Vascular risk factors for depression and apathy | Part II 90 hypothesize that vascular risk factors and (cerebro)vascular disease would also have been associated with apathy in remitted depression. Nonetheless, patients with depression are a selection of the general population and the pathophysiology of apathy in these patients might differ from that in the general population. Possibly, in depressed populations apathy might be related to either disturbances in functional connectivity patterns between brain areas 44 and/or psychosocial circumstances (e.g., non-challenging environments) 45. In our population, the contribution of structural cerebrovascular damage to the origin of apathy might be too small, especially as we have only indirectly assessed the cerebrovascular disease burden by its risk factors and peripheral diseases. Nonetheless, a recent study on severe late-life depression also found much overlap between depression and apathy, but again, both were not related with vascular hyperintensities identified by brain imaging 46. Therefore, we accordingly wonder whether apathy in remitted depression should not be regarded as a residual symptom of the depression itself. Especially as loss of interest and psychomotor changes are among the residual symptoms most often seen after depression and related to impairment in psychosocial functioning, such as maintaining work and a family life 47 48 8. A diagnostic dilemma, -which warrants future research-, arises here. Should a clinician treat apathy as a residual symptom of successfully treated depression 49, because in general such symptoms are a risk factor for relapse 50 51. Or should a clinician consider apathy as a syndrome unrelated to depression and in need of targeted treatment? Methodological considerations Although in essence a cross sectional design, a strength of our study is that the diagnosis of remitted depression was established prospectively. Another strength is the sample size and wide age range of the study population. Most studies on vascular disease include older populations and in studies of younger populations cardiovascular diseases are often disregarded. Finally, we adjusted for the use of antidepressants, antipsychotics and benzodiazepines which might confound results due to their sedative or dopaminergic modulating properties 52 53 54 and ruled out that apathy might be due to functional limitations by adjusting for handgrip strength as an indicator of fitness 37. In our attempt to identify determinants of apathy, we tried to avoid confounding due to overlap between apathy scales and depression scales 55. Based on a principal factor analysis on the items of the Starkstein Apathy Scale (SAS) as well as the Inventory of Depressive Symptomatology (IDS) we distinguished two dimensions of apathy, i.e., amotivation and loss of initiative. Nonetheless, a factor analysis combining items from different scales, may artificially result in separate dimensions. This issue cannot be discarded as both apathy factors only included items of the SAS and the ‘pure mood’ factor only items of the IDS. Nonetheless, dichotomizing all items, thereby minimizing the impact of different response tendencies between the items of both scales, resulted in the same factor solution. Since specific items of the SAS and IDS did not load on the factors of interest, the present approach might still be a valuable addition to the use of the SAS sum score and an improvement over the use of the IDS sum score. Moreover, a sensitivity analysis using the IDS sum score did not change our results.
RkJQdWJsaXNoZXIy MjY0ODMw