Part II | Vascular risk factors for depression and apathy 83 5 Introduction Despite successful treatment of a depressive episode, many patients still suffer from residual symptoms placing them at an increased risk of relapse 1 2. A frequently observed residual symptom by depressed patients who achieved remission is apathy 3 4. Apathy is generally considered a lack of goal-directed behavior, cognition and/or emotion 5. Over the past decades, apathy has been identified as a common and clinically relevant behavioral syndrome in many neuropsychiatric disorders 6. While symptoms and signs of apathy are highly common among depressed patients 7, studies on apathy in depression are scarce. In the Netherlands Study of Depression in Older Persons (NESDO) 199/266 (75%) of depressed patients had a clinically relevant level of apathy at baseline. Of these apathic depressed patients, at two-year follow-up, 80% were still classified as apathic, while only 41%was still depressed. Moreover, among the non-apathic depressed patients at baseline, 36% became apathic at follow-up 7. These figures are alarming, as apathy predicts a lower return to work after remitted depression 8. These findings corroborate findings that a low interest in work and activities are among the most frequently encountered residual symptoms in remitted depression 9 10. Empirical studies on apathy in depression, however, are easily confounded due to overlap in symptoms and signs. Considering the symptom-domain level of apathy, apathy is described as a loss of initiative in behavioral terms, and as loss of interest or anhedonia in cognitive/emotional terms 11 12. The observed ‘inability to want’ has also been defined as amotivation 11. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; 2013) loss of interest and anhedonia is a core criterion of a depressive disorder next to or in addition to depressed mood. Furthermore, the observable reduction in physical activity among depressed patients may easily be confused with or be a result of a loss of initiative. To avoid bias due to overlapping criteria, studies on apathy in remitted depression should adjust for the residual level (severity) of pure ‘mood’ symptoms, without correcting for loss of interest, anhedonia and a reduction of physical activity (see methods). From a neurobiological perspective, apathy is related to dysfunctioning of prefrontalbasal ganglia circuitries 13. Neuroimaging studies have shown that the frontal regions with their projections to prefrontal regions, and the basal ganglia, the parietal regions, and the anterior cingulate play a role in planning, motivation, and auto-activation 14. Structural damage of these regions and projections, as seen in Alzheimer’s disease 15 or functional impairment of these, as seen in Parkinson’s disease (dopaminergic and serotonergic depletion) 16 are associated with apathy. Apathy in late-life depression has also been related to structural damage 17 18; although the depressive symptoms that overlap with apathy (anhedonia, loss of interest and an observable reduction in physical activity) in theory would be linked with functional impairment of the frontolimbic networks. Apathy during a depression and persisting after seemingly successful depression treatment has been linked to structural damage to the frontolimbic network 19 ; and with persisting abnormalities in the salience network 20.
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