Cognitive impairment in patients with stress-related exhaustion.

Patients who seek medical care for stress-related mental health problems frequently report cognitive impairments as the most pronounced symptom. The purpose of the present study was to compare cognitive function in patients with stress-related exhaustion with that in healthy controls, using a comprehensive battery of cognitive tests. We also explored whether neuropsychological findings were related to severity of illness measured using the Shirom-Melamed burnout questionnaire and hospital anxiety and depression scale. Thirty-three patients (15 males) and 37 healthy controls (11 males), mean age 46 years [standard deviation (SD) 3.9] and 47 years (SD 4.3), respectively, were included in the final analysis. Five cognitive domains were assessed: (1) speed, attention and working memory, (2) learning and episodic memory, (3) executive functions, (4) visuospatial functions and (5) language. The most pronounced difference between patients and controls was seen on executive function, when tested with a multidimensional test, including aspects of speed, control and working memory. The patients also performed poorer on Digit span, measuring attention span and working memory as well as on learning and episodic memory, when measured as delayed recall and the difference between immediate and delayed recall. Delayed recall was the only test that was significantly related to severity of burnout symptoms among the patients. This could reflect poor cognitive sustainability in the patients with the highest burnout scores, as this particular test was the last one performed during the test session. This study clearly shows that cognitive impairment should be considered when evaluating and treating patients who seek medical care for stress-related exhaustion.

Self-reported exhaustion: a possible indicator of reduced work ability and increased risk of sickness absence among human service workers.

OBJECTIVE: The aim of this study was to assess the construct and predictive validity of a new instrument for self-rating of stress-related Exhaustion Disorder (s-ED). METHODS: Public healthcare workers and social insurance officers, 85% females, were included (N = 2,683) in a longitudinal study. The s-ED instrument, based on clinical criteria for Exhaustion Disorder, was used at baseline to classify participants into three categories: non-s-ED, light/moderate s-ED and pronounced s-ED. Other assessments include burnout, anxiety, depression and work ability. Sick leave at follow-up after 2 years was defined as 14 days of ongoing sick leave (SA14) or a period of 60 days of sick leave during the last 12 months (SA60). Associations at baseline were expressed as prevalence ratios, and adjusted relative risks (RR) were calculated using Cox regression. RESULTS: At baseline, 16% reported s-ED. Scores of depression, anxiety and burnout and the rate of poor work ability increased with increasing severity of s-ED. Self-reported exhaustion at baseline increased the risk of reporting sickness absence at follow-up; pronounced s-ED RR 2.7; CI 1.8-4.0 for SA14 and RR 3.4; CI 2.3-5.2 for SA60. CONCLUSIONS: Self-rated ED corresponded well to established scales for mental health, indicating sufficient construct validity. Individuals reporting s-ED at baseline were more likely to report sickness absence at follow-up, confirming its predictive properties. The s-ED instrument may be a useful tool for occupational health services in identifying human service workers at risk of having or developing a potentially disabling stress-related mental illness.

Influence of TNF-alpha and biomechanical stress on endothelial anti- and prothrombotic genes.

Biomechanical stress modulates vascular tone, vascular remodelling and the spatial localisation of atherosclerotic plaques. Inflammatory cytokines, such as TNF-alpha, regulate expression of genes that impair the function of endothelial cells. This study investigates the combinatory effect of different biomechanical stresses and TNF-alpha on the expression of endothelial anti- and prothrombotic genes. Human umbilical vein endothelial cells were exposed to TNF-alpha and different levels of static/pulsatile tensile stress or shear stress. The response in endothelial cells to TNF-alpha was not modulated by tensile stress. However, shear stress was a more potent stimulus. Shear stress counteracted the cytokine-induced expression of VCAM-1, and the cytokine-suppressed expression of thrombomodulin and eNOS. Shear stress and TNF-alpha additively induced PAI-1, whereas shear stress blocked the cytokine effect on t-PA and u-PA. A flow profile characterized by high laminar shear stress seems to render the endothelial cell more resistant to inflammatory stress.

Reflex suppression of gastric motility during laparotomy and gastroduodenal nociceptive stimulation.

The effects on gastric motility of laparotomy or of nociceptive stimuli directed to the antro-duodenal area were studied in anaesthetized cats. A diathermic lesion of the duodenal or gastric antral wall induced pronounced gastric relaxation, which could either fade off within 0.5--1.5 h or persist for several hours. This gastric relaxatory response persisted after administration of antiadrenergic and anticholinergic drugs but was eliminated by vagotomy or cold blockade of the vagi. Vagotomy performed during the relaxed gastric state after diathermy immediately resulted in a more or less complete recovery of gastric tone. Blunt mechanical stimulation of the duodenum also caused a prompt gastric relaxation, which showed the same characteristics as the response to diathermy as regards the effects of nerve-blocking drugs and vagotomy. The laparotomy incision per se caused temporary inhibition of rhythmic gastric contraction, but this effect was largely abolished if atropine or guanethidine had been given. It is concluded that nociceptive stimuli against the gastric or duodenal wall induce, besides a sympathoadrenergic reflex inhibition of gastric motility, a profound long-lasting gastric relaxation via a reflex activation of the vagal nonadrenergic inhibitory fibres. This vagally mediated relaxation of the stomach is likely to contribute to the suppression of gastric motility seen in 'paralytic ileus'.