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Objectives: Stroke is the second most common cause of death and a major cause of disability. Besides the physical consequences, depressive symptoms are frequent in the aftermath after stroke. Every year, approximately 15 million stroke survivors worldwide are at risk of developing post-stroke depression. In this study we describe the natural course of depressive symptoms in stroke patients over a long-period of time post stroke and identify associated determinants., Materials and Methods: From the Second Manifestations of ARTerial disease-Memory, depression and aging (SMART-Medea) study, an observational prospective cohort study, we selected patients with cerebrovascular disease, and used the biannually collected data of the Patient Health Questionnaire-9 for depressive symptoms. A score of ≥10 indicated the presence of depressive symptoms. A multinomial logistic regression analysis was used to identify prognostic determinants for courses of depressive symptoms after stroke., Results: During a mean follow-up time of 7.9 years, 62% of the 172 participants was never depressed, 19% had a single episode and 19% had recurrent depressive symptoms. Physical function was associated with increased risk for single episode and recurrent depressive symptoms (OR=1.06 [1.01-1.11]). OR's for social, mental and (vascular) comorbidities variables were not significant. Participants' physical function was only measured at baseline. Several relevant variables were not present in this dataset, including information about clinical events during follow-up., Conclusion: Nearly 40% of the participants are confronted with depressive symptoms on the long-term. Physical function plays a substantial part for stroke survivors in the development of these symptoms., Competing Interests: Declaration of Competing Interest All authors declare no conflict of interest., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

Objective: To estimate the association between hippocampal and total brain volume and the course of depressive symptoms over eight years of follow-up in patients with a history of vascular disease., Method: Within the SMART-Medea study, 636 participants (62 ± 10 years) had a 1.5-tesla brain MRI obtaining hippocampal and total brain volumes. Depressive symptoms were assessed with the Patient Health Questionnaire-9 biannually during eight-year follow-up. Generalized estimating equation models with robust standard errors were used to assess the associations of hippocampal and total brain volumes with depressive symptoms during follow-up adjusting for age, sex, education, and intracranial volume. An interaction term between volume and time (6-month intervals) was included to examine whether the course of depressive symptoms differed according to hippocampal and total brain volume., Results: The mean PHQ-9 score was 2.8 ± 3.5. Smaller hippocampal volumes were associated with an increasing course of depressive symptom levels, while larger volumes were associated with decreasing levels (P-value interaction = 0.07). Smaller total brain volume was associated with consistently higher levels of depressive symptoms, but not with change in course of depressive symptoms (P-value interaction = 0.45)., Conclusion: Smaller hippocampal volume but not total brain volume is associated with poorer course of depressive symptoms over eight years of follow-up., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Depressive symptoms and cognitive impairment often co-occur, but their interactive relationship is complex and the direction of causation is still a topic of research. We examined the influence of cognitive performance on the course of depressive symptoms during 7 years of follow-up in patients with vascular disease., Method: Within the SMART-MR study, 736 patients (mean age 62 ± 10 years) had neuropsychological assessment on four cognitive domains at baseline [memory (MEM), working memory (WMEM), executive functioning (EXEC), and information processing speed (SPEED)]. Depressive symptoms were assessed with the Patient Health Questionnaire-9 (PHQ-9) at baseline and every 6 months during 7 years of follow-up. Generalized Estimating Equation (GEE) models were used to assess the association between cognitive performance with depressive symptoms at multiple time points during follow-up. Interaction terms between the respective cognitive domains and time was included to examine if the course of depressive symptoms differed according to baseline cognitive performance., Results: The GEE analyses showed no significant interactions between the respective cognitive domains and time indicating no different course of depressive symptoms according to baseline cognitive performance. Lower MEM, EXEC or SPEED, but not WMEM performance, was significantly associated with more depressive symptoms during follow-up per z score decrease: MEM [B = 0.70, 95% confidence interval (CI) 0.35-1.05]; EXEC (B = 0.88, 95% CI 0.41-1.36), and SPEED (B = 0.57, 95% CI 0.21-0.92)., Conclusions: Poorer cognitive performance on the domains MEM, EXEC and SPEED, but not WMEM, was associated with higher levels of depressive symptoms over 7 years of follow-up, but not with a different course of depressive symptoms over time.

Background: The 'vascular depression' hypothesis states that brain changes located in frontal-subcortical pathways increase vulnerability for specific depressive symptom profiles, but studies examining locations of small-vessel and degenerative changes with individual symptoms are scarce. We examined whether location and progression of white-matter lesions (WMLs), lacunar infarcts and atrophy were associated with motivational and mood symptoms in patients with symptomatic atherosclerotic disease., Method: In 578 patients [63 (s.d.=8) years] of the Second Manifestations of ARTerial disease (SMART)-Medea study, volumes of WMLs and atrophy and visually rated infarcts were obtained with 1.5 T magnetic resonance imaging at baseline and after 3.9 (s.d.=0.4) years' follow-up. Depressive symptoms were assessed with Patient Health Questionnaire-9 at follow-up and categorized into motivational and mood symptoms., Results: Regression analyses adjusted for age, gender, education, Mini-Mental State Examination, physical functioning, antidepressant use and vascular risk factors showed that location in mainly deep white-matter tracts and progression of WMLs were associated with symptoms of anhedonia, concentration problems, psychomotor retardation and appetite disturbance. Lacunar infarcts in deep white matter were associated with greater motivational [Incidence rate ratio (IRR) 1.7, 95% confidence interval (CI) 1.2-2.4] and mood (IRR 1.7, 95% CI 1.1-2.6) sumscores, and with symptoms of psychomotor retardation, energy loss and depressed mood; lacunar infarcts in the thalamus were associated with psychomotor retardation only. Cortical atrophy was associated with symptoms of anhedonia and appetite disturbance. Excluding patients with major depression did not materially change the results., Conclusions: Our findings suggest that disruption of frontal-subcortical pathways by small-vessel lesions leads to a symptom profile that is mainly characteristic of motivational problems, also in the absence of major depression.

Aims/hypothesis: Although current literature suggests an association between diabetes and depression, the direction of the association is unclear. We examined the temporal association between diabetes and depression by studying antidepressant and benzodiazepine use around the initiation of diabetes treatment., Methods: From a pharmacy registry database we selected 49,593 diabetic patients and a random sample of non-diabetic individuals (n = 154,441), all >40 years old. Antidepressant and benzodiazepine use was calculated for the 7 years before and 7 years after the index date. The index date in diabetes patients was defined as the date of initiation of diabetes medication. A random index date was assigned to non-diabetic individuals. Time-specific incidence rate ratios of antidepressant and benzodiazepine use were calculated for intervals of 1 year, 3 months and 1 month., Results: Antidepressant and benzodiazepine use was increased 2 months before and 3 months after the initiation of diabetes treatment compared with non-diabetic individuals. The strongest increase in incidence of antidepressant and benzodiazepine use was seen in the month after initiation of diabetes treatment with incidence rate ratios of 2.4 (95% CI 2.0-3.0) and 3.4 (95% CI 3.0-3.8) respectively, after adjustment for age, sex and Chronic Disease Score., Conclusions/interpretation: The increased incidence of antidepressant and benzodiazepine use may be a consequence of the burden of disease, of starting with diabetes medication or of being diagnosed with diabetes. Our findings could also reflect earlier detection by their physician.

Context: Depression is associated with an increased mortality risk. It is not known to what extent depression characteristics such as severity and length of exposure to depression contribute to the association with excess mortality., Objectives: To investigate the association between depression severity and duration with mortality in community-living elderly., Design: Two-wave prospective cohort study with 10-year follow-up of vital status. Assessment of depression at baseline and at three year follow-up (GMS-AGECAT). Cox proportional hazards analyses of mortality with depression according to severity and length of exposure, adjusted for demographic variables, physical illnesses, cognitive decline and functional disabilities., Setting and Participants: Randomly selected cohort of 3 746 non-demented older community-living persons in the city of Amsterdam., Main Outcome Measures: Excess mortality of both the baseline cohort, and of non-demented subjects participating in both assessments (n = 1989)., Results: Both moderate (MHR 1.29, 95% CI 1.03-1.61) and severe depression (MHR 1.34, 95% CI 1.07-1.68) predicted 10-year mortality after multivariate adjustment. Chronic depression was associated with a 41% higher mortality risk in 6-year follow-up compared to subjects without depression., Conclusions: Severity and chronicity of depression are associated with a higher mortality risk. In combination with other findings this is suggestive of a causal relationship and may have implications for both preventive and treatment strategies of late-life depression., ((c) 2008 John Wiley & Sons, Ltd.)

Objective: Low B-vitamin status and high levels of serum homocysteine are found in depressed inpatients, but results of population-based studies of this association are inconclusive. We investigated whether a low dietary intake of B(6-9-12) vitamins and high levels of serum homocysteine are associated with depressive symptoms in elderly men., Methods: The study sample included a total of 332 men aged 70-90 years who were free from cardiovascular diseases and diabetes at baseline in 1990. Depressive symptoms were measured with the Zung Self-rating Depression Scale at baseline in 1990 and dietary factors with the crosscheck dietary history method in 1985 and 1990. Serum levels of homocysteine were obtained in 1985. Multiple linear and logistic regression analyses were performed., Results: Dietary intake of folate (-1.19, 95% CI -2.03; -0.36) and vitamin B(6) (-2.09, 95% CI -2.92; -1.26) per standard deviation increase was associated with lower levels of serum homocysteine, while vitamin B(12) was not associated with serum homocysteine. Intake of folate, vitamin B(6), vitamin B(12) and levels of serum homocysteine were not related to depressive symptoms., Conclusions: Our results do not support the hypothesis that a low dietary intake of B(6-9-12) vitamins and high levels of serum homocysteine are related to depression in healthy elderly men.

Background: The association between depression and increased mortality risk in older persons may depend on the severity of the depressive disorder and gender., Aims: To investigate the association between major and mild depressive syndromes and excess mortality in community-living elderly men and women., Method: Depression (Geriatric Mental State AGECAT) was assessed in 4051 older persons, with a 6-year follow-up of community death registers. The mortality risk of neurotic and psychotic depression was calculated after adjustment for demographic variables, physical illness, cognitive decline and functional disabilities., Results: A total of 75% of men and 41% of women with psychotic depression had diet at follow-up. Psychotic depression was associated with significant excess mortality in both men and women. Neurotic depression was associated with a 1.67-fold higher mortality risk in men only., Conclusions: In the elderly, major depressive syndromes increase the risk of death in both men and women, but mild depression increases the risk of death only in men.

Background and Objective: In an earlier study we observed that a depressive syndrome was highly predictive of developing Alzheimer's disease (AD) in older persons with normal baseline cognition and higher levels of education. We interpreted these findings as the depression being an early noncognitive manifestation of AD in persons with more cognitive reserve. The present study examines whether specific symptoms of depression can be identified that predict AD among older subjects with higher levels of education., Design and Participants: In the community-based Amsterdam Study of the Elderly (AMSTEL), a sample of 3,147 nondemented persons with normal cognition, 65 to 84 years old, was selected and divided into subjects with >8 years and < or =8 years of education. At baseline, the presence or absence of 12 specific symptoms of depression was assessed. At follow-up, patients with incident AD were diagnosed according to DSM-IV criteria in a two-step diagnostic procedure., Results: After an average follow-up of 3.2 years, 1,911 persons were reevaluated, of whom 22 with > 8 years and 31 with < or =8 years of education had developed AD. Multivariate logistic regression analyses showed that among persons with >8 years of education depressed mood and subjective bradyphrenia were strongly associated with incident AD. No association between depressive symptoms and AD was observed among subjects with < or =8 years of education., Conclusions: Both depressed mood and subjective bradyphrenia seem to indicate subclinical AD in older people with higher levels of education. Clinicians should be alert that in these persons, AD may become apparent within a relatively short period of time.

Background: Depression in the elderly was found to be associated with a variety of risk-factors in cross sectional designs. Based on the vulnerability-stress model, etiologic pathways for depression have been suggested, with vulnerability modifying the effect of stress factors. The current prospective study tests an etiologic model for depression incidence, by assessing modifying effects of three types of vulnerability: genetic/familial vulnerability, organic vulnerability, and environmental vulnerability., Methods: 1940 non-depressed community-living elderly were interviewed at baseline, and at follow-up three years later. Bivariate and multivariate relationships between risk factors and incident depression (GMS-AGECAT) were studied., Results: Higher age, personal history of depression, death of spouse, health related factors and comorbid organic or anxiety syndrome showed significant bivariate associations with depression incidence. In multivariate analysis, the effect of stress factors on incident depression was not modified by a genetic/familial vulnerability, nor by an organic vulnerability. Effect modification by environmental factors was however evident; having a marital partner, and if unmarried having social support, significantly reduced the impact of functional disabilities on the incidence of depression., Limitations: The study consisted of two measurements with a three years interval, depressive episodes with a short duration may be under-represented., Conclusions: In the elderly, the effect of stress on incident depression is modified by environmental vulnerability. No evidence was found of effect modification by either genetic/familial or organic vulnerability. The results have implications for both recognition and treatment of late-life depression.

BackgroundTo examine whether lifetime DSM-IV diagnosis of major depressive disorder (MDD), including age at onset and number of episodes, is associated with brain atrophy in older persons without dementia.MethodWithin the population-based Age, Gene/Environment Susceptibility (AGES)–Reykjavik Study, 4354 persons (mean age 76 ± 5 years, 58% women) without dementia had a 1.5-T brain magnetic resonance imaging (MRI) scan. Automated brain segmentation total and regional brain volumes were calculated. History of MDD, including age at onset and number of episodes, and MDD in the past 2 weeks was diagnosed according to DSM-IV criteria using the Mini-International Neuropsychiatric Interview (MINI).ResultsOf the total sample, 4.5% reported a lifetime history of MDD; 1.5% had a current diagnosis of MDD (including 75% with a prior history of depression) and 3.0% had a past but no current diagnosis (remission). After adjusting for multiple covariates, compared to participants never depressed, those with current MDD (irrespective of past) had more global brain atrophy [B = –1.25%, 95% confidence interval (CI) −2.05 to −0.44], including more gray- and white-matter atrophy in most lobes, and also more atrophy of the hippocampus and thalamus. Participants with current, first-onset MDD also had more brain atrophy (B = –1.62%, 95% CI −3.30 to 0.05) whereas those remitted did not (B = 0.06%, 95% CI −0.54 to 0.66).ConclusionsIn older persons without dementia, current MDD, irrespective of prior history, but not remitted MDD was associated with widespread gray- and white-matter brain atrophy. Prospective studies should examine whether MDD is a consequence of, or contributes to, brain volume loss and development of dementia. [ABSTRACT FROM PUBLISHER]

BackgroundThe different incidence rates of, and risk factors for, depression in different countries argue for the need to have a specific risk algorithm for each country or a supranational risk algorithm. We aimed to develop and validate a predictD-Spain risk algorithm (PSRA) for the onset of major depression and to compare the performance of the PSRA with the predictD-Europe risk algorithm (PERA) in Spanish primary care.MethodA prospective cohort study with evaluations at baseline, 6 and 12 months. We measured 39 known risk factors and used multi-level logistic regression and inverse probability weighting to build the PSRA. In Spain (4574), Chile (2133) and another five European countries (5184), 11 891 non-depressed adult primary care attendees formed our at-risk population. The main outcome was DSM-IV major depression (CIDI).ResultsSix variables were patient characteristics or past events (sex, age, sex×age interaction, education, physical child abuse, and lifetime depression) and six were current status [Short Form 12 (SF-12) physical score, SF-12 mental score, dissatisfaction with unpaid work, number of serious problems in very close persons, dissatisfaction with living together at home, and taking medication for stress, anxiety or depression]. The C-index of the PSRA was 0.82 [95% confidence interval (CI) 0.79–0.84]. The Integrated Discrimination Improvement (IDI) was 0.0558 [standard error (s.e.)=0.0071, Zexp=7.88, p<0.0001] mainly due to the increase in sensitivity. Both the IDI and calibration plots showed that the PSRA functioned better than the PERA in Spain.ConclusionsThe PSRA included new variables and afforded an improved performance over the PERA for predicting the onset of major depression in Spain. However, the PERA is still the best option in other European countries. [ABSTRACT FROM PUBLISHER]