Hypertension and white matter lesions are independently associated with apathetic behavior in healthy elderly subjects: The Sefuri brain MRI study
ABSTRACT Apathy is defined as a syndrome of primary loss of motivation not attributable to emotional distress, intellectual impairment or consciousness disturbance. The aim of our study was to investigate the effects of vascular risk factors and silent ischemic brain lesions on apathetic behavior of community-dwelling elderly subjects. Brain MRI and other medical examinations were performed on 222 non-demented community-dwelling elderly subjects (96 men and 126 women, average age 70.1 years). The apathy group was defined as the most apathetic quintile determined by Starkstein's apathy scale. Silent infarction, deep white matter lesions (DWMLs) and periventricular hyperintensities were detected in 12.2, 39.2 and 22.5%, respectively. Linear regression analysis (Pearson) revealed that the scores on the apathy scale correlated slightly but significantly with logarithmically transformed scores of the Modified Stroop Test (r=0.135, P=0.045), but not with the Mini-Mental State Examination. The apathy group tended to have more high blood pressure (141.6/82.6 vs. 136.1/79.6 mm Hg), less prevalent hyperlipidemia (18 vs. 35%) and lower serum albumin. Multivariate analysis (the forward stepwise method of logistic analysis) revealed an independent correlation between the apathy and grade of DWMLs (odds ratio 1.826, 95% confidence interval (CI) 1.129-2.953 per grade) or diastolic blood pressure (DBP) (odds ratio 1.055, 95% CI 1.014-1.098 per mm Hg) after adjusting for possible confounders. The mean apathy scale score in the DBP>or=90 mm Hg group was significantly lower (more apathetic) than that in the DBP<80 group (P=0.011, analysis of covariance). This study showed that hypertension and DWMLs are independently associated with apathy in healthy elderly subjects.
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- "The association of symptoms of apathy and depression with incident cardiovascular disease and stroke was analyzed using logistic regression analysis with incident non-fatal and fatal cardiovascular disease and stroke as dependent variables. Because silent ischemic brain lesions might contribute to apathy symptoms (Lavretsky et al., 2008; Yao et al., 2009) and subjects affected by this may have an increased risk of clinically overt stroke (Bernick et al., 2001), cardiovascular disease and stroke were analyzed as separate dependent variables. If participants suffered from incident stroke and cardiovascular disease, both events were analyzed separately. "
ABSTRACT: Although depression is considered to be associated with cardiovascular disease (CVD), specifically symptoms of apathy have been strongly associated with a history of CVD in recent studies. In this study, we prospectively assess whether symptoms of apathy and depression are independent risk factors for incident CVD and stroke. We carried out a prospective cohort study of 1810 community-dwelling older individuals (70-78 years) without a history of CVD or stroke. Symptoms of apathy and depression were assessed with the 15-item Geriatric Depression Scale. Incident CVD and stroke were assessed after 2 years follow-up. The associations of symptoms of apathy and depression with incident CVD and stroke were analyzed separately using logistic regression analysis. Symptoms of apathy and depression were present in 281 (15.5%) and 266 (14.7%) participants, respectively. Incident CVD occurred in 62 (3.5%) participants and stroke in 55 (3.1%) participants. Apathy was associated with incident CVD after adjustment for demographics and cardiovascular risk factors (odds ratio (OR) = 2.60, 95% CI = 1.46-4.65). Exclusion of subjects with depressive symptoms yielded a similar OR (2.94, 95% CI = 1.45-5.96, n = 1544). No association was found between depressive symptoms and incident CVD. Neither apathy symptoms nor depressive symptoms were associated with incident stroke. Apathy, but not depression, is a strong, independent risk factor for incident CVD. It may be a marker of underlying vascular disease. By its nature, apathy may cause non-adherence to a healthy lifestyle, diminished activities, and possibly even withdrawal from clinical care aimed at improving vascular risk profiles. Copyright © 2013 John Wiley & Sons, Ltd.International Journal of Geriatric Psychiatry 05/2014; 29(5). DOI:10.1002/gps.4026 · 3.09 Impact Factor
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- "Consistent with our finding of low FC among medial frontal structures and the ventral striatum are findings suggesting that lesions in the basal ganglia and in frontal subcortical regions have been associated with apathy (Levy and Dubois, 2006; van Reekum et al., 2005). Healthy elders with apathy have more subcortical white matter hyperintensities (WMH) than those without apathy (Yao et al., 2009). Apathy was associated with history of stroke/ TIA as well as cardiovascular risk factors in a large probability sample of community residing elders (Ligthart et al., 2012). "
ABSTRACT: BACKGROUND: Apathy is common in late-life depression and is associated with disability and poor antidepressant response. This study examined whether resting functional connectivity (FC) of the nucleus accumbens (NAcc) and the dorsal anterior cingulate (dACC) with other structures can distinguish apathetic depressed older patients from non-apathetic depressed patients and normal subjects. METHODS: Twenty-six non-demented, non-MCI older adults were studied. Of these, 16 had major depression (7 also had apathy) and 10 had no psychopathology. Resting state fMRI was performed prior to treatment in subjects who were psychotropic-free for at least two weeks. FC was determined by placing seeds in the NAcc and the dACC bilaterally. RESULTS: Apathetic depressed patients had lower FC of the NAcc with the amygdala, caudate, putamen, globus pallidus, and thalamus and increased FC with the dorsomedial prefrontal cortex, the superior frontal cortex, and the insula than non-apathetic patients. Further, apathetic patients had lower FC of the dACC with dorsolateral and ventrolateral prefrontal cortices and higher FC with the insula and the orbitofrontal cortex than non-apathetic patients. LIMITATIONS: Small number of subjects, lack of random sampling, use of a 1.5T MRI scanner. CONCLUSIONS: This preliminary study suggests that FC between the NAcc and the dACC and structures related to reward and related behavioral responses constitute the functional topography of abnormalities characterizing apathy of late life depression. However, replication is needed.Journal of Affective Disorders 12/2012; 149(1-3). DOI:10.1016/j.jad.2012.11.023 · 3.71 Impact Factor
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- "In dementia, apathy as mental slowness was more frequently associated with vascular white-matter changes . In a community-dwelling elderly subject sample, an association was found between apathy and hypertension and white matter lesions . This relation had been otherwise considered as a depression-executive dysfunction syndrome of late life . "
ABSTRACT: Though the core symptoms of Parkinson's disease (PD) are motor-related, a majority of patients also have neuropsychiatric symptoms concerning mood, behavior and cognition. Apathy and depression are considered among the most frequent ones, and have a negative impact on global functioning and quality of life. Recent neuroimaging studies have provided specific findings related with these symptoms. Depression in PD has been specifically associated with morphological and functional changes in prefrontal cortex, cingulate and thalamus, as with 5-HT transmission reduction in posterior cingulated and amygdala-hippocampus complex. Apathy has received less attention, but has been related with gray matter volume reductions or functional deficits in many regions, as anterior and posterior cingulate and dorsolateral or inferior frontal gyrus. Some of these deficits may be also related with a more pronounced reduction in striatal dopamine transmission. As neuroimaging studies give more arguments to the mechanisms of these symptoms, they also stimulate research for a better individualization of specific affective dimensions in Parkinson's disease.Journal of the neurological sciences 08/2011; 310(1-2):58-60. DOI:10.1016/j.jns.2011.07.006 · 2.26 Impact Factor