Treatment response in late-onset depressionCitation formats

  • External authors:
  • R Baldwin
  • S Jeffries
  • C Sutcliffe
  • M Scott
  • A Burns

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Treatment response in late-onset depression : relationship to neuropsychological, neuroradiological and vascular risk factors. / Baldwin, R; Jeffries, S; Jackson, Alan; Sutcliffe, C; Thacker, N; Scott, M; Burns, A.

In: Psychological Medicine, Vol. 34, No. 1, 01.2004, p. 125-136.

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Baldwin, R ; Jeffries, S ; Jackson, Alan ; Sutcliffe, C ; Thacker, N ; Scott, M ; Burns, A. / Treatment response in late-onset depression : relationship to neuropsychological, neuroradiological and vascular risk factors. In: Psychological Medicine. 2004 ; Vol. 34, No. 1. pp. 125-136.

Bibtex

@article{af24f7dbed3642288242d5e1a20221df,
title = "Treatment response in late-onset depression: relationship to neuropsychological, neuroradiological and vascular risk factors",
abstract = "BACKGROUND: Late-onset depressive disorder is associated with white matter lesions and neuropsychological deficits that in some studies are linked to a poorer outcome for depression. Some white matter lesions may be vascular in origin. This study investigated the relationship between response or non-response to antidepressant monotherapy and neuropsychological function, structural brain measures and vascular factors.METHOD: This was a case control study. Fifty patients with late-onset major depressive disorder (29 who were responders to antidepressant monotherapy and 21 who were not) were compared with 35 non-depressed control subjects. Measures included assessment of vascular risk factors, neuropsychological testing and a magnetic resonance imaging (MRI) scan.RESULTS: After adjustment for depressed mood and medication at evaluation, both patient groups had significantly more impairment compared to control subjects on verbal learning tasks involving immediate or delayed recall. Patients who did not respond to antidepressant monotherapy had significantly poorer performance than controls on tests involving visuospatial ability, language, word recognition and tests of executive function, whereas there were no differences between control subjects and responders. On two tests of executive function (verbal fluency and the Stroop test) non-responders scored significantly worse than responders. There were no significant group differences on MRI measures of atrophy or of white matter lesions apart from a higher periventricular hyperintensity score in non-responders compared to controls. There were no group differences on measures of vascular disease.CONCLUSION: The results lend support to the emerging evidence that resistance to treatment in late-onset depression may be associated with impaired executive function. Subtle cerebrovascular mechanisms may be involved.",
keywords = "Age of Onset, Aged, Aged, 80 and over, Analysis of Variance, Antidepressive Agents, Case-Control Studies, Depressive Disorder, Major, Electroconvulsive Therapy, England, Female, Humans, Hypertension, Magnetic Resonance Imaging, Male, Mental Processes, Middle Aged, Neuropsychological Tests, Risk Factors, Treatment Outcome, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't",
author = "R Baldwin and S Jeffries and Alan Jackson and C Sutcliffe and N Thacker and M Scott and A Burns",
year = "2004",
month = jan
doi = "10.1017/S0033291703008870",
language = "English",
volume = "34",
pages = "125--136",
journal = "Psychological Medicine, accepted 9 December 2014",
issn = "0033-2917",
publisher = "Cambridge University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Treatment response in late-onset depression

T2 - relationship to neuropsychological, neuroradiological and vascular risk factors

AU - Baldwin, R

AU - Jeffries, S

AU - Jackson, Alan

AU - Sutcliffe, C

AU - Thacker, N

AU - Scott, M

AU - Burns, A

PY - 2004/1

Y1 - 2004/1

N2 - BACKGROUND: Late-onset depressive disorder is associated with white matter lesions and neuropsychological deficits that in some studies are linked to a poorer outcome for depression. Some white matter lesions may be vascular in origin. This study investigated the relationship between response or non-response to antidepressant monotherapy and neuropsychological function, structural brain measures and vascular factors.METHOD: This was a case control study. Fifty patients with late-onset major depressive disorder (29 who were responders to antidepressant monotherapy and 21 who were not) were compared with 35 non-depressed control subjects. Measures included assessment of vascular risk factors, neuropsychological testing and a magnetic resonance imaging (MRI) scan.RESULTS: After adjustment for depressed mood and medication at evaluation, both patient groups had significantly more impairment compared to control subjects on verbal learning tasks involving immediate or delayed recall. Patients who did not respond to antidepressant monotherapy had significantly poorer performance than controls on tests involving visuospatial ability, language, word recognition and tests of executive function, whereas there were no differences between control subjects and responders. On two tests of executive function (verbal fluency and the Stroop test) non-responders scored significantly worse than responders. There were no significant group differences on MRI measures of atrophy or of white matter lesions apart from a higher periventricular hyperintensity score in non-responders compared to controls. There were no group differences on measures of vascular disease.CONCLUSION: The results lend support to the emerging evidence that resistance to treatment in late-onset depression may be associated with impaired executive function. Subtle cerebrovascular mechanisms may be involved.

AB - BACKGROUND: Late-onset depressive disorder is associated with white matter lesions and neuropsychological deficits that in some studies are linked to a poorer outcome for depression. Some white matter lesions may be vascular in origin. This study investigated the relationship between response or non-response to antidepressant monotherapy and neuropsychological function, structural brain measures and vascular factors.METHOD: This was a case control study. Fifty patients with late-onset major depressive disorder (29 who were responders to antidepressant monotherapy and 21 who were not) were compared with 35 non-depressed control subjects. Measures included assessment of vascular risk factors, neuropsychological testing and a magnetic resonance imaging (MRI) scan.RESULTS: After adjustment for depressed mood and medication at evaluation, both patient groups had significantly more impairment compared to control subjects on verbal learning tasks involving immediate or delayed recall. Patients who did not respond to antidepressant monotherapy had significantly poorer performance than controls on tests involving visuospatial ability, language, word recognition and tests of executive function, whereas there were no differences between control subjects and responders. On two tests of executive function (verbal fluency and the Stroop test) non-responders scored significantly worse than responders. There were no significant group differences on MRI measures of atrophy or of white matter lesions apart from a higher periventricular hyperintensity score in non-responders compared to controls. There were no group differences on measures of vascular disease.CONCLUSION: The results lend support to the emerging evidence that resistance to treatment in late-onset depression may be associated with impaired executive function. Subtle cerebrovascular mechanisms may be involved.

KW - Age of Onset

KW - Aged

KW - Aged, 80 and over

KW - Analysis of Variance

KW - Antidepressive Agents

KW - Case-Control Studies

KW - Depressive Disorder, Major

KW - Electroconvulsive Therapy

KW - England

KW - Female

KW - Humans

KW - Hypertension

KW - Magnetic Resonance Imaging

KW - Male

KW - Mental Processes

KW - Middle Aged

KW - Neuropsychological Tests

KW - Risk Factors

KW - Treatment Outcome

KW - Comparative Study

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1017/S0033291703008870

DO - 10.1017/S0033291703008870

M3 - Article

C2 - 14971633

VL - 34

SP - 125

EP - 136

JO - Psychological Medicine, accepted 9 December 2014

JF - Psychological Medicine, accepted 9 December 2014

SN - 0033-2917

IS - 1

ER -