Vascular Depression

2019 ◽  
pp. 175-186
Keyword(s):  
Vascular Depression

scholarly journals Corticostriatothalamic reward prediction error signals and executive control in late-life depression

2014 ◽  
Vol 45 (7) ◽  
pp. 1413-1424 ◽  
Author(s):  
A. Y. Dombrovski ◽  
K. Szanto ◽  
L. Clark ◽  
H. J. Aizenstein ◽  
H. W. Chase ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Executive Control ◽  
Late Life ◽  
Vascular Lesions ◽  
Contingency Learning ◽  
Late Life Depression ◽  
Vascular Depression ◽  
Fmri Study ◽  
Core Feature ◽  
Control Functional

BackgroundAltered corticostriatothalamic encoding of reinforcement is a core feature of depression. Here we examine reinforcement learning in late-life depression in the theoretical framework of the vascular depression hypothesis. This hypothesis attributes the co-occurrence of late-life depression and poor executive control to prefrontal/cingulate disconnection by vascular lesions.MethodOur fMRI study compared 31 patients aged ⩾60 years with major depression to 16 controls. Using a computational model, we estimated neural and behavioral responses to reinforcement in an uncertain, changing environment (probabilistic reversal learning).ResultsPoor executive control and depression each explained distinct variance in corticostriatothalamic response to unexpected rewards. Depression, but not poor executive control, predicted disrupted functional connectivity between the striatum and prefrontal cortex. White-matter hyperintensities predicted diminished corticostriatothalamic responses to reinforcement, but did not mediate effects of depression or executive control. In two independent samples, poor executive control predicted a failure to persist with rewarded actions, an effect distinct from depressive oversensitivity to punishment. The findings were unchanged in a subsample of participants with vascular disease. Results were robust to effects of confounders including psychiatric comorbidities, physical illness, depressive severity, and psychotropic exposure.ConclusionsContrary to the predictions of the vascular depression hypothesis, altered encoding of rewards in late-life depression is dissociable from impaired contingency learning associated with poor executive control. Functional connectivity and behavioral analyses point to a disruption of ascending mesostriatocortical reward signals in late-life depression and a failure of cortical contingency encoding in elderly with poor executive control.

The External Validity of MRI-defined Vascular Depression

2013 ◽  
Vol 21 (3) ◽  
pp. S66-S67 ◽  
Author(s):  
Monique A. Pimontel ◽  
Michelle E. Reinlieb ◽  
Lauren C. Johnert ◽  
Ernst Garcon ◽  
Joel R. Sneed ◽  
...  
Keyword(s):  
External Validity ◽  
Vascular Depression

The Cerebrovascular Model of Depression in Late Life

CNS Spectrums ◽  
2002 ◽  
Vol 7 (10) ◽  
pp. 712-715 ◽  
Author(s):  
Jeffrey M. Lyness
Keyword(s):  
Stroke Risk ◽  
Age Of Onset ◽  
Cognitive Impairments ◽  
Late Life ◽  
Executive Dysfunction ◽  
Brain Disease ◽  
Future Research ◽  
Late Life Depression ◽  
Vascular Depression ◽  
Cerebrovascular Risk

ABSTRACTDepression in older people, especially depression with an older age of onset, may be a manifestation of acquired brain disease. The cerebrovascular model of depression, often referred to as “vascular depression,” hypothesizes that otherwise clinically occult small vessel brain disease contribute to the pathogeneses of some late-life depressive conditions. This paper reviews several lines of evidence supporting the cerebrovascular model and addresses the limitations of the existing literature. Several directions for future research are noted, including empirical testing of the notion that cerebrovascular disease might underlie the pathogeneses of depression with prominent executive dysfunction or other cognitive impairments. At this time, there are no specific therapeutic options for patients with suspected vascular depression beyond standard approaches to depression treatments, although education about the possibly greater risks of chronicity should be included in treatment planning. Therapy of cerebrovascular risk factors and stroke-risk reduction are important as consistent with general practice guidelines, although it is not known whether this will reduce the incidence or improve the outcome of late-life depression.

scholarly journals Asymptomatic cerebral infarction and vascular depression

Nosotchu ◽  
2004 ◽  
Vol 26 (4) ◽  
pp. 670-674
Author(s):  
Tokumi Fujikawa
Keyword(s):  
Cerebral Infarction ◽  
Vascular Depression

scholarly journals BROODING MODERATES THE RELATIONSHIP BETWEEN CEREBROVASCULAR BURDEN AND VASCULAR DEPRESSION

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S877-S878
Author(s):  
Manuel Herrera Legon ◽  
Daniel Paulson
Keyword(s):  
Older Adults ◽  
Depressive Symptomatology ◽  
Depression Scale ◽  
Late Life ◽  
Community Dwelling ◽  
Self Report ◽  
Future Research ◽  
Late Life Depression ◽  
Vascular Depression ◽  
The Relationship

Abstract Objective: The vascular depression hypothesis posits that cerebrovascular burden confers risk for late-life depression. Though neuroanatomical correlates of vascular depression (prefrontal white matter hyperintensities) are well established, little is known about cognitive correlates; the identification of which may suggest therapeutic targets. Aims of this study are to examine the hypothesis that the relationship between cerebrovascular burden and depressive symptoms is moderated by brooding, a type of rumination. Method: A sample of 52 community-dwelling, stroke-free, individuals over the age of 70, without history of severe mental illness or dementia completed the Ruminative Responses Scale, and provided self-report (cardiac disease, hypertension, diabetes, high cholesterol) CVB data. The Geriatric Depression Scale was used to assess depressive symptomatology. Results: Results of a bootstrapped model were that self-reported measures of CVB predicted depressive symptomatology. This relationship was significantly moderated by brooding. Among older adults, those who self-reported high CVB and medium to elevated levels of rumination experienced disproportionately more depressive symptomatology. Conclusions: These findings suggest that brooding rumination may be one correlate of the vascular depression syndrome. Future research should examine neuroanatomical correlates of rumination among older adults, and further explore brooding as a therapeutic target for those with late-life depression.

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