Search

Stress is a ubiquitous challenge in modern societies. Symptoms range from mood swings and cognitive impairment to autonomic symptoms. This study explores the link between work-related stress and the neurobiological element of brain processing, testing the hypothesis that patients with occupational stress have altered cerebral glucose consumption compared to healthy controls. The participants' present conditions were evaluated using an adapted WHO SCAN interview. Neural activity at rest was assessed by positron emission tomography (PET) with the glucose analogue [18F]fluorodeoxyglucose. Participants were genotyped for the Val158Met polymorphism of the COMT gene, believed to influence stress resilience. This study included 11 women with work-related stress and 11 demographically comparable healthy controls aged 28–62 years, with an average of 46.2 years. The PET scans indicated clusters of decreased glucose consumption primarily located in the white matter of frontal lobe sub-gyral areas in stress patients. COMT Val158Met polymorphism detection indicated no immediate relation of the homozygous alleles and stress resilience; however, healthy controls mainly had the heterozygous allele. In conclusion, the results support that work-related stress does affect the brain in the form of altered glucose metabolism, suggesting neurobiological effects could be related to white matter abnormalities rather than gray matter deterioration. Genotyping indicates a more complex picture than just that of the one type being more resilient to stress. Further studies recruiting a larger number of participants are needed to confirm our preliminary findings. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to assess whether frequency of occupational violence (OV) affects posttraumatic stress disorder (PTSD) symptoms through nontraumatic strains in the occupational context. Methods: Twelve-month prospective survey data on 1763 Social educators were used. Path-analysis measured direct and indirect pathways of frequency of OV on PTSD through change in time pressure, change in burnout, change in sense of safety at work, and change in coping with regret in patient work. Results: Forty-two pet. of the variance in PTSD symptoms was predicted; F (20, 1541) = 36.8, P<0.001, R² = 042. Frequency of OV indirectly affected level of PTSD through all the mediators; estimated indirect effects = 0.14, 95% confidence interval 0.07 to 0.22. Conclusion: PTSD resulting from OV is not only a result of the violent acts themselves but is also caused by nontraumatic strains. It is essential to include the broader context of work environment factors in prevention of work-related PTSD. [ABSTRACT FROM AUTHOR]

High workload seems to increase the risk of patient-initiated workplace violence (patient-initiated violence). However, the temporal association between workload and violence remains uncertain. Understanding the interplay of factors in the psychosocial working environment and patient-initiated violence is important to future preventive initiatives. To assess whether a high workload increases the risk of patient-initiated violence, and whether intraorganizational relationships based on trust, reciprocity, justice and collaboration, known as workplace social capital, moderate this risk. Baseline survey data on 1823 social educators was collected followed by 12 monthly surveys on patient-initiated violence exposure. Poisson regressions, in mixed models, were conducted to assess the risk of violence at four levels of workload. Further, moderation analyses were conducted to assess the moderating effects of three sub-types of workplace social capital. High and very high workload increased the risk of patient-initiated violence: RR = 1.5 [1.4–1.6], p <.001 and RR = 1.4 [1.3–1.4], p <.001. All three levels of workplace social capital had a moderating effect on the workload-violence association: Workload*Workplace social capital (co-worker) : F (3, 16,712) = 3.4, p =.017, Workload*Workplace social capital (local management) : F (3, 16,748) = 11.9, p <.001, Workload*Workplace social capital (general management) : F (3, 16,556) = 5.5, p <.001. Only high Workplace social capital (co-workers) reduced the risk of violence at all levels of workload. Workplace social capital (general management) reduced the risk of violence at high, medium and low workload, and Workplace social capital (local management) reduced the risk of violence at medium and low workload. High workload clearly increases the risk of patient-initiated violence. A high workplace social capital appears to be a viable protective factor and should be investigated further in studies of patient-initiated violence prevention. [ABSTRACT FROM AUTHOR]