Treatment of Post-Stroke Depression

Research output: Contribution to journalReview article

4 Citations (Scopus)

Abstract

Purpose of reviewThis review presents a critical appraisal of current therapeutic strategies for patients with post-stroke depression (PSD). We present the reader with the most recent evidence to support pharmacological, psychosocial, and neuromodulation interventions in PSD. We also discuss the relevance of using antidepressants and psychotherapy to prevent PSD and discuss evidence that antidepressant treatment may reduce mortality after stroke.Recent findingsNeuroinflammation and decrease neurogenesis and plasticity may play an important role in the mechanism of PSD. The strongest predictors of PSD are stroke severity, early physical disability, and severity of loss of functioning. Nevertheless, populations at risk for PSD are yet to be identified. Recent meta-analysis examined the efficacy of pharmacotherapy and psychotherapy. There is consensus that antidepressants such as escitalopram and paroxetine produce a significantly greater response and remission rate of PSD than placebo. Randomised controlled trials (RCTs) using psychotherapy are fewer, but recent meta-analysis tend to suggest efficacy for this treatment modality. Neuromodulation using repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS), as well as novel psychosocial interventions are potentially useful treatments in need of further research.SummaryPharmacological therapy with antidepressants and psychotherapy should be considered as first line of treatment for PSD. The most effective antidepressants are the selective serotonin reuptake inhibitors escitalopram and paroxetine, whereas cognitive behavioural therapy is the most effective psychotherapeutic intervention.

Original languageEnglish
Article number31
Number of pages10
JournalCurrent Treatment Options in Neurology
Volume21
Issue number7
DOIs
Publication statusPublished - Jul 2019

Cite this

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title = "Treatment of Post-Stroke Depression",
abstract = "Purpose of reviewThis review presents a critical appraisal of current therapeutic strategies for patients with post-stroke depression (PSD). We present the reader with the most recent evidence to support pharmacological, psychosocial, and neuromodulation interventions in PSD. We also discuss the relevance of using antidepressants and psychotherapy to prevent PSD and discuss evidence that antidepressant treatment may reduce mortality after stroke.Recent findingsNeuroinflammation and decrease neurogenesis and plasticity may play an important role in the mechanism of PSD. The strongest predictors of PSD are stroke severity, early physical disability, and severity of loss of functioning. Nevertheless, populations at risk for PSD are yet to be identified. Recent meta-analysis examined the efficacy of pharmacotherapy and psychotherapy. There is consensus that antidepressants such as escitalopram and paroxetine produce a significantly greater response and remission rate of PSD than placebo. Randomised controlled trials (RCTs) using psychotherapy are fewer, but recent meta-analysis tend to suggest efficacy for this treatment modality. Neuromodulation using repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS), as well as novel psychosocial interventions are potentially useful treatments in need of further research.SummaryPharmacological therapy with antidepressants and psychotherapy should be considered as first line of treatment for PSD. The most effective antidepressants are the selective serotonin reuptake inhibitors escitalopram and paroxetine, whereas cognitive behavioural therapy is the most effective psychotherapeutic intervention.",
keywords = "Stroke, Depression, Anxiety, Pharmacotherapy, Psychotherapy, Neuromodulation, PROBLEM-SOLVING THERAPY, BEHAVIORAL-THERAPY, CONTROLLED-TRIAL, STROKE, METAANALYSIS, PREVENTION, STIMULATION, PREDICTORS, FREQUENCY, MORTALITY",
author = "Starkstein, {Sergio E.} and Hayhow, {Bradleigh D.}",
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Treatment of Post-Stroke Depression. / Starkstein, Sergio E.; Hayhow, Bradleigh D.

In: Current Treatment Options in Neurology, Vol. 21, No. 7, 31, 07.2019.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Treatment of Post-Stroke Depression

AU - Starkstein, Sergio E.

AU - Hayhow, Bradleigh D.

PY - 2019/7

Y1 - 2019/7

N2 - Purpose of reviewThis review presents a critical appraisal of current therapeutic strategies for patients with post-stroke depression (PSD). We present the reader with the most recent evidence to support pharmacological, psychosocial, and neuromodulation interventions in PSD. We also discuss the relevance of using antidepressants and psychotherapy to prevent PSD and discuss evidence that antidepressant treatment may reduce mortality after stroke.Recent findingsNeuroinflammation and decrease neurogenesis and plasticity may play an important role in the mechanism of PSD. The strongest predictors of PSD are stroke severity, early physical disability, and severity of loss of functioning. Nevertheless, populations at risk for PSD are yet to be identified. Recent meta-analysis examined the efficacy of pharmacotherapy and psychotherapy. There is consensus that antidepressants such as escitalopram and paroxetine produce a significantly greater response and remission rate of PSD than placebo. Randomised controlled trials (RCTs) using psychotherapy are fewer, but recent meta-analysis tend to suggest efficacy for this treatment modality. Neuromodulation using repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS), as well as novel psychosocial interventions are potentially useful treatments in need of further research.SummaryPharmacological therapy with antidepressants and psychotherapy should be considered as first line of treatment for PSD. The most effective antidepressants are the selective serotonin reuptake inhibitors escitalopram and paroxetine, whereas cognitive behavioural therapy is the most effective psychotherapeutic intervention.

AB - Purpose of reviewThis review presents a critical appraisal of current therapeutic strategies for patients with post-stroke depression (PSD). We present the reader with the most recent evidence to support pharmacological, psychosocial, and neuromodulation interventions in PSD. We also discuss the relevance of using antidepressants and psychotherapy to prevent PSD and discuss evidence that antidepressant treatment may reduce mortality after stroke.Recent findingsNeuroinflammation and decrease neurogenesis and plasticity may play an important role in the mechanism of PSD. The strongest predictors of PSD are stroke severity, early physical disability, and severity of loss of functioning. Nevertheless, populations at risk for PSD are yet to be identified. Recent meta-analysis examined the efficacy of pharmacotherapy and psychotherapy. There is consensus that antidepressants such as escitalopram and paroxetine produce a significantly greater response and remission rate of PSD than placebo. Randomised controlled trials (RCTs) using psychotherapy are fewer, but recent meta-analysis tend to suggest efficacy for this treatment modality. Neuromodulation using repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS), as well as novel psychosocial interventions are potentially useful treatments in need of further research.SummaryPharmacological therapy with antidepressants and psychotherapy should be considered as first line of treatment for PSD. The most effective antidepressants are the selective serotonin reuptake inhibitors escitalopram and paroxetine, whereas cognitive behavioural therapy is the most effective psychotherapeutic intervention.

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KW - Anxiety

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KW - BEHAVIORAL-THERAPY

KW - CONTROLLED-TRIAL

KW - STROKE

KW - METAANALYSIS

KW - PREVENTION

KW - STIMULATION

KW - PREDICTORS

KW - FREQUENCY

KW - MORTALITY

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DO - 10.1007/s11940-019-0570-5

M3 - Review article

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JO - Current Treatment Options in Neurology

JF - Current Treatment Options in Neurology

SN - 1092-8480

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M1 - 31

ER -