Prolonged stress (≥ six months) may cause a condition which has been named exhaustion disorder (ED) with ICD-10 code F43.8. ED is characterised by exhaustion, cognitive problems, poor sleep and reduced tolerance to further stress. ED can cause long term disability and depressive symptoms may develop. The aim was to construct and evaluate a self-rating scale, the Karolinska Exhaustion Disorder Scale (KEDS), for the assessment of ED symptoms. A second aim was to examine the relationship between self-rated symptoms of ED, depression, and anxiety using KEDS and the Hospital Anxiety and Depression Scale (HAD). Items were selected based on their correspondence to criteria for ED as formulated by the Swedish National Board of Health and Welfare (NBHW), with seven response alternatives in a Likert-format. Self-ratings performed by 317 clinically assessed participants were used to analyse the scale’s psychometric properties. KEDS consists of nine items with a scale range of 0–54. Receiver operating characteristics analysis demonstrated that a cut-off score of 19 was accompanied by high sensitivity and specificity (each above 95%) in the discrimination between healthy subjects and patients with ED. Reliability was satisfactory and confirmatory factor analysis revealed that ED, depression and anxiety are best regarded as different phenomena. KEDS may be a useful tool in the assessment of symptoms of Exhaustion Disorder in clinical as well as research settings. There is evidence that the symptom clusters of ED, anxiety and depression, respectively, reflect three different underlying dimensions.
Background
We recently reported marked hyporeactivity of the hypothalamo-pituitary-adrenal (HPA) axis in depressed females on job-stress related long-term sick-leave (LTSL). This unexpected finding prompted the question whether HPA-axis hypofunction in this group results from stress exposure, or reflects pre-existing vulnerability. Here, as a first step toward addressing this question, we assessed temporal stability of HPA-axis reactivity in these subjects.
Methods
We used the combined dexamethasone/corticotropin-releasing hormone (DEX-CRH) test to retest HPA-axis reactivity in 29 patients and 27 controls after 12 months follow-up. Clinical status and cognitive performance was also retested.
Results
Despite marked clinical improvement, and normalization of initially observed impairments in attention and working memory, marked HPA-axis hyporeactivity persisted in patients. A high test – retest correlation was found both at the level of ACTH (R=0.85, p<0.001) and cortisol (R=0.76, p<0.001) responses.
Conclusions
Hyporeactivity of the HPA was stable over 12 months in LTSL subjects, independently of clinical improvement and normalized cognitive function. The stability of this response over time suggests that decreased DEX-CRH responses in this group may be a trait rather than a state marker. This finding is compatible with a hypothesis that HPA-axis hyporeactivity may reflect a pre-existing vulnerability in these subjects.
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