Late-life depression

2014 ◽  
Vol 29 (S3) ◽  
pp. 577-577 ◽  
Author(s):  
K. Ritchie
Keyword(s):  
Depressive Symptomatology ◽  
Late Onset ◽  
Late Life ◽  
Later Life ◽  
The Elderly ◽  
Conclusive Evidence ◽  
First Episode ◽  
Hormonal Changes ◽  
Late Life Depression ◽  
Incident Cases

Late-life depression is highly heterogeneous in clinical presentation, and is also commonly resistant to treatment. While some cases are a continuation of the chronic course of illness beginning in early adulthood, a large number of persons will have a first episode of depression in later life following alife-time of relatively good mental health. While incident cases of major depression tend to decrease with age, the number of persons with clinically significant depressive symptomatology rises. À distinction has often been made between early-onset and late-onset depression, however, there is no conclusive evidence to suggest these are distinct clinical entities. On the other hand observations from a fifteen year prospective population study of psychiatric disorder in the elderly (the ESPRIT Study) supports the alternative idea that depression may be divided into sub-types according to postulated aetiology; for example depression with a strong genetic component, related to hormonal changes, the consequence of trauma; the result of cerebrovascular insult. Exposure to these putative causes may be more common at different points in the life span, thus suggesting age-differences. Our research further suggests that even cases of depression appearing for the first time in late-life, may be initially triggered by risk factors occurring decades before. Our findings suggest, for example, that childhood events may lead to changes in the biology of stress management, which continue throughout life, increasing vulnerability to depression and persisting even after effective treatment of symptoms. Together these observations suggest it may be more meaningful to classify depression in the elderly according to probable principle precipitating factors rather than age.

Mood disorders in the elderly

2012 ◽  
pp. 1550-1558
Author(s):  
Robert Baldwin
Keyword(s):  
Bipolar Disorder ◽  
Mood Disorders ◽  
Late Life ◽  
Later Life ◽  
The Elderly ◽  
Clinical Syndrome ◽  
Late Life Depression ◽  
Increased Risk

This chapter considers some of the commonly asked questions about mood disorders in later life. Is depression in later life a distinct clinical syndrome? How common is it? Is there an organic link, for example to cerebral changes, and if so, is there an increased risk of later dementia? Is it more difficult to diagnose and treat late-life depression, and once treated, is the outcome good, bad, or indifferent? The emphasis will be on depression but bipolar disorder and mania will also be considered.

Is the Clinical Expression of Late-Life Depression Influenced by Brain Changes? MRI Subcortical Neuroanatomical Correlates of Depressive Symptoms

2000 ◽  
Vol 12 (4) ◽  
pp. 425-434 ◽  
Author(s):  
Steve Simpson ◽  
Robert C. Baldwin ◽  
Alan Jackson ◽  
Alistair Burns ◽  
Peter Thomas
Keyword(s):  
Depressive Symptoms ◽  
White Matter ◽  
Late Onset ◽  
Late Life ◽  
Psychomotor Retardation ◽  
First Episode ◽  
Late Life Depression ◽  
Clinical Expression ◽  
Cross Sectional ◽  
Vascular Depression

Background: “Vascular depression” has recently been proposed. It is characterized by magnetic resonance imaging (MRI) T2-weighted subcortical lesions, a late onset of first episode of depression, and reduced heritability; a cerebrovascular etiology is suggested. The validity of “vascular depression” might be strengthened if an association was found between the subcortical lesions used to define it and particular depressive symptoms. Methods: A blinded cross-sectional examination of DSM-III-R depressive symptoms (American Psychiatric Association, 1987) and MRI T2-weighted subcortical lesions in 44 patients with late-life depression. Results: Many associations were found; however, because of multiple comparisons, their significance is viewed with caution. The most robust finding was that psychomotor retardation was independently related to total white-matter score. The odds of showing psychomotor retardation was increased 1.9 times for every point increase in severity of white-matter change. Conclusion: In late-life depression the clinical expression of the depression is influenced by the pattern of MRI T2-weighted subcorticallesions. This gives some validity to the concept of an MRI-defined “vascular” subtype of late-life depression and strengthens the argument for including neuroimaging in the classification of late-life depression.

P.309 Late-life depression: How do patients with early-onset vs late-onset differ in clinical features and treatment response?

2020 ◽  
Vol 31 ◽  
pp. S52-S53
Author(s):  
W.R. Chae ◽  
M. Fuentes Casan ◽  
F. Gutknecht ◽  
A. Ljubez ◽  
S.M. Gold ◽  
...  
Keyword(s):  
Treatment Response ◽  
Clinical Features ◽  
Early Onset ◽  
Late Onset ◽  
Late Life ◽  
Late Life Depression

scholarly journals When Cognitive Decline and Depression Coexist in the Elderly: CSF Biomarkers Analysis Can Differentiate Alzheimer's Disease from Late-Life Depression

2018 ◽  
Vol 10 ◽  
Author(s):  
Claudio Liguori ◽  
Mariangela Pierantozzi ◽  
Agostino Chiaravalloti ◽  
Giulia M. Sancesario ◽  
Nicola B. Mercuri ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Late Life ◽  
The Elderly ◽  
Csf Biomarkers ◽  
Late Life 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.

Metabolic dysregulation and late-life depression: a prospective study

2016 ◽  
Vol 47 (6) ◽  
pp. 1041-1052 ◽  
Author(s):  
R. M. Marijnissen ◽  
N. Vogelzangs ◽  
M. E. Mulder ◽  
R. H. S. van den Brink ◽  
H. C. Comijs ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Waist Circumference ◽  
Depressive Symptomatology ◽  
Hdl Cholesterol ◽  
Late Life ◽  
Late Life Depression ◽  
Metabolic Dysregulation ◽  
The Metabolic Syndrome ◽  
Co Morbidity ◽  
Severity Of Depression

BackgroundDepression is associated with the metabolic syndrome (MS). We examined whether metabolic dysregulation predicted the 2-year course of clinical depression.MethodA total of 285 older persons (⩾60 years) suffering from depressive disorder according to DSM-IV-TR criteria was followed up for 2 years. Severity of depression was assessed with the Inventory of Depressive Symptomatology (IDS) at 6-month intervals. Metabolic syndrome was defined according the National Cholesterol Education Programme (NCEP-ATP III). We applied logistic regression and linear mixed models adjusted for age, sex, years of education, smoking, alcohol use, physical activity, somatic co-morbidity, cognitive functioning and drug use (antidepressants, anti-inflammatory drugs) and severity of depression at baseline.ResultsMS predicted non-remission at 2 years (odds ratioper component = 1.26, 95% confidence interval 1.00–1.58), p = 0.047), which was driven by the waist circumference and HDL cholesterol. MS was not associated with IDS sum score. Subsequent analyses on its subscales, however, identified an association with the somatic symptom subscale score over time (interaction time × somatic subscale, p = 0.005), driven by higher waist circumference and elevated fasting glucose level.ConclusionsMetabolic dysregulation predicts a poor course of late-life depression. This finding supports the concept of ‘metabolic depression’, recently proposed on population-based findings of a protracted course of depressive symptoms in the presence of metabolic dysregulation. Our findings seem to be driven by abdominal obesity (as indicated by the waist circumference) and HDL cholesterol dysregulation.

The pattern and course of cognitive impairment in late-life depression

2009 ◽  
Vol 40 (4) ◽  
pp. 591-602 ◽  
Author(s):  
S. Köhler ◽  
A. J. Thomas ◽  
N. A. Barnett ◽  
J. T. O'Brien
Keyword(s):  
Cognitive Impairment ◽  
Executive Functioning ◽  
Cognitive Deficits ◽  
Processing Speed ◽  
Age Of Onset ◽  
Late Onset ◽  
Late Life ◽  
Late Life Depression ◽  
Remission Status ◽  
Current Mood

BackgroundCognitive deficits persist despite clinical recovery in subjects with late-life depression, but more needs to be known about their longer-term outcome and factors affecting their course. To investigate this, we followed the pattern of cognitive impairments over time and examined the effects of current mood, remission status, age of depression onset and antidepressant (AD) treatment on these deficits.MethodSixty-seven subjects aged ⩾60 years with DSM-IV major depressive disorder and 36 healthy comparison subjects underwent tests of global cognition, memory, executive functioning and processing speed at baseline, 6 and 18 months, with some subjects tested again after 4 years. z scores were compared between groups, with analyses of clinical factors that may have influenced cognitive performance in depressed subjects.ResultsHalf of the patients exhibited a generalized cognitive impairment (GCI) that persisted after 18 months. Patients performed worse across all cognitive domains at all time points, without substantial variability due to current mood, remission status or AD treatment. Late age of onset was associated significantly with decline in memory and executive functioning. Impaired processing speed may be a partial mediator of some deficits, but was insufficient to explain differences between patients and controls. Four-year follow-up data suggest impairments persist, but do not further decline.ConclusionsCognitive deficits in late-life depression persist up to 4 years, affect multiple domains and are related to trait rather than state effects. Differences in severity and course between early and late onset depression suggest different pathogenic processes.

Depression and mild cognitive impairment – Comorbidity and/or continuum?

2016 ◽  
Vol 33 (S1) ◽  
pp. S190-S191
Author(s):  
G. Sobreira ◽  
M.A. Aleixo ◽  
C. Moreia ◽  
J. Oliveira
Keyword(s):  
Risk Factors ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Late Life ◽  
The Elderly ◽  
Late Life Depression ◽  
Pubmed Database ◽  
Competing Interest ◽  
The Relationship

IntroductionDepression and mild cognitive impairment are common among the elderly. Half the patients with late-life depression also present some degree of cognitive decline, making the distinction between these conditions difficult.ObjectivesTo conduct a database review in order to understand the relationship between these entities, and treatment approaches.AimsTo create and implement clinical guidelines at our institution, to evaluate and treat elderly patients presenting with depression and mild cognitive impairment.MethodsA PubMed database search using as keywords “late life depression”, “depression”; “cognitive impairment”; “mild cognitive impairment” and “dementia” between the year 2008 and 2015.ResultsLate-life depression and cognitive impairment are frequent among the elderly (10–20%). Depression is also common in the early stages of dementia decreasing as the cognitive decline progresses. The causal relationship between these entities is not well understood and some authors advocate a multifactorial model (genetic risk factors; neuroendocrine changes; vascular risk factors) and the cognitive impairment of said changes is dependent on the individual's cognitive reserve. Regarding treatment of depression in patients with cognitive impairment, most authors advocate a stepped approach with watchful waiting and then, if symptoms persist, the introduction of pharmacotherapy and psychosocial intervention.ConclusionsThe relationship between cognitive impairment and depression is still not clear and probably multifactorial. The diagnosis of depressive symptoms in patients with severe cognitive impairment can be difficult and most forms of pharmacological treatment in this population are not beneficial, making it important to carefully evaluate the benefits of introducing new medication.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Late-onset bipolar disorder: What else?

2016 ◽  
Vol 33 (S1) ◽  
pp. S121-S121
Author(s):  
C.P. Ferreira ◽  
S. Alves ◽  
C. Oliveira ◽  
M.J. Avelino
Keyword(s):  
Elderly Patient ◽  
Bipolar Disorder ◽  
Treatment Guidelines ◽  
Late Onset ◽  
Mood Stabilizer ◽  
The Elderly ◽  
First Episode ◽  
Therapeutic Implications ◽  
Psychiatric Conditions ◽  
New Onset

IntroductionGeriatric-onset of a first-episode mania is a rare psychiatric condition, which may be caused by a heterogeneous group of non-psychiatric conditions. To confirm late-onset bipolar disorder (LOBD) diagnosis, secondary-mania causes should be ruled out.ObjectivesTo provide a comprehensive review reporting prevalence, features, differential diagnosis, comorbidity and treatment of LOBD.MethodsThe literature was systematically reviewed by online searching using PubMed®. The authors selected review papers with the words “Late-onset mania” and/or “Late-onset bipolar” in the title and/or abstract published in the last 10 years.Results and discussionWith population ageing, LOBD is becoming a more prevalent disorder. Clinical presentation may be atypical and confounding, making the diagnosis not always obvious. Several non-psychiatric conditions must be considered in an elderly patient presenting with new-onset mania, namely stroke, dementia, hyperthyroidism or infection causing delirium. Only then LOBD diagnosis may be done, making that an exclusion diagnosis. Comorbidities, such as hypertension or renal insufficiency are often present in the elderly and must be taken into account when choosing a mood stabilizer.ConclusionsLOBD remains a complex and relatively understudied disorder with important diagnostic and therapeutic implications. This diagnosis must be kept in mind for every elderly patient presenting with new-onset mania. Further investigations could contribute to a better understanding of LOBD etiopathogenesis and to set out better treatment guidelines.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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