive outreach team for patients suffering from SMI compared 61 control subjects without healthcare-related working conditions. EI was assessed by means of the German version of the Mayer-Salovey-Caruso-Emotional-Intelligence Test (MSCEIT), resilience was assessed using the German version of the Resilience Scale. Both groups showed an average level of EI in all categories of the MSCEIT and indicated high levels of resilience. They did not differ significantly from each other, neither in terms of EI nor resilience. Correlation analysis revealed a positive association between EI and resilience, albeit small in magnitude. Our results suggest that mental health professionals are not more resilient and therefore not more ‘protected’ from stressors than the general population. Though this finding warrants cautious interpretation, the positive correlation between EI and resilience suggests that EI may be a potential target for education and training in order to strengthen resilience even in healthy individuals and vice versa.     

LAC-Depressionsstudie

The study on long-term therapy of chronic depression (LAC depression study) is one of the first prospective studies to compare psychoanalytic with cognitive behavioral long-term treatment and also investigates the impact of patient assignment by randomization and preference. This comprehensive multicenter study combines a naturalistic and a randomized controlled approach. The long-term follow-up is based on a broad spectrum of quantitative and qualitative research methods and is expected to contribute to the further development of psychotherapeutic treatment methods in this hard to treat patient group as well as to research on the effectiveness of long-term treatment. The background, design and current state of the assessment are presented. A total of 402 patients with chronic depression were included in the trial and the 1 and 2?year follow-up results are currently being analyzed.     

The consequences of job crafting: a three-wave study

This longitudinal study examined the consequences of job crafting on two important employee outcomes: psychological capital (PsyCap) as a work-related personal resource and work engagement as an indicator of employee well-being. The study also tested the reverse causation effects of PsyCap and work engagement on job crafting. It used a three-wave, three-month panel design to survey 940 employees from three European countries working in a broad range of economic sectors and occupations. The results of the cross-lagged longitudinal structural equation modelling demonstrated that job crafting predicted PsyCap and work engagement over time. No reverse causation effects were found. Overall, this study shows that when individuals proactively build a resourceful and challenging work environment for themselves, it can lead to diverse positive outcomes that are crucial to employee health and well-being. Employees should therefore be encouraged and be given the opportunity to craft their own jobs.     

Incremental Validity of Perceived Control Dimensions in the Differential Prediction of Interpretive Biases for Threat

This study evaluated whether a diminished perception of control over environmental and interoceptive events differentially predicted interpretive biases for threat for ambiguous scenarios. The sample had 95 participants without a history of psychopathology. Results indicated that the internal dimension of the Anxiety Control Questionnaire (ACQ; R. M. Rapee, M. G. Craske, T. A. Brown, & D. H. Barlow, 1996) was predictive of interpretive biases for internal scenarios above and beyond demographic variables, subclinical panic attack history, and state anxiety; the external control subscale of the ACQ also was predictive of internal rank-ordered responses. The ACQ external dimension was predictive of interpretive responses for external scenarios beyond the effects accounted for by the other predictor variables, including perceived control for internal events. These findings provide initial correlational evidence consistent with cognitive–behavioral accounts of panic disorder that posit a perceived lack of control over aversive events may exacerbate an interpretive bias for threat.     

The impact of visual flow stimulation on anxiety, dizziness, and body sway in individuals with and without fear of heights

Individuals with acrophobia experience anxiety and dizziness when exposed to heights. It may be that their balance system is disturbed and that they therefore have to rely more strongly on visual information.We tested this hypothesis by exposing 20 individuals with high fear of heights and 20 healthy control participants to nine different visual flow stimuli through a head mounted display, thereby inducing a conflict between visual input and somatosensory information. Anxiety and dizziness were assessed repeatedly by means of self-reports, while resultant body sway was measured continuously with a force plate individuals stood on.Individuals with fear of heights felt more anxious and dizzier, and also showed stronger body sway than healthy control participants.Merely receiving visual balance information contradictory to somatosensory balance information is sufficient to induce anxiety, dizziness, and body sway in individuals with fear of heights. An underlying balance dysfunction may contribute to the development of height phobia.     

Behavioral deficits and subregion-specific suppression of LTP in mice expressing a population of mutant NMDA receptors throughout the hippocampus

The NMDA receptor (NMDAR) subunit GluN1 is an obligatory component of NMDARs without a known functional homolog and is expressed in almost every neuronal cell type. The NMDAR system is a coincidence detector with critical roles in spatial learning and synaptic plasticity. Its coincidence detection property is crucial for the induction of hippocampal long-term potentiation (LTP). We have generated a mutant mouse model expressing a hypomorph of the Grin1^N598R allele, which leads to a minority (about 10%) of coincidence detection-impaired NMDARs. Surprisingly, these animals revealed specific functional changes in the dentate gyrus (DG) of the hippocampal formation. Early LTP was expressed normally in area CA1 in vivo, but was completely suppressed at perforant path-granule cell synapses in the DG. In addition, there was a pronounced reduction in the amplitude of the evoked population spike in the DG. These specific changes were accompanied by behavioral impairments in spatial recognition, spatial learning, reversal learning, and retention. Our data show that minor changes in GluN1-dependent NMDAR physiology can cause dramatic consequences in synaptic signaling in a subregion-specific fashion despite the nonredundant nature of the GluN1 gene and its global expression.According to Hebb''s postulate, neurons require a molecular mechanism to detect synchronous activity in order to change the strength of synaptic connectivity (Hebb 1949). NMDA receptors (NMDARs) are molecular coincidence detectors, and selective NMDAR antagonists block the induction of long-term potentiation (LTP) in both the dentate gyrus (DG) and CA1 regions of the hippocampus (Bliss and Collingridge 1993; Martin et al. 2000). NMDARs have been long known for their role in spatial learning, but more recently have been implicated in other forms of cognitive function and dysfunction (Gruart et al. 2006; Whitlock et al. 2006; Castner and Williams 2007; Kristiansen et al. 2007; Wilson and Linster 2008).Neuronal NMDARs are hetero-tetrameric ligand-gated ion channels typically comprised of two types of subunits. Two copies of the mandatory GluN1 subunit (or NR1 subunit [Collingridge et al. 2009] encoded by Grin1) are associated with two copies from the GluN2 family, GluN2A–D (or NR2A–D). The GluN1 subunit is expressed ubiquitously both spatially and temporally throughout the developing and adult brain. Global knockout mice models of the GluN1 subunit are postnatally lethal within hours after birth (Forrest et al. 1994; Li et al. 1994), and cell-specific GluN1 mice knockouts (Tsien et al. 1996; Nakazawa et al. 2002; McHugh et al. 2007; Niewoehner et al. 2007) have provided insights on how specific synapses and regional neuronal networks are dependent on NMDAR function.The early postnatal lethality of the global GluN1 knockout is in contrast to the null mutants of the four AMPA receptor genes and other major synaptic proteins, such as αCaMKII (Silva et al. 1992a,b; Jia et al. 1996; Zamanillo et al. 1999; Meng et al. 2003). This can be at least partially explained by the absence of any close GluN1 homologs, which could functionally compensate for the absence of the GluN1 subunit. Recombinant expression studies defined the GluN1 subunit as a mandatory component of NMDARs. This constellation provides a specific opportunity to test whether different local neuronal subnetworks are affected differentially by mutant Grin1 alleles associated with subtle alterations of the functional properties of NMDARs.GluN1 subunits with the N598R point mutation (GluN1^R) yield functional NMDARs that are Mg²⁺ insensitive and Ca²⁺ impermeable (Burnashev et al. 1992; Mori et al. 1992). The Grin1^N598R allele that codes for GluN1^R subunits is a gain-of-function mutation that is dominant lethal, even in heterozygous and hemizygous lines (Single et al. 2000; Rudhard et al. 2003). NMDARs with GluN1^R subunits do not act as coincidence detectors and, interestingly, mice expressing exclusively the GluN1^R allele lack whisker-related pattern formation in the neonate brainstem (Rudhard et al. 2003).To investigate the functional importance of GluN1 subunits with the N598R point mutation, we took advantage of the generation of a variant mutant line of mice (GluN1^Rneo/+) expressing a minority (around 10%) of these mutant NMDARs. Even though the majority of the NMDARs are normal, all neurons expressing NMDARs will contain a subset of receptors carrying this mutation.Therefore, this mouse model is an ideal candidate to study the impact of subtle alterations of NMDAR function on different neuronal networks, such as those comprising the hippocampal formation.Studies examining region-specific targeted disruption of GluN1 expression in subregions of the hippocampus have revealed subtle yet important contributions of this NMDAR subunit in synaptic plasticity and spatial learning and memory. CA1-restricted knockout of GluN1 expression in the hippocampus caused impaired spatial learning and memory as well as reduced CA1-LTP (Tsien et al. 1996). In the case of the disruption of GluN1 expression in the DG region of the hippocampus, more subtle behavioral impairments were apparent, including the inability to discriminate between two similar contexts (pattern separation) and deficits in spatial working memory despite normal LTP in the CA1 region (McHugh et al. 2007; Niewoehner et al. 2007).Our GluN1^Rneo/+ mice differ from the region-specific GluN1 mutant mice in that they express the mutant hypomorph at the same level in different subregions of the hippocampus. Interestingly, we found that this allele leads to substantial differences in short- and long-term plasticity between area CA1 and the DG of the hippocampus. The specific impairment in the DG was accompanied by impaired spatial recognition, spatial learning, reversal learning, and retention. Our data establish the possibility of a circuit-specific phenotype caused by a mutant variant of a globally expressed major nonredundant synaptic protein.     

Recognizing group cognition

In this paper, we approach the idea of group cognition from the perspective of the “extended mind” thesis, as a special case of the more general claim that systems larger than the individual human, but containing that human, are capable of cognition (Clark, 2008, Clark and Chalmers, 1998). Instead of deliberating about “the mark of the cognitive” (Adams & Aizawa, 2008), our discussion of group cognition is tied to particular cognitive capacities. We review recent studies of group problem solving and group memory which reveal that specific cognitive capacities that are commonly ascribed to individuals are also aptly ascribed at the level of groups. These case studies show how dense interactions among people within a group lead to both similarity-inducing and differentiating dynamics that affect the group’s ability to solve problems. This supports our claim that groups have organization-dependent cognitive capacities that go beyond the simple aggregation of the cognitive capacities of individuals. Group cognition is thus an emergent phenomenon in the sense of Wimsatt (1986). We further argue that anybody who rejects our strategy for showing that cognitive properties can be instantiated at multiple levels in the organizational hierarchy on a priori grounds is a “demergentist,” and thus incurs the burden of proof for explaining why cognitive properties are “stuck” at a certain level of organizational structure. Finally, we show that our analysis of group cognition escapes the “coupling-constitution” charge that has been leveled against the extended mind thesis (Adams & Aizawa, 2008).