Guideline AVC 2

AHA/ASA Scientific Statement
Poststroke Depression
A Scientific Statement for Healthcare Professionals From the American
Heart Association/American Stroke Association
The American Academy of Neurology affirms the value of this statement as an educational
tool for neurologists.
Amytis Towfighi, MD, Chair; Bruce Ovbiagele, MD, MSc, MAS, FAHA, Vice Chair;
Nada El Husseini, MD, MHSc; Maree L. Hackett, PhD; Ricardo E. Jorge, MD;
Brett M. Kissela, MD, MS, FAHA; Pamela H. Mitchell, PhD, RN, FAHA;
Lesli E. Skolarus, MD; Mary A. Whooley, MD; Linda S. Williams, MD, FAHA; on behalf of the
American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; and
Council on Quality of Care and Outcomes Research
Abstract—Poststroke depression (PSD) is common, affecting approximately one third of stroke survivors at any one
time after stroke. Individuals with PSD are at a higher risk for suboptimal recovery, recurrent vascular events, poor quality
of life, and mortality. Although PSD is prevalent, uncertainty remains regarding predisposing risk factors and optimal
strategies for prevention and treatment. This is the first scientific statement from the American Heart Association on the
topic of PSD. Members of the writing group were appointed by the American Heart Association Stroke Council’s Scientific
Statements Oversight Committee and the American Heart Association’s Manuscript Oversight Committee. Members
were assigned topics relevant to their areas of expertise and reviewed appropriate literature, references to published
clinical and epidemiology studies, clinical and public health guidelines, authoritative statements, and expert opinion.
This multispecialty statement provides a comprehensive review of the current evidence and gaps in current knowledge
of the epidemiology, pathophysiology, outcomes, management, and prevention of PSD, and provides implications for
Downloaded from http://ahajournals.org by on October 20, 2021
clinical practice. (Stroke. 2017;48:e30-e43. DOI: 10.1161/STR.0000000000000113.)

Key Words: AHA Scientific Statements ◼ depression ◼ management ◼ prevention & control
◼ screening ◼ stroke ◼ treatment
D epression occurs in approximately one third of stroke

survivors at any one time1 and is associated with
poor functional outcomes2 and higher mortality.3 Although
literature; and provides management implications for clini-
cal practice.
poststroke depression (PSD) is one of the most common Methods

complications after stroke, few guidelines exist regarding Writing group members were nominated by the committee
assessment, treatment, and prevention of PSD. This sci- chair on the basis of their previous work in relevant topic
entific statement summarizes published evidence on the areas and were approved by the American Heart Association
causes, predisposing factors, epidemiology, screening, Stroke Council’s Scientific Statement Oversight Committee
treatment, and prevention of PSD; illuminates gaps in the and the American Heart Association’s Manuscript Oversight
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship
or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete
and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on June 1, 2016, and the American Heart
Association Executive Committee on July 20, 2016. A copy of the document is available at http://professional.heart.org/statements by using either “Search
for Guidelines & Statements” or the “Browse by Topic” area. To purchase additional reprints, call 843-216-2533 or e-mail [email protected].
The American Heart Association requests that this document be cited as follows: Towfighi A, Ovbiagele B, El Husseini N, Hackett ML, Jorge RE, Kissela
BM, Mitchell PH, Skolarus LE, Whooley MA, Williams LS; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular and
Stroke Nursing; and Council on Quality of Care and Outcomes Research. Poststroke depression: a scientific statement for healthcare professionals from the
American Heart Association/American Stroke Association. Stroke. 2017;48:e30–e43. doi: 10.1161/STR.0000000000000113.
Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines
development, visit http://professional.heart.org/statements. Select the “Guidelines & Statements” drop-down menu, then click “Publication Development.”
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-
Permission-Guidelines_UCM_300404_Article.jsp. A link to the “Copyright Permissions Request Form” appears on the right side of the page.
© 2016 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STR.0000000000000113
e30
Towfighi et al Poststroke Depression e31
Committee. Multiple disciplines were represented, includ- other measures of natural history of PSD: incidence in year
ing neurology, psychiatry, psychology, neurorehabilitation, 1 ranged from 10% to 15% (2 studies); cumulative incidence
primary care, epidemiology, biostatistics, and nursing. The ranged from 39% to 52% (3 studies with follow-up periods
writing group met by telephone to determine subcategories to between 1 and 5 years); and 15% to 50% of patients with PSD
evaluate. These included 9 sections that covered the following: within 3 months of stroke recovered 1 year later. All longi-
incidence, prevalence, and natural history; pathophysiology; tudinal studies revealed a dynamic natural history, with new
predictors; functional outcomes; quality of life (QOL); health- cases and recovery of depression occurring over time.8 Little
care use; mortality; screening; and management and preven- is known about whether the natural course of PSD differs in
tion. Each subcategory was led by a primary author, with 1 those with a history of depression before stroke.
to 3 additional coauthors. Full searches of PubMed, Ovid Hackett et al updated their systematic review and meta-
MEDLINE, Ovid Cochrane Database of Systematic Reviews, analysis in 20141 to include all published observational studies
Ovid Central Register of Controlled Trials databases, Internet with prospective consecutive recruitment of stroke patients and
Stroke Center/Clinical Trials Registry (http://www.strokecen- assessment of depression or depressive symptoms at prespeci-
ter.org/trials/), and National Guideline Clearinghouse (http:// fied time points (until May of 2013; 61 studies; n=25 488; 29
guideline.gov/) were conducted of all English-language cohorts were also in Ayerbe et al’s review). Their study revealed
articles on human subjects, published through February of similar results, with depression present in 33% (95% CI, 26%–
2015. The evidence was organized within the context of the 39%) at 1 year after stroke, with a decline beyond 1 year: 25%
American Heart Association Framework. Drafts of summa- (95% CI, 16%–33%) up to 5 years, and 23% (95% CI, 14%–
ries and suggestions/considerations for clinical practice were 31%) at 5 years.1 Prevalence of PSD was lower beyond 1 year:
circulated to the entire writing group for feedback. Sections Subgroup analyses revealed a pooled prevalence estimate of
were revised and merged by the Chair. The resulting draft was 31% (95% CI, 27%–35%) for the 48 studies (n=23 654) includ-
reviewed and edited by the Vice-Chair, and the entire com- ing individuals with a history of depression; 34% (95% CI,
mittee was asked to approve the final draft. Changes to the 29%–39%) for the 25 studies (n=19 218) including individuals
document were made by the Chair and Vice-Chair in response with aphasia; and 33% (95% CI, 28%–38%) for the 25 studies
to peer review, and the document was again sent to the entire (n=5658) of people with first-ever stroke.1
writing group for suggested changes and approval. A sum- In Hackett’s and Ayerbe’s meta-analyses, the prevalence
mary of findings is available in the Table. rates did not differ significantly over time during the first year
after stroke (within 1 month from stroke, 1–6 months, or 6–12
months) or by setting (hospital, rehabilitation, or popula-
Incidence, Prevalence, and
tion based). The studies included in Hackett’s and Ayerbe’s

Natural History of PSD reviews were heterogeneous in nature, using a variety of
Depression is common after stroke, affecting approximately methods to diagnose depression and different thresholds for
one third of stroke survivors at any one time after stroke (com- the same scale. The hospital- and rehabilitation-based stud-
pared with 5%–13% of adults without stroke), with a cumula- ies had numerous exclusion criteria (such as excluding those
tive incidence of 55%.4–6 Hackett et al performed a systematic with a history of depression), thus limiting their generalizabil-
review and meta-analysis of 51 studies conducted before June ity. Statistical quality and presentation of methods and results
2004 and revealed a pooled frequency estimate of PSD of were poor in many studies, and important covariates (such
33% (95% confidence interval [CI], 29%–36%).7 All studies as history of depression) were not included in multivariable
included ischemic stroke, most included intracerebral hemor- models in most studies. Few of the multivariable models were
rhage, and the majority excluded subarachnoid hemorrhage and likely to be stable as the ratio of events per variable in the
transient ischemic attack. Valid methods were used to ascertain model met or surpassed the recommended minimum.
depression in these studies. The primary end point was the pro- In summary, approximately one third develop PSD at
portion of patients who met the diagnostic category of depres- some point after stroke. The frequency is highest in the first
sion, which included the following: (1) depressive disorder, year, at nearly 1 in 3 stroke survivors, and declines thereafter.
depressive symptoms, or psychological distress, as defined by
scores above a cut point for abnormality on a standard scale; (2) Pathophysiology of PSD
major depression, or minor depression (or dysthymia) accord- The pathophysiology of PSD is poorly understood. The cause
ing to the third, fourth, and fifth editions of the Diagnostic of PSD is likely multifactorial—with biological and psy-
and Statistical Manual of Mental Disorders, or other standard chosocial components—and may vary depending on timing
diagnostic criteria using structured or semistructured psychi- after event. An understanding of the pathophysiology of PSD
atric interviews. Ayerbe et al’s subsequent systematic review may aid in its management; for example, PSD resulting from
and meta-analysis of 43 cohorts published before August 2011 biological causes could potentially respond better to pharma-
(n=20 293) revealed a similar pooled frequency of PSD of 29% cological therapy, whereas PSD resulting from psychosocial
(95% CI, 25%–32%).8 The frequency remained fairly constant causes could possibly respond more favorably to psychother-
for the first year after stroke and diminished slightly thereafter apy and social support interventions.
(28%; 95% CI, 23%–34% within 1 month of stroke; 31%; 95% Studies have revealed an association between PSD and
CI, 24%–39% at 1–6 months; 33%; 95% CI, 23%–43% at 6 poststroke cognitive and functional deficits, indirectly sug-
months to 1 year; and 25%; 95% CI, 19%–32% beyond 1 year). gesting that PSD may be a psychological reaction to these
Only 5 studies in Ayerbe et al’s systematic review reported deficits.9,10 In addition, numerous psychosocial risk factors for
e32 Stroke February 2017
PSD are also risk factors for depression without stroke, such PSD has been observed in individuals with anosognosia.16
as past psychiatric history, premorbid neurotic personality Third, late-onset depression has been associated with white
traits, and social isolation.11,12 matter disease and small silent infarcts.12,17,18 Fourth, poststroke
In contrast, evidence suggests that PSD has underlying bio- depressive-like symptoms have been noted in several animal
logical causes and is not merely a psychological response to models.19,20 Last, depression has been reported after transient
new disability or a life-threatening event. First, 1 study showed ischemic attack and minor stroke (National Institutes of Health
that depression was more common after stroke than other physi- Stroke Scale score ≤5 at discharge).21,22
cal illnesses with similar levels of physical disability13; however, Proposed biological factors contributing to PSD include
other studies have not corroborated these findings.14,15 Second, lesion location, genetic susceptibility, inflammation,
Table. Summary of Findings

Topic Summary of Findings
Epidemiology Approximately one third of stroke survivors develop PSD at some point after stroke. The frequency is highest in the
first year, at nearly 1 in 3 stroke survivors, and declines thereafter.
Pathophysiology The pathophysiology of PSD is complex and likely involves a combination of biological and psychosocial factors.
Further research is needed to develop a better understanding of PSD pathophysiology with an aim to develop
targeted interventions for prevention and treatment.
Predictors A multitude of studies have evaluated predictors of PSD, but because of differences in inclusion and exclusion
criteria, statistical methods, and inadequate sample sizes for multivariate analyses, generalizability is limited. The
most consistent predictors of PSD have been physical disability, stroke severity, history of depression, and cognitive
impairment. Further studies are needed to develop a better understanding of predictors of PSD.
PSD and functional outcomes PSD is associated with poorer functional outcomes after stroke. Treatment with fluoxetine was associated with lower
PSD occurrence rates and improvement in motor recovery in 1 RCT. Further research is needed to assess the effect
of PSD on outcomes and to develop optimal strategies to counteract these effects.
PSD and QOL A few studies suggest that PSD adversely affects QOL. Further research is needed to further elucidate the
independent effect of PSD on QOL and to determine how to improve QOL in individuals with or at risk for PSD.
PSD and healthcare use A few studies have shown an association between PSD and healthcare use. Further studies are needed to evaluate
the effect of treatment of PSD on subsequent healthcare use.
PSD and mortality PSD is associated with higher mortality after stroke.
Screening Twenty-four studies (n=2907 participants) showed that the CES-D, HDRS, and PHQ-9 had high sensitivity
for detecting PSD; however, the studies had several limitations, including generalizability. Systematic
screening for PSD with the 9-item PHQ-9 is pragmatic, has high sensitivity for detecting PSD, and may improve
outcomes, provided that processes are in place to assure accurate diagnosis, timely and effective treatment,
and follow-up. Further research is needed to determine whether screening for PSD—in conjunction with
collaborative care to ensure timely intervention, treatment, and follow-up—improves outcomes in diverse
populations of stroke survivors.
Management: pharmacotherapy Twelve trials (n=1121) suggest that antidepressant medications may be effective in treating PSD; further research is
needed to determine optimal timing, threshold, and medications for treatment.
Management: neuromodulation Further studies are needed to determine the efficacy of neuromodulation on treating PSD.
Management: psychosocial interventions Seven trials (n=775) suggest that brief psychosocial interventions may be useful and effective in treatment of PSD.
Whether antidepressant medication is a necessary or beneficial adjuvant cannot be established from these trials
because of a lack of placebo controls.
Management: stroke liaison workers Fifteen trials (n=2743) have not revealed a beneficial effect from stroke liaison workers on PSD; however, the trials
included individuals without a diagnosis of PSD. Further studies are needed to determine the effect of liaison worker
on those with established PSD.
Management: information provision Seven trials (n=720) suggest that information provision provides a small benefit in depression scores; however, the
clinical significance of this improvement is unclear.
Management: self-management Few studies have assessed the effectiveness of self-management strategies on PSD; further studies are needed to
determine whether these strategies are beneficial.
Prevention: pharmacotherapy Eight trials (n=776) suggest that pharmacological treatment may be effective in preventing PSD; however, further
studies are needed in more representative samples of stroke survivors, and additional study is required to determine
the optimal timing and duration of treatment.
Prevention: psychosocial interventions Five trials (n= 1078) suggest that psychosocial therapies may prevent the development of PSD; however, the studies
are not generalizable to all stroke survivors, given their narrow inclusion and exclusion criteria. Further research with
more rigorous methods is needed to assess the effect of psychotherapy on prevention of PSD.
CES-D indicates Center of Epidemiological Studies-Depression Scale; HDRS, Hamilton Depression Rating Scale; PHQ, Patient Health Questionnaire; PSD, poststroke
depression; QOL, quality of life; and RCT, randomized controlled trial.
neurogenesis in response to ischemia, alterations in neurotrophic between PSD and high postdexamethasone cortisol levels
factors, disruption of cortico-striato-pallido-thalamic-cortical (OR, 3.28; 95% CI, 1.28–8.39), lower serum brain-derived
projections, and alterations in serotonergic, noradrenergic, and neurotrophic factor levels (standardized mean difference,
dopaminergic pathways, leading to changes in amine levels.19 −0.52; 95% CI, −0.84 to −0.21), smaller amygdala volumes
The hypothesis that lesion location was associated with PSD (standardized mean difference, −0.45; 95% CI, −0.89 to
gained popularity in the 1970s when Robinson et al reported −0.02), and overall brain perfusion reduction (standardized
associations between laterality of experimentally induced mean difference, −0.35; 95% CI, −0.64 to −0.06). There
stroke, brain catecholamine concentrations, and activity in rats were no significant associations between PSD and inflam-
and subsequently between left hemispheric (particularly fron- matory markers such as C-reactive protein, interleukin-6,
tal) strokes and PSD in humans.23,24 Numerous cohort studies interleukin-18, or tumor necrosis factor-alpha (7 stud-
subsequently investigated the association between lesion loca- ies; inflammation assessed within a mean of 35 days after
tion and PSD; a meta-analysis of 35 cohorts published before stroke); however, the studies included individuals with tran-
August of 199925 and a subsequent systematic review and sient ischemic attack and silent stroke and apathy (without
meta-analysis of 43 cohorts published before January of 2014 diagnosis of depression), potentially obscuring the results.
(n=5507)26 found no association between PSD and lesion loca- Despite the aforementioned weaknesses and additional limi-
tion. Subgroup analyses stratified by time since stroke onset tations (relatively small number of studies, different scales
to assessment for PSD showed that between 1 and 6 months to assess depression), this meta-analysis suggested that cere-
after stroke, right hemispheric strokes were associated with bral perfusion reduction, higher cortisol levels and low lev-
lower odds of PSD (odds ratio [OR]=0.79; 95% CI, 0.66– els of neurotrophic factors, and amygdala volume reduction
0.93).26 In contrast, a meta-analysis of 52 studies published may be promising biological markers for PSD.34
before July 2003 (n=3668) found a weak relationship between In summary, the pathophysiology of PSD is complex and
PSD and right hemispheric lesions (overall weighted mean likely involves a combination of biological and psychosocial
effect size=−0.0801; 95% CI, −0.146;−0.014; P=0.014). The factors. Further research is needed to develop a better under-
authors of this meta-analysis appropriately indicated that the standing of PSD pathophysiology with an aim to develop tar-
effect size was small and may not have practical significance. geted interventions for prevention and treatment.
When they only included high-quality studies, there was no
relationship between PSD and lesion location.27 The various Predictors of PSD
systematic reviews used slightly different selection criteria Three independent systematic reviews of observational
for the included studies and distinct statistical methods for the studies without corresponding meta-analyses (Hackett
meta-analysis. All 3 systematic reviews identified limitations et al: 20 cohorts, n=17 93435; Kutlubaev et al: 23 cohorts,
to the analyses because of multiple sources of heterogeneity n=18 3742,35; De Ryck et al: 24 cohorts, n=14 64236; Ayerbe
such as varying time intervals between stroke and depression et al: 10 cohorts, n=16 0458) have identified consistent pre-
assessment, different depression scales, exclusion of patients dictors of depression after stroke. There were few overlap-
with aphasia, and heterogeneous methods of reporting results. ping cohorts in the reviews reflecting the different inclusion
Studies assessing genetic associations with PSD have been and exclusion criteria set by the review authors. The data
limited and small. Higher serotonin transporter gene (SLC6A4) indicated that physical disability, stroke severity, depres-
promoter methylation status in the presence of the SLC6A4 sion before stroke, and cognitive impairment consistently
linked promoter region (5-HTTLPR) s/s genotype was asso- had a positive association with the development of PSD.
ciated with PSD at 2 weeks and 1 year after stroke, as well Other factors that have been identified as predictors include
as worsening of depressive symptoms over the first year after a lack of family and social support after stroke36 and anxiety
stroke (n=286 stroke subjects).28 In that same cohort, a higher after stroke.8 Older age, female sex, diabetes mellitus, stroke
brain-derived neurotrophic factor methylation status and the subtype, education level, living alone, and previous stroke
brain-derived neurotrophic factor val66met polymorphism have not shown a consistent association with the subsequent
were independently associated with prevalent PSD (n=286 development of depression.2 People with transient ischemic
stroke subjects).29 Alleles associated with reduced anti-inflam- attacks and those with obvious speech disturbances or com-
matory cytokine function such as the interleukin-4 + 33C/C and munication difficulties (eg, aphasia, confusion, or dementia),
the interleukin-10 -1082A/A genotypes have also been asso- impaired consciousness, severe cognitive decline or sub-
ciated with PSD (n=276 stroke subjects).30 Proinflammatory arachnoid hemorrhage were excluded from most studies lim-
cytokines may play a role in PSD by inducing alterations of the iting our ability to generalize these findings. The statistical
hypothalamus-pituitary-adrenal axis and decreasing serotonin methods in most of the studies included in these systematic
synthesis.31 Studies have alluded to a direct involvement of the reviews were poor, and most of the samples were too small
serotonergic system, regardless of the degree of disability and for multivariate analyses.
lesion location.32,33 In summary, a multitude of studies have evaluated pre-
A meta-analysis of the most studied biological markers dictors of PSD, but because of differences in inclusion and
of PSD (cerebral blood flow, cortisol levels, inflammatory exclusion criteria, statistical methods, and inadequate sample
marker levels, brain-derived neurotrophic factor levels, and sizes for multivariate analyses, generalizability is limited. The
brain volume/atrophy) including studies through June of most consistent predictors of PSD have been physical dis-
2012 (33 studies; n=1893 participants) showed associations ability, stroke severity, history of depression, and cognitive
impairment. Further studies are needed to develop a better In summary, a few studies suggest that PSD adversely
understanding of predictors of PSD. affects QOL. Further research is needed to elucidate the
independent effect of PSD on QOL and to determine how to
Association Between PSD and improve QOL in individuals with or at risk for PSD.
Functional Outcomes
PSD might conceivably influence functional outcome by Effect of PSD on Healthcare Use
limiting participation in rehabilitation, directly decreasing To date, no systematic review has assessed the association
physical, social, and cognitive function, or perhaps affecting between PSD and healthcare use; however, individual studies
the biological process of neuroplasticity.37,38 A systematic have shown that PSD is associated with higher rates of health-
review of 14 studies before May of 2013 with 4498 par- care use after stroke, including inpatient healthcare use and
ticipants assessing the association between PSD and stroke total healthcare use. In 2 large Veterans Health Administration
outcome (4 population-based studies [n=2800], 5 hospital- cohorts in the United States, those with PSD had longer
based [n=800], and 5 rehabilitation-based [n=898]) revealed lengths of stay52 and higher outpatient and inpatient use in the
that PSD had a consistent adverse effect on outcomes. In 6 12 months after stroke.52,53 In addition to PSD, other mental
of 8 studies, depression was associated with poor functional health diagnoses after stroke have also been associated with
outcomes (3 of 5 with multivariable analyses); the other 2 increased healthcare use.53,54
studies found no association between PSD and functional Although the relationship between PSD and subsequent
improvement.2 A lifetime history of depression and active healthcare use is established, few studies, and none specifi-
depression affected functional outcome at 3 and 12 months cally in stroke patients, have assessed whether treatment of
in 1 cohort study.39 depression is associated with a decrease in healthcare use.
A randomized controlled trial (RCT) comparing fluox- Addressing this question is complex, given that healthcare
etine to placebo within 5 to 10 days after stroke showed use and depression treatment are understandably confounded.
lower PSD occurrence rates and significant improvement One study among patients aged 65 years and older with prior
in motor function in the fluoxetine group.40 Even after sta- thromboembolic events (including some with stroke) found
tistically controlling for the reduction in depression, motor that antidepressant use was not associated with an increase
improvement was improved in the fluoxetine group. This or decrease in healthcare use,55 but no large, high-quality
finding raises the question of whether depression prevents studies of the relationship between depression treatment and
motor recovery (and this negative effect is reversed by treat- subsequent healthcare use in patients with PSD have been
ment), or whether there may be some effect of fluoxetine published.
or selective serotonin reuptake inhibitors (SSRIs) in general In summary, a few studies have shown an association between
on neuroplasticity and motor recovery. Indeed, other studies PSD and healthcare use. Further studies are needed to evaluate
have shown that SSRI use after stroke generally improves the effect of treatment of PSD on subsequent healthcare use.
motor recovery.41–45 The factors influencing whether PSD
worsens outcome, and methods to counteract these effects, Association Between PSD and Mortality
require further exploration. PSD has been associated with higher mortality rates after
In summary, PSD is associated with poorer functional stroke. A systematic review and meta-analysis of studies
outcomes after stroke. Treatment with fluoxetine was asso- published before November of 2012 (13 studies; 59 598
ciated with lower PSD occurrence rates and improvement in individuals with stroke: 6052 with PSD and 53 546 from
motor recovery in 1 RCT. Further research is needed to assess comparison groups) revealed a pooled OR of 1.22 (95% CI,
the effect of PSD on outcomes and to develop optimal strate- 1.02–1.47) and pooled hazard ratio (HR) of 1.52 (95% CI,
gies to counteract these effects. 1.02–2.26) for increased/early mortality at follow-up for
individuals with PSD.3 Ayerbe et al’s 2013 meta-analysis
Association Between PSD and QOL found an association between PSD and mortality in 2 out
To date, the association between PSD and poststroke QOL of 3 studies that investigated this association.8 A subsequent
has not been explored in a systematic review or meta-anal- study of stroke survivors followed in the South London
ysis. Individual studies have found that poststroke depres- Stroke Register revealed that individuals with PSD had a
sive symptoms are associated with reduced poststroke QOL greater risk of mortality (HR, 1.41; 95% CI, 1.13–1.77).56
as measured by the Short-Form General Health Survey,46,47 The association between PSD and mortality was strongest in
EuroQoL questionnaire48 and Assessment of Quality of individuals <65 years of age. Adjustment for comorbidities,
Life.49 Poststroke mood change is 1 of the factors with the smoking, alcohol use, SSRI use, social support, and adher-
greatest effect on poststroke QOL.47,50 Stroke survivors’ ence with medications did not change these associations.
cognitive and language impairments may necessitate proxy Individuals who started SSRIs after stroke had higher risk
responses for self-reported outcomes. Proxies tend to report of mortality, independently of PSD at 3 months (HR, 1.72;
worse QOL scores than do stroke survivors themselves.51 95% CI, 1.34–2.20).57 This study should be interpreted with
These differences make it necessary to carefully examine caution because numerous models were used to describe the
the composition of outcomes, cohorts, and use of proxies to association between depression and mortality, and the only
look for potential biases in studies exploring the association common factors between these models were age, sex, eth-
of PSD and QOL. nicity, and stroke severity. The relationship between SSRIs
and mortality requires a rigorous analysis of the interactions has excellent sensitivity for diagnosing major depression in
with other key variables such as depression, disability, and the general population,59 screens positive if 1 or both of the
comorbid medical conditions. 2 core symptoms (depressed mood and anhedonia) is pres-
In summary, PSD is associated with higher mortality after ent. The multiple-choice version, developed in 2003, has a
stroke. 6-point scale and the cut point for a positive screen varies by
population (≥2 or ≥3). The 3 studies of PHQ-2 in the Meader
Screening for PSD meta-analysis60–62 used the multiple choice version.58 Further
Stroke patients present unique challenges to identifying studies are needed to determine the sensitivity and specificity
depression. Stroke-related neurological symptoms such as of the yes/no PHQ-2 in individuals with stroke; however, in
aprosodic speech, abulia, or flat affect may hinder healthcare an analysis of 1024 participants with coronary heart disease
practitioners’ identification of PSD,75 whereas aphasia may enrolled in the Heart and Soul Study, of which 147 (14%)
lead to undiagnosed and inadequate treatment of depression. had a history of stroke, the yes/no PHQ-2 had sensitivity of
A high index of suspicion by all members of the interdisciplin- 0.90 (95% CI, 0.86–0.94) and specificity of 0.69 (95% CI,
ary treatment team is therefore necessary to accurately recog- 0.66–0.73).63
nize depression. Clues of PSD can be subtle, such as refusal to Another factor to consider is the timing of screening for
participate in therapy. Patients can experience emotional labil- PSD. The optimal screening tool may vary by time since
ity or a pseudobulbar affect after a stroke, often prompting the stroke and the optimal time to screen is unknown. Meader et
team to erroneously diagnose a patient with PSD. Emotional al performed subgroup analyses by time frame after stroke and
lability can be frustrating for the patient and family; however, found that 6 scales had sufficient data for meta-analysis in the
symptoms typically decline over time and do not require treat- acute (eg, hospital setting and within 6 months of stroke) set-
ment for depression.75 ting: Geriatric Depression Scale 15 (GDS 15), Montgomery
Screening is useful for prevalent conditions that can be Asberg Depression Rating Scale, HDRS, Hospital Anxiety
effectively treated but not readily detected without screen- and Depression Scale (HADS-Total and HADS-D), and Beck
ing. Three key factors are important to consider when deter- Depression Inventory. The HDRS had the highest sensitivity
mining whether screening is useful for PSD: (1) the validity and positive predictive value, while HADS-Total was most
and reliability of screening tools to detect PSD; (2) whether specific. There were 4 scales where meta-analysis was pos-
treatment of PSD improves depressive symptoms, QOL, func- sible in postacute (receiving outpatient or inpatient rehabilita-
tional outcomes, and mortality; and (3) whether PSD screen- tion treatment) settings: HDRS, CES-D, HADS-D, and Beck
ing improves outcomes. In this section, we address the first Depression Inventory. CES-D had the highest positive predic-
and third points. The second point will be addressed in the tive value and the highest utility for screening, followed by
following section on management. the HDRS.58 One must also take into account the feasibility of
depression screening.
Screening Tools for PSD Implication for Clinical Practice
The optimal screening tool for PSD remains unclear. Meader In summary, 24 studies (n=2907 participants) showed that the
et al conducted a meta-analysis to determine which screening CES-D, HDRS, and PHQ-9 had high sensitivity for detecting
tools were most accurate for detecting PSD.58 They included PSD; however, the studies had several limitations, including
studies through November of 2012 (24 studies; n=2907 par- generalizability.
ticipants). Limitations included significant heterogeneity
between studies, narrow inclusion and exclusion criteria, not Effects of Screening for PSD on Outcomes
reporting stroke type (ischemic vs hemorrhagic), inadequate The controversy surrounding routine screening for PSD lies
reporting of blinding of assessments, not reporting predefined in the third question: does screening for PSD improve out-
cutoffs, rarely comparing multiple tools in the same popula- comes? In the primary care setting, initial RCTs found little
tion, not assessing scales in different languages, race/ethnic if any benefit from screening for depression64–67; although
groups, and cultures, and lack of information concerning screening improved recognition and treatment, it did not
dropout. Overall, the 20-item Center of Epidemiological improve depressive symptoms or outcomes. Subsequent
Studies-Depression Scale (CES-D) (sensitivity: 0.75; 95% RCTs showed that depression screening in combination
CI, 0.60–0.85; specificity: 0.88; 95% CI, 0.71–0.95), 21-item with a collaborative care intervention—a multiprofessional
Hamilton Depression Rating Scale (HDRS) (sensitivity: 0.84; approach to patient care involving a structured patient man-
95% CI, 0.75–0.90; specificity: 0.83; 95% CI, 0.72–0.90), agement plan and interventions, scheduled patient follow-ups,
and 9-item Patient Health Questionnaire (PHQ-9) (sensitiv- and enhanced interprofessional communication—improved
ity: 0.86; 95% CI, 0.70–0.94; specificity: 0.79; 95% CI, 0.60– outcomes.68 Collaborative care for depression can include a
0.90) appeared to be the optimal measures for screening. variety of interventions from the simple (telephone calls to
Although CES-D and HDRS had high sensitivity, they may encourage medication compliance) to the complex (intensive
not be feasible in a busy clinical practice, and PHQ-9 may be follow-up including structured complex psychosocial inter-
more pragmatic. PHQ-2 performed poorly (sensitivity 0.79; ventions). Studies that are based in primary care have shown
95% CI, 0.55–0.92; specificity 0.76; 95% CI, 0.62–0.85). that essential elements of collaborative care programs are the
It is important to note, however, that there are 2 versions of use of evidence-based protocols for treatment, structured col-
the PHQ-2. The yes/no version, developed in 1997, which laboration between primary care providers and mental health
specialists, active monitoring of adherence to treatment health support when there is suspicion for depression or mal-
and of outcomes, and (in some cases) structured programs adaptive behavior.
of psychotherapy delivered in primary care.69 In nonstroke
populations, collaborative care programs have resulted in Management and Prevention of PSD
improved control of depression70 and comorbid illness68 in a
Management: Pharmacotherapy to Treat PSD
cost-effective manner.71 On the basis of this evidence, the US
Few RCTs have examined the efficacy of antidepressants to
Preventive Services Task Force recommends routine screen-
treat PSD. These RCTs were heterogeneous, typically had
ing for depression in primary care settings where adequate
small sample sizes, often were of short duration, and varied
systems are in place to ensure accurate diagnosis, effective
in critical aspects of their design including characteristics of
treatment, and appropriate follow-up.72
the study population, method for screening and diagnosing
The studies of PSD screening combined with collabora-
PSD, and operational definitions of primary and secondary
tive care in populations with stroke are scarce and small. The
outcomes. Rather than relying on a structured psychiatric inter-
AIM (Activate-Initiate-Monitor) RCT (N=188) used a care
view and established diagnostic criteria, many pharmacother-
management strategy (n=89 at 12 weeks) in which nurse care
apy trials defined PSD with an arbitrary cutoff score on a scale
managers supervised by study physicians used psychoeduca-
measuring the severity of depressive symptoms. Furthermore,
tional sessions to Activate survivors and families to understand the RCT that enrolled the greatest number of patients with
depression and accept treatment, Initiate antidepressant treat- PSD to date (n=285) did not use a rigorous operational diag-
ment, and Monitor treatment with scripted bimonthly telephone nosis of depression to ascertain cases.82 Most trials excluded
calls. The control condition (n=93 at 12 weeks) was usual care individuals with aphasia, cognitive impairment and psychi-
with the same number of telephone sessions that focused only atric comorbidity, limiting their generalizability. In addition,
on recognition and monitoring of stroke symptoms and risks. patients with PSD were enrolled at different times after an
Remission (HDRS<8) was achieved in 39% vs 23% (P=0.01) index stroke, although clinical correlates of depression vary
favoring the intervention group. Reduction of depression symp- with time, affecting the probability of response. Treatment
toms (HDRS<8 or a 50% reduction in scores from baseline) objectives have been vague; few of the RCTs provided a clear
was achieved in 51% versus 30% (P=0.005), favoring the inter- definition of what they considered remission or response and
vention group.73 Although another study (n=652) revealed that consequently failed to report their respective rates.
implementation of clinical improvement teams increased the A meta-analysis by Hackett et al83 tried to overcome these
diagnosis and provision of treatment for PSD, the presence or shortfalls while reviewing 12 RCTs of the efficacy of antide-
absence of depression was not measured as an outcome.74
pressant medication to treat PSD (n=1121). Given the limi-

Other facts to consider are costs associated with screen- tations described above, the authors were mostly restricted
ing, the yield of systematic screening (ie, will it identify to providing a narrative review of the available evidence.
more cases than would be identified without routine screen- Nonetheless, the data suggested a beneficial effect of antide-
ing), and whether treatment of depression in those who pressants on remission (pooled OR for meeting criteria for
may have been missed without screening (ie, milder cases) depression: 0.47; 95% CI, 0.22–0.98) and response, measured
is effective. Although multiple guidelines recommend rou- as a >50% reduction in mood scores (pooled OR, 0.22; 95%
tine screening for depression in poststroke patients,75–79 it CI, 0.09–0.52). Adverse events were more frequent among
is important to note that the guidelines were not developed those subjects who received the active medication compared
on the basis of RCT evidence showing that PSD screening with those who received placebo. These included central ner-
improves outcomes. vous system side effects (OR, 1.96; 95% CI, 1.19–3.24), gas-
trointestinal side effects (OR, 2.37; 95% CI, 1.38–4.06) and
Implication for Clinical Practice
other side effects (OR, 1.51; 95% CI, 0.91–2.34). There were
Systematic screening for PSD may improve outcomes, pro-
insufficient trials of each of the antidepressants to conduct
vided that processes are in place to assure accurate diagno-
meta-analyses by antidepressant. Since the aforementioned
sis, timely and effective treatment, and follow-up. Further
systematic review, there have been no new publications of
research is needed to determine whether screening for PSD— double-blinded, placebo-controlled trials examining the effi-
in conjunction with collaborative care to ensure timely inter- cacy of pharmacological agents to treat PSD, with the excep-
vention, treatment, and follow-up—improves outcomes in tion of a trial of nefiracetam that proved to be equivalent to
diverse populations of stroke survivors. placebo in treating PSD.84
The available evidence on the efficacy of psychostimu-
Depression in Caregivers lants is mostly limited to case reports and open label trials.
Caregivers are also at particular risk for depression and declin- Methylphenidate may be useful in inpatient settings or when
ing health. Depression rates of stroke caregivers may even promptness of response is required. A small RCT (n=21) of
exceed that of stroke patients.80 Risk factors include older its efficacy was conducted in the late 1990s in stroke rehabili-
age of caregiver, stroke severity, and spouse compared with tation settings. When compared to placebo, methylphenidate
next of kin. Caregivers who experience strain associated with significantly reduced the severity of depressive symptoms and
caring for a disabled elderly person are at increased risk of was associated with improved motor recovery.85 Stimulants
mortality themselves.81 The members of the stroke care team have been used to augment partial responses to SSRIs, espe-
should also be cognizant of the caregiver and offer mental cially in the presence of residual cognitive impairments or
fatigue; however, given their cardiovascular side effects and psychosocial nurse practitioners about behavioral observation,
potential for inducing reversible vasoconstriction syndrome, information about adapting to stroke and mood, and problem
larger, adequately powered RCTs, with long-term follow-up solving, versus usual care (n=53) including follow-up with their
are needed to determine whether they are effective in improv- own provider and informational literature from the American
ing outcomes after stroke. Stroke Association. Antidepressants were recommended by the
participants’ providers for both groups. Remission or greater
reduction in depression symptoms was achieved more often
In summary, 12 trials (n=1121) suggested that antidepressant
in the intervention group than usual care at all time points
medications may be effective in treating PSD; further research
(9 weeks, 6 months, and 1 year). Remission (HDRS ≤9) was
is needed to determine optimal timing, threshold, and medica-
47% versus 19% (P=0.001) at 9 weeks and 48% versus 27%
tions for treatment.
(P=0.031) at 1 year, both favoring intervention.87
A second Living Well With Stroke Study (N=100)
Management: Neuromodulation included participants with ischemic and hemorrhagic stroke,
Preliminary evidence (n=92 patients) from a small RCT sug- had a shortened intervention (6 sessions), and compared in-
gested that noninvasive brain stimulation techniques such as person versus telephone delivery versus usual care. HDRS
repetitive transcranial magnetic stimulation might be effective scores were reduced by 42% (telephone) and 40% (in person)
among depressed stroke patients who do not respond to a trial immediately after intervention compared with 30% for usual
with antidepressants.86
care. Although this difference favored the intervention, it was
There are no RCTs of electroconvulsive therapy in stroke
not significant. By 12 months after intervention, there was
survivors with PSD; however, electroconvulsive therapy has
no significant difference among the 3 conditions, with all 3
been used as a last resort to treat refractory PSD.83 Treatment
groups achieving a 40% reduction in scores.88
should be started at the lowest effective energy levels, using
The findings of the Living Well With Stroke Study RCTs
pulsatile currents, increased spacing of treatments (2–5 days
were supported by a much smaller, multifaceted intervention,
between treatments), and fewer treatments in an entire course
conducted during rehabilitation.90 Twenty-four patients with
(ie, 4–6). Nondominant unilateral electroconvulsive therapy is
ischemic or hemorrhagic stroke in a rehabilitation hospital
the preferred technique.
were randomly assigned to receive 12 weekly sessions of eco-
In summary, further studies are needed to determine the
system-focused therapy (n=12), which emphasized a family-
efficacy of neuromodulation on treating PSD.
focused, problem-solving identification of valued activities
and coordination of therapies. The comparison group (n=12)
Management: Psychosocial Interventions had 12 weekly sessions focused on education about stroke and
to Treat PSD depression and reviewed written materials. Participants were
A Cochrane review and meta-analysis first published in 2004 included in the trial based on the PHQ-9, with depression
and updated in 2008 (3 trials including 445 participants) indi- diagnosis confirmed by Diagnostic and Statistical Manual of
cated a paucity of well-designed trials of psychosocial inter- Mental Disorders, 4th Edition criteria and depression severity
ventions for the treatment of PSD with no evidence of benefit measured by HDRS scores. At week 12, 66.7% of the ecosys-
of psychotherapy (cognitive behavioral therapy, motivational tem focused therapy participants had achieved remission of
interviewing, a supportive psychological intervention) over depression (HDRS<10), which was significantly greater than
control conditions for treating PSD. Several ongoing trials the 16.7% achieving remission in the control group.90
were identified in that review,83 4 of which have been pub- The CALM trial (Communication and Low Mood)
lished since 2007. Three of these individual trials indicated (N=105)89 randomized stroke survivors with aphasia to receive
a benefit of brief psychosocial therapies for established PSD up to 20 1-hour sessions of behavioral therapy over 3 months
and for prevention. (n=51), delivered by an assistant psychologist supervised
Two RCTs included people with ischemic stroke screened by a clinical psychologist and supported by an intervention
for depressive symptoms within 1 to 4 months after stroke. The manual developed from studies of cognitive behavioral ther-
diagnosis of major or minor depression was confirmed with a apy or usual care (n=54). Mean Stroke Aphasic Depression
structured clinical interview consistent with the Diagnostic Questionnaire scores decreased from baseline to 6 months by
and Statistical Manual of Mental Disorders, 4th Edition crite- 6 points in the intervention group compared with an increase
ria87,88 or the Stroke Aphasic Depression Questionnaire 10-item of 1.9 points in the control group. When baseline values and
hospital version (cutoff ≥6) or the visual analogue sad item communication impairment were controlled for, participants
(cutoff ≥50) completed by a nurse, relative, or caregiver.89 The in the intervention group had improved mood compared with
primary outcome of depression was measured using HDRS at controls (P=0.002).89
9 weeks, 6 months, and 1 year87,88 in 2 trials by outcome asses- These 4 trials of 330 participants were relatively small,
sors masked to the participant’s study group and uninvolved and 3 were conducted at single institutions, but the reduction
in the treatment, and at 3 and 6 months after randomization in depression results were consistent with the exception of the
using the Stroke Aphasic Depression Questionnaire 21-item second Living Well With Stroke Study.
hospital version completed by a relative or caregiver.89
In the Living Well With Stroke Study (N=101),87 ischemic Implication for Clinical Practice
stroke survivors were randomized to a brief psychosocial inter- In summary, 7 trials (n=775) suggest that brief psychosocial
vention (n=48), which comprised 9 sessions of counseling by interventions may be useful and effective in treatment of PSD.
Whether antidepressant medication is a necessary or benefi- to assess the effect of self-management teaching on PSD inci-
cial adjuvant cannot be established from these trials because dence and outcomes.
of a lack of placebo controls. In summary, few studies have assessed the effectiveness
of self-management strategies on PSD; further studies are
Management: Stroke Liaison Workers needed to determine whether these strategies are beneficial.
Stroke liaison workers provide services including education,
information provision, social support, and liaison with other ser- Prevention of PSD Using Pharmacological
vices. A systematic review of 15 interventions (2743 participants) Interventions
in unselected groups of stroke survivors (ie, trials were not limited PSD is a disorder in which the ratio between recent incidence
to people with or without depression) did not show any evidence and prevalence is high (ie, high influx disorder).95 Given the
of a beneficial effect from stroke liaison workers on depres- high prevalence and association with functional impairment,
sion, when compared with controls (standardized mean reduc- poor QOL, and increased morbidity and mortality, PSD is an
tion in depression scores, −0.04; 95% CI, −0.12 to 0.04).91 ideal target for selective prevention.
Salter et al performed a meta-analysis summarizing the
Implication for Clinical Practice findings of 8 RCTs (from 1990 through 2011) assessing the
In summary, 15 trials (n=2743) have not revealed a beneficial efficacy of preventive pharmacological interventions among
effect from stroke liaison workers on PSD; however, the tri- 776 initially nondepressed stroke patients.96 Pooled analyses
als included individuals without a diagnosis of PSD. Further revealed that the likelihood of developing PSD was reduced
studies are needed to determine the effect of liaison worker on among patients receiving active pharmacological treatment
those with established PSD. (OR, 0.34; 95% CI, 0.22–0.53), especially after a 1 year treat-
ment (OR, 0.31; 95% CI, 0.18–0.56), and with the use of an
Management: Information Provision SSRI (OR, 0.37; 95% CI, 0.22–0.61). The most commonly
In a systematic review of studies assessing the effectiveness reported side effects were nausea, diarrhea, fatigue, and dizzi-
of information provision strategies in improving outcomes in ness. There were no significant differences between the active
stroke survivors (17 RCTs; n=2831), 12 trials evaluated the treatment and placebo groups in the frequency of these symp-
effect of passive or active information provision on depression. toms. Only tremor was significantly associated with sertraline
Dichotomous data were available for 956 of 1280 participants in 1 of the RCTs.96 This review included 2 publications from
from 8 trials and revealed no significant difference on depres- the same cohort and an open trial (drug vs usual care). These
sion. Continuous data were available for 720 of 1016 partici- review results are contrary to an earlier 2008 Cochrane sys-
pants in 7 trials and showed a small benefit of information tematic review including 12 placebo-controlled trials of 611
provision on depression scores (weighted mean reduction in individuals, finding no evidence that antidepressant drugs
scores of −0.52; 95% CI, −0.93 to −0.10; P=0.01); however, prevented depression after stroke.97 The Salter meta-analysis
the clinical significance of this improvement is unclear. Active included 3 small trials40,98,99 of antidepressant medications
information provision was significantly more effective than was published after the Cochrane review, and 1 other trial has
since been published.100 All 4 trials (401 participants) showed
passive information for depression (P<0.02 for all trials), and
benefit of their respective antidepressant (fluoxetine n=59,
anxiety (P<0.05 for trials reporting dichotomous data, P<0.01
placebo n=59; milnacipran n=56, placebo n=46; paroxetine
for trials reporting continuous data).92 There was considerable
n=32, placebo n=32; and escitalopram n=59, placebo n=58)
variability in the interventions evaluated and quality of the trials.
over placebo. With the exception of the single open label trial,
Implication for Clinical Practice the studies had satisfactory methodological quality; however,
In summary, 7 trials (n=720) suggest that information provi- only 3 studies reported their mechanism for concealed alloca-
sion provides a small benefit in depression scores; however, tion, and all studies excluded those with aphasia and/or sig-
the clinical significance of this improvement is unclear. nificant cognitive impairment, limiting generalizability.
Management: Self-Management In summary, 8 trials (n=776) suggest that pharmacologi-
The US Institute of Medicine has defined self-management cal treatment may be effective in preventing PSD; however,
as “the tasks that individuals must undertake to live with further studies are needed in more representative samples of
one or more chronic conditions. These tasks include having stroke survivors, and additional study is required to determine
the confidence to deal with medical management, role man- the optimal timing and duration of treatment.
agement and emotional management of their conditions.”93
Self-efficacy, an individual’s confidence in their ability to Prevention of PSD Using Psychosocial Interventions
carry out a specific task or behavior, is a mediator in the A Cochrane review and meta-analysis first published in 2004,
causal pathway between acquiring self-management skills and updated in 2008 (4 trials including 902 participants), indi-
and enactment of self-management behaviors. A systematic cated a small but significant effect of psychosocial strategies
review without meta-analysis assessed the effectiveness of (problem-solving therapy, a broad home-based therapy, moti-
self-management strategies on depression, as a secondary vational interviewing) to prevent PSD (OR, 0.64; 95% CI,
end point, after stroke. No evidence of benefit was seen in 2 0.42–0.98).97 Limitations included considerable heterogeneity
RCTs including 303 participants.94 Further research is needed in design, analysis, and reporting of clinical trials, variable
inclusion criteria, exclusion of individuals with aphasia, cog- determine whether screening for PSD—in conjunction
nitive impairment, and previous psychiatric illness (limiting with collaborative care to ensure timely intervention,
generalizability), inadequate concealment of randomization, treatment, and follow-up—improves outcomes.
and high numbers of drop outs. In trial results published since • Conduct large, multicenter, international RCTs to iden-
the 2008 review, 1 long-term follow-up study of people with tify safe and effective treatments for PSD, optimal timing
and without high depressive symptom burden at baseline and thresholds for treatment, and to determine whether
(n=411), the group that received motivational interviewing effective treatment of PSD improves survival and other
sessions (n=204) was more likely to have normal mood (48% outcomes after stroke.
vs 38% control, OR, 1.66; 95% CI, 1.08–2.55) and to have • Determine optimal strategies to prevent PSD.
survived at 12 months (6.5% died in intervention vs 12.8%
control; OR, 2.14; 95% CI, 1.06–4.38). Formal diagnoses of Conclusions
depression were not made in this study.101 Depression is common after stroke, affecting up to one
A multisite prevention trial included pharmacological and third of stroke survivors at any one time. The natural his-
psychosocial treatment for 176 nondepressed stroke survivors tory of PSD is dynamic; however, symptoms most fre-
enrolled within 3 months of stroke. Participants were randomized quently develop in the first year. The pathophysiology of
to 1 year of treatment either with a double-blind trial of escita- PSD is poorly understood; proposed mechanisms include
lopram (n=59) versus placebo (n=58) or a nonblinded problem- psychosocial factors such as psychological response to new
solving therapy group (n=59). Those taking placebo were more disability and social isolation, as well as biological factors
likely to report clinical depression (HR, 4.5; 95% CI, 2.4–8.2) such as genetic susceptibility, inflammation, alterations in
than those who participated in the problem-solving treatment neurotrophic factors, disruption of neural networks, and
(HR, 2.2; 95% CI, 1.4–3.5) and than those taking escitalopram.99 alterations in serotonergic, noradrenergic, and dopaminergic
However, 4 of those in the escitalopram group developed new pathways. The most consistent predictors of PSD include
symptoms of major depression when the drug was discontinued physical disability, stroke severity, depression before stroke,
after 1 year, whereas no one in the placebo or problem-solving and cognitive impairment. Individuals with PSD have higher
group developed new symptoms of depression.102 healthcare use, poorer functional outcomes and QOL, and
higher mortality. Numerous screening tools are reliable in
Implication for Clinical Practice identifying depression in stroke survivors; however, fur-
In summary, 5 trials (n=1078) suggest that psychosocial thera- ther studies are needed to determine the optimal timing,
pies may prevent the development of PSD; however, the stud- setting, and follow-up for screening. Clinical trials of anti-
ies are not generalizable to all stroke survivors, given their
depressants in individuals with PSD have shown a benefi-

narrow inclusion and exclusion criteria. Further research with cial effect on depression remission and response, but trials
more rigorous methods are needed to assess the effect of psy- were limited by small samples, variable criteria for PSD,
chotherapy on prevention of PSD. and vague definitions for remission and response. Several
recent trials have indicated a benefit of brief psychosocial
Recommendations for Future Research therapies for treatment. The effect of information provision,
• Further elucidate pathophysiology of PSD, including collaborative care interventions, and clinical improvement
relative contributions of biological and psychosocial fac- teams on PSD require further study; however, preliminary
tors in the development of PSD. data suggest a benefit of the latter 2. Pharmacological and
• Determine whether the pathophysiology of early PSD psychosocial interventions have been shown to reduce the
differs from late PSD.
likelihood of developing PSD. The high prevalence and
• Assess the effect of PSD on outcomes and develop opti- poor prognosis of depression in patients with stroke sup-
mal strategies to counteract these effects.
• Further elucidate the independent effect of PSD on QOL ports a strategy of increased awareness, timely screening,
and determine how to improve QOL in individuals with and prompt evidence-based management; however, further
or at risk for PSD. studies are needed to determine the optimal timing and
• Evaluate the effect of treatment of PSD on subsequent method for screening, and ideal treatment strategy. This sci-
healthcare use. entific statement aimed to draw attention to this underrec-
• Assess the risks and benefits of routine screening for ognized, underinvestigated, and undertreated problem with
PSD and determine optimal timing, frequency, setting, the goal of summarizing current knowledge, emphasizing
and method for screening. implications for clinical practice, and recommending areas
• Conduct large, multicenter, international RCTs to for future research.
Disclosures
Writing Group Disclosures
Speakers’ Consultant/
Writing Group Research Other Research Bureau/ Expert Ownership Advisory
Member Employment Grant Support Honoraria Witness Interest Board Other
Amytis Towfighi University of Southern California None None None None None None None
Bruce Ovbiagele Medical University of South None None None None None None None
Carolina
Nada El Husseini Wake Forest University Baptist None None None None None None None
Medical Center
Maree L. Hackett The George Institute for Global None None None None None None None
Health/Royal Prince Alfred
Hospital
Ricardo E. Jorge Baylor College of Medicine None None Janssen Cilag None None None None
China*
Brett M. Kissela University of Cincinnati None None None None None None None
Academic Health Center
Pamela H. Mitchell University of Washington None None None None None None None
Lesli E. Skolarus University of Michigan NIH† University of Michigan None None None Bracket None
(Institutional Grant)† Global†
Mary A. Whooley University of California, San None None None None None None None
Francisco Department of
Veteran Affairs Medical Center
Linda S. Williams Roudebush VA Medical Center Veterans None None None None None None
Administration*
This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on
the Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be “significant” if (a) the
person receives $10 000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock
or share of the entity, or owns $10 000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under
the preceding definition.
*Modest.
†Significant.
Reviewer Disclosures
Other Speakers’ Consultant/
Research Research Bureau/ Expert Ownership Advisory
Reviewer Employment Grant Support Honoraria Witness Interest Board Other
Moira Kapral University of Toronto, None None None None None None None
Canada
Anjail Z Sharrief University of Texas None None None None None None None
Medical School at
Houston
Brian Silver Rhode Island Hospital None None None Medicolegal None None Joint Commission
expert review* (Surveyor)*;
Women’s
Health Initiative
(Adjudicator of
stroke outcomes)*;
UCSF (Adjudicator
for stroke outcomes
in SOCRATES trial)*
This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure
Questionnaire, which all reviewers are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $10 000 or more during
any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000 or
more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
*Significant.
References 24. Robinson RG, Kubos KL, Starr LB, Rao K, Price TR. Mood changes
in stroke patients: relationship to lesion location. Compr Psychiatry.
1. Hackett ML, Pickles K. Part I: frequency of depression after stroke: an
1983;24:555–566.
updated systematic review and meta-analysis of observational studies.
25. Carson AJ, MacHale S, Allen K, Lawrie SM, Dennis M, House A, Sharpe
Int J Stroke. 2014;9:1017–1025. doi: 10.1111/ijs.12357.
M. Depression after stroke and lesion location: a systematic review.
2. Kutlubaev MA, Hackett ML. Part II: predictors of depression after stroke
Lancet. 2000;356:122–126. doi: 10.1016/S0140-6736(00)02448-X.
and impact of depression on stroke outcome: an updated systematic
26. Wei N, Yong W, Li X, Zhou Y, Deng M, Zhu H, Jin H. Post-stroke depres-
review of observational studies. Int J Stroke. 2014;9:1026–1036. doi:
sion and lesion location: a systematic review. J Neurol. 2015;262:81–90.
10.1111/ijs.12356.
doi: 10.1007/s00415-014-7534-1.
3. Bartoli F, Lillia N, Lax A, Crocamo C, Mantero V, Carrà G, Agostoni
27. Yu L, Liu CK, Chen JW, Wang SY, Wu YH, Yu SH. Relationship
E, Clerici M. Depression after stroke and risk of mortality: a system-
between post-stroke depression and lesion location: a meta-
atic review and meta-analysis. Stroke Res Treat. 2013;2013:862978. doi:
analysis. Kaohsiung J Med Sci. 2004;20:372–380. doi: 10.1016/
10.1155/2013/862978.
S1607-551X(09)70173-1.
4. Hasin DS, Goodwin RD, Stinson FS, Grant BF. Epidemiology of 28. Kim JM, Stewart R, Kang HJ, Kim SW, Shin IS, Kim HR, Shin MG,
major depressive disorder: results from the National Epidemiologic Kim JT, Park MS, Cho KH, Yoon JS. A longitudinal study of SLC6A4
Survey on Alcoholism and Related Conditions. Arch Gen Psychiatry. DNA promoter methylation and poststroke depression. J Psychiatr Res.
2005;62:1097–1106. doi: 10.1001/archpsyc.62.10.1097. 2013;47:1222–1227. doi: 10.1016/j.jpsychires.2013.04.010.
5. Kessler RC, Chiu WT, Demler O, Merikangas KR, Walters EE. 29. Kim JM, Stewart R, Kang HJ, Kim SY, Kim SW, Shin IS, Park MS,
Prevalence, severity, and comorbidity of 12-month DSM-IV disorders Kim HR, Shin MG, Cho KH, Yoon JS. A longitudinal study of BDNF
in the National Comorbidity Survey Replication. Arch Gen Psychiatry. promoter methylation and genotype with poststroke depression. J Affect
2005;62:617–627. doi: 10.1001/archpsyc.62.6.617. Disord. 2013;149:93–99. doi: 10.1016/j.jad.2013.01.008.
6. Ayerbe L, Ayis S, Crichton S, Wolfe CD, Rudd AG. The natural his- 30. Kim JM, Stewart R, Kim SW, Shin IS, Kim JT, Park MS, Park SW, Kim
tory of depression up to 15 years after stroke: the South London Stroke YH, Cho KH, Yoon JS. Associations of cytokine gene polymorphisms
Register. Stroke. 2013;44:1105–1110. doi: 10.1161/STROKEAHA. with post-stroke depression. World J Biol Psychiatry. 2012;13:579–587.
111.679340. doi: 10.3109/15622975.2011.588247.
7. Hackett ML, Yapa C, Parag V, Anderson CS. Frequency of depres- 31. Spalletta G, Bossù P, Ciaramella A, Bria P, Caltagirone C, Robinson RG.
sion after stroke: a systematic review of observational studies. Stroke. The etiology of poststroke depression: a review of the literature and a
2005;36:1330–1340. doi: 10.1161/01.STR.0000165928.19135.35. new hypothesis involving inflammatory cytokines. Mol Psychiatry.
8. Ayerbe L, Ayis S, Wolfe CD, Rudd AG. Natural history, predictors and 2006;11:984–991. doi: 10.1038/sj.mp.4001879.
outcomes of depression after stroke: systematic review and meta-analy- 32. Rocco A, Afra J, Toscano M, Sirimarco G, Di Clemente L, Altieri M,
sis. Br J Psychiatry. 2013;202:14–21. doi: 10.1192/bjp.bp.111.107664. Lenzi GL, Di Piero V. Acute subcortical stroke and early serotonergic
9. Ng KC, Chan KL, Straughan PT. A study of post-stroke depression in a modification: a IDAP study. Eur J Neurol. 2007;14:1378–1382. doi:
rehabilitative center. Acta Psychiatr Scand. 1995;92:75–79. 10.1111/j.1468-1331.2007.01985.x.
10. Nys GM, van Zandvoort MJ, van der Worp HB, de Haan EH, de Kort PL, 33. Newberg AR, Davydow DS, Lee HB. Cerebrovascular disease basis
Kappelle LJ. Early depressive symptoms after stroke: neuropsychologi- of depression: post-stroke depression and vascular depression. Int Rev
cal correlates and lesion characteristics. J Neurol Sci. 2005;228:27–33. Psychiatry. 2006;18:433–441. doi: 10.1080/09540260600935447.
doi: 10.1016/j.jns.2004.09.031. 34. Noonan K, Carey LM, Crewther SG. Meta-analyses indicate asso-
11. Murphy E. Social origins of depression in old age. Br J Psychiatry. ciations between neuroendocrine activation, deactivation in neu-
1982;141:135–142. rotrophic and neuroimaging markers in depression after stroke.
12. Whyte EM, Mulsant BH. Post stroke depression: epidemiology, patho- J Stroke Cerebrovasc Dis. 2013;22:e124–e135. doi: 10.1016/j.
physiology, and biological treatment. Biol Psychiatry. 2002;52:253–264. jstrokecerebrovasdis.2012.09.008.
13. Folstein MF, Maiberger R, McHugh PR. Mood disorder as a specific 35. Hackett ML, Anderson CS. Predictors of depression after stroke: a sys-
complication of stroke. J Neurol Neurosurg Psychiatry. 1977;40: tematic review of observational studies. Stroke. 2005;36:2296–2301. doi:
1018–1020. 10.1161/01.STR.0000183622.75135.a4.
14. Burvill P, Johnson G, Jamrozik K, Anderson C, Stewart-Wynne E. 36. De Ryck A, Brouns R, Geurden M, Elseviers M, De Deyn PP,
Risk factors for post-stroke depression. Int J Geriatr Psychiatry. Engelborghs S. Risk factors for poststroke depression: identification
1997;12:219–226. of inconsistencies based on a systematic review. J Geriatr Psychiatry
15. Lieberman D, Friger M, Fried V, Grinshpun Y, Mytlis N, Tylis R, Neurol. 2014;27:147–158. doi: 10.1177/0891988714527514.
Galinsky D, Lieberman D. Characterization of elderly patients in reha- 37. Parikh RM, Robinson RG, Lipsey JR, Starkstein SE, Fedoroff JP, Price
bilitation: stroke versus hip fracture. Disabil Rehabil. 1999;21:542–547. TR. The impact of poststroke depression on recovery in activities of daily
16. Starkstein SE, Fedoroff JP, Price TR, Leiguarda R, Robinson RG. living over a 2-year follow-up. Arch Neurol. 1990;47:785–789.
Anosognosia in patients with cerebrovascular lesions. A study of caus- 38. Robinson RG, Bolla-Wilson K, Kaplan E, Lipsey JR, Price TR.
ative factors. Stroke. 1992;23:1446–1453. Depression influences intellectual impairment in stroke patients. Br J
17. Fujikawa T, Yamawaki S, Touhouda Y. Incidence of silent cerebral Psychiatry. 1986;148:541–547.
infarction in patients with major depression. Stroke. 1993;24:1631–1634. 39. Wulsin L, Alwell K, Moomaw CJ, Lindsell CJ, Kleindorfer DO,
18. Alexopoulos GS, Meyers BS, Young RC, Kakuma T, Silbersweig D, Woo D, Flaherty ML, Khatri P, Adeoye O, Ferioli S, Broderick JP,
Charlson M. Clinically defined vascular depression. Am J Psychiatry. Kissela BM. Comparison of two depression measures for predicting
1997;154:562–565. doi: 10.1176/ajp.154.4.562. stroke outcomes. J Psychosom Res. 2012;72:175–179. doi: 10.1016/j.
19. Loubinoux I, Kronenberg G, Endres M, Schumann-Bard P, Freret T, jpsychores.2011.11.015.
Filipkowski RK, Kaczmarek L, Popa-Wagner A. Post-stroke depression: 40. Chollet F, Tardy J, Albucher JF, Thalamas C, Berard E, Lamy C, Bejot Y,
mechanisms, translation and therapy. J Cell Mol Med. 2012;16:1961– Deltour S, Jaillard A, Niclot P, Guillon B, Moulin T, Marque P, Pariente
1969. doi: 10.1111/j.1582-4934.2012.01555.x. J, Arnaud C, Loubinoux I. Fluoxetine for motor recovery after acute isch-
20. Craft TK, DeVries AC. Role of IL-1 in poststroke depressive-like aemic stroke (FLAME): a randomised placebo-controlled trial. Lancet
behavior in mice. Biol Psychiatry. 2006;60:812–818. doi: 10.1016/j. Neurol. 2011;10:123–130. doi: 10.1016/S1474-4422(10)70314-8.
biopsych.2006.03.011. 41. Dam M, Tonin P, De Boni A, Pizzolato G, Casson S, Ermani M, Freo U,
21. Snaphaan L, van der Werf S, Kanselaar K, de Leeuw FE. Post-stroke Piron L, Battistin L. Effects of fluoxetine and maprotiline on functional
depressive symptoms are associated with post-stroke characteristics. recovery in poststroke hemiplegic patients undergoing rehabilitation
Cerebrovasc Dis. 2009;28:551–557. doi: 10.1159/000247598. therapy. Stroke. 1996;27:1211–1214.
22. Altieri M, Maestrini I, Mercurio A, Troisi P, Sgarlata E, Rea V, Di 42. Pariente J, Loubinoux I, Carel C, Albucher JF, Leger A, Manelfe C,
Piero V, Lenzi GL. Depression after minor stroke: prevalence and pre- Rascol O, Chollet F. Fluoxetine modulates motor performance and
dictors. Eur J Neurol. 2012;19:517–521. doi: 10.1111/j.1468-1331. cerebral activation of patients recovering from stroke. Ann Neurol.
2011.03583.x. 2001;50:718–729.
23. Robinson RG, Shoemaker WJ, Schlumpf M, Valk T, Bloom FE. Effect 43. Zittel S, Weiller C, Liepert J. Citalopram improves dexterity in chronic
of experimental cerebral infarction in rat brain on catecholamines and stroke patients. Neurorehabil Neural Repair. 2008;22:311–314. doi:
behaviour. Nature. 1975;255:332–334. 10.1177/1545968307312173.
44. Acler M, Robol E, Fiaschi A, Manganotti P. A double-blind placebo RCT 64. Dowrick C, Buchan I. Twelve month outcome of depression in gen-
to investigate the effects of serotonergic modulation on brain excitability eral practice: does detection or disclosure make a difference? BMJ.
and motor recovery in stroke patients. J Neurol. 2009;256:1152–1158. 1995;311:1274–1276.
doi: 10.1007/s00415-009-5093-7. 65. Callahan CM, Hendrie HC, Dittus RS, Brater DC, Hui SL, Tierney WM.
45. Mead GE, Hsieh CF, Lee R, Kutlubaev MA, Claxton A, Hankey GJ, Improving treatment of late life depression in primary care: a random-
Hackett ML. Selective serotonin reuptake inhibitors (SSRIs) for stroke ized clinical trial. J Am Geriatr Soc. 1994;42:839–846.
recovery. Cochrane Database Syst Rev. 2012;11:CD009286. doi: 66. Williams JW Jr, Mulrow CD, Kroenke K, Dhanda R, Badgett RG, Omori
10.1002/14651858.CD009286.pub2. D, Lee S. Case-finding for depression in primary care: a randomized
46. Naess H, Waje-Andreassen U, Thomassen L, Nyland H, Myhr KM. trial. Am J Med. 1999;106:36–43.
Health-related quality of life among young adults with ischemic stroke 67. Whooley MA, Stone B, Soghikian K. Randomized trial of case-find-
on long-term follow-up. Stroke. 2006;37:1232–1236. doi: 10.1161/01. ing for depression in elderly primary care patients. J Gen Intern Med.
STR.0000217652.42273.02. 2000;15:293–300.
47. Paolucci S, Gandolfo C, Provinciali L, Torta R, Toso V; DESTRO 68. Katon WJ, Lin EH, Von Korff M, Ciechanowski P, Ludman EJ, Young
Study Group. The Italian multicenter observational study on post-stroke B, Peterson D, Rutter CM, McGregor M, McCulloch D. Collaborative
depression (DESTRO). J Neurol. 2006;253:556–562. doi: 10.1007/ care for patients with depression and chronic illnesses. N Engl J Med.
s00415-006-0058-6. 2010;363:2611–2620. doi: 10.1056/NEJMoa1003955.
48. Christensen MC, Mayer SA, Ferran JM, Kissela B. Depressed mood 69. Simon G. Collaborative care for depression. BMJ. 2006;332:249–250.
after intracerebral hemorrhage: the FAST trial. Cerebrovasc Dis. doi: 10.1136/bmj.332.7536.249.
2009;27:353–360. doi: 10.1159/000202012. 70. Archer J, Bower P, Gilbody S, Lovell K, Richards D, Gask L,
49. Sturm JW, Donnan GA, Dewey HM, Macdonell RA, Gilligan AK, Dickens C, Coventry P. Collaborative care for depression and anxi-
Srikanth V, Thrift AG. Quality of life after stroke: the North East ety problems. Cochrane Database Syst Rev. 2012;10:CD006525. doi:
Melbourne Stroke Incidence Study (NEMESIS). Stroke. 2004;35:2340– 10.1002/14651858.CD006525.pub2.
2345. doi: 10.1161/01.STR.0000141977.18520.3b. 71. Katon W, Russo J, Lin EH, Schmittdiel J, Ciechanowski P, Ludman
50. Pan JH, Song XY, Lee SY, Kwok T. Longitudinal analysis of quality of E, Peterson D, Young B, Von Korff M. Cost-effectiveness of a mul-
life for stroke survivors using latent curve models. Stroke. 2008;39:2795– ticondition collaborative care intervention: a randomized con-
2802. doi: 10.1161/STROKEAHA.108.515460. trolled trial. Arch Gen Psychiatry. 2012;69:506–514. doi: 10.1001/
51. Williams LS, Bakas T, Brizendine E, Plue L, Tu W, Hendrie H, Kroenke archgenpsychiatry.2011.1548.
K. How valid are family proxy assessments of stroke patients’ health- 72. Siu AL, Bibbins-Domingo K, Grossman DC, Baumann LC, Davidson
related quality of life? Stroke. 2006;37:2081–2085. doi: 10.1161/01. KW, Ebell M, García FA, Gillman M, Herzstein J, Kemper AR, Krist
STR.0000230583.10311.9f. AH, Kurth AE, Owens DK, Phillips WR, Phipps MG, Pignone MP; US
52. Jia H, Damush TM, Qin H, Ried LD, Wang X, Young LJ, Williams Preventive Services Task Force (USPSTF). Screening for depression in
LS. The impact of poststroke depression on healthcare use by veter- adults: US Preventive Services Task Force recommendation statement.
ans with acute stroke. Stroke. 2006;37:2796–2801. doi: 10.1161/01. JAMA. 2016;315:380–387. doi: 10.1001/jama.2015.18392.
STR.0000244783.53274.a4. 73. Williams LS, Kroenke K, Bakas T, Plue LD, Brizendine E, Tu W,
53. Ghose SS, Williams LS, Swindle RW. Depression and other mental Hendrie H. Care management of poststroke depression: a random-
health diagnoses after stroke increase inpatient and outpatient medical ized, controlled trial. Stroke. 2007;38:998–1003. doi: 10.1161/01.
utilization three years poststroke. Med Care. 2005;43:1259–1264. STR.0000257319.14023.61.
54. Dossa A, Glickman ME, Berlowitz D. Association between mental 74. Williams LS, Ofner S, Yu Z, Beyth RJ, Plue L, Damush T. Pre-post
health conditions and rehospitalization, mortality, and functional out- evaluation of automated reminders may improve detection and manage-
comes in patients with stroke following inpatient rehabilitation. BMC ment of post-stroke depression. J Gen Intern Med. 2011;26:852–857.
Health Serv Res. 2011;11:311. doi: 10.1186/1472-6963-11-311. doi: 10.1007/s11606-011-1709-6.
55. Blanchette CM, Simoni-Wastila L, Shaya F, Orwig D, Noel J, Stuart 75. Duncan PW, Zorowitz R, Bates B, Choi JY, Glasberg JJ, Graham
B. Health care use in depressed, elderly, cardiac patients and the effect GD, Katz RC, Lamberty K, Reker D. Management of Adult Stroke
of antidepressant use. Am J Health Syst Pharm. 2009;66:366–372. doi: Rehabilitation Care: a clinical practice guideline. Stroke. 2005;36:e100–
10.2146/ajhp080092. e143. doi: 10.1161/01.STR.0000180861.54180.FF.
56. Ayerbe L, Ayis S, Rudd AG, Heuschmann PU, Wolfe CD. Natural his- 76. Miller EL, Murray L, Richards L, Zorowitz RD, Bakas T, Clark P,
tory, predictors, and associations of depression 5 years after stroke: Billinger SA; on behalf of the American Heart Association Council on
the South London Stroke Register. Stroke. 2011;42:1907–1911. doi: Cardiovascular Nursing and the Stroke Council. Comprehensive over-
10.1161/STROKEAHA.110.605808. view of nursing and interdisciplinary rehabilitation care of the stroke
57. Ayerbe L, Ayis S, Crichton SL, Rudd AG, Wolfe CD. Explanatory factors patient: a scientific statement from the American Heart Association.
for the increased mortality of stroke patients with depression. Neurology. Stroke. 2010;41:2402–2448. doi: 10.1161/STR.0b013e3181e7512b.
2014;83:2007–2012. doi: 10.1212/WNL.0000000000001029. 77. Intercollegiate Stroke Working Party. National Clinic Guideline for
58. Meader N, Moe-Byrne T, Llewellyn A, Mitchell AJ. Screening for post- Stroke. 4th ed. London: Royal College of Physicians; 2012.
stroke major depression: a meta-analysis of diagnostic validity stud- 78. Stroke Foundation of New Zealand and New Zealand Guidelines Group,
ies. J Neurol Neurosurg Psychiatry. 2014;85:198–206. doi: 10.1136/ Clinical Guidelines for Stroke Management 2010. Wellington, New
jnnp-2012-304194. Zealand: Stroke Foundation of New Zealand; 2010.
59. Whooley MA, Avins AL, Miranda J, Browner WS. Case-finding instru- 79. National Stroke Foundation. Clinical Guidelines for Stroke Management.
ments for depression. Two questions are as good as many. J Gen Intern Melbourne, Australia: National Stroke Foundation; 2010.
Med. 1997;12:439–445. 80. Berg A, Palomäki H, Lönnqvist J, Lehtihalmes M, Kaste M. Depression
60. Turner A, Hambridge J, White J, Carter G, Clover K, Nelson L, Hackett among caregivers of stroke survivors. Stroke. 2005;36:639–643. doi:
M. Depression screening in stroke: a comparison of alternative measures 10.1161/01.STR.0000155690.04697.c0.
with the structured diagnostic interview for the diagnostic and statisti- 81. Schulz R, Beach SR. Caregiving as a risk factor for mortality: the
cal manual of mental disorders, fourth edition (major depressive epi- Caregiver Health Effects Study. JAMA. 1999;282:2215–2219.
sode) as criterion standard. Stroke. 2012;43:1000–1005. doi: 10.1161/ 82. Ohtomo E, Hirai S, Terashi A, Hasegawa K, Tazaki Y, Araki G, Ito E,
STROKEAHA.111.643296. Nishimura T and Furukawa T. Clinical evaluation of aniracetam on psy-
61. de Man-van Ginkel JM, Hafsteinsdóttir T, Lindeman E, Burger H, Grobbee D, chiatric symptoms related to cerebrovascular disease. J Clin Exp Med.
Schuurmans M. An efficient way to detect poststroke depression by subse- 1991;156:143–187.
quent administration of a 9-item and a 2-item Patient Health Questionnaire. 83. Hackett ML, Anderson CS, House A, Xia J. Interventions for treating
Stroke. 2012;43:854–856. doi: 10.1161/STROKEAHA.111.640276. depression after stroke. Cochrane Database Syst Rev. 2008:CD003437.
62. Williams LS, Brizendine EJ, Plue L, Bakas T, Tu W, Hendrie H, Kroenke K. 84. Robinson RG, Jorge RE, Clarence-Smith K. Double-blind randomized
Performance of the PHQ-9 as a screening tool for depression after stroke. treatment of poststroke depression using nefiracetam. J Neuropsychiatry
Stroke. 2005;36:635–638. doi: 10.1161/01.STR.0000155688.18207.33. Clin Neurosci. 2008;20:178–184. doi: 10.1176/jnp.2008.20.2.178.
63. McManus D, Pipkin SS, Whooley MA. Screening for depression in 85. Grade C, Redford B, Chrostowski J, Toussaint L, Blackwell B.
patients with coronary heart disease (data from the Heart and Soul Study). Methylphenidate in early poststroke recovery: a double-blind, placebo-
Am J Cardiol. 2005;96:1076–1081. doi: 10.1016/j.amjcard.2005.06.037. controlled study. Arch Phys Med Rehabil. 1998;79:1047–1050.
86. Jorge RE, Moser DJ, Acion L, Robinson RG. Treatment of vascular 94. Jones F, Riazi A. Self-efficacy and self-management after stroke: a
depression using repetitive transcranial magnetic stimulation. Arch systematic review. Disabil Rehabil. 2011;33:797–810. doi: 10.3109/
Gen Psychiatry. 2008;65:268–276. doi: 10.1001/archgenpsychiatry. 09638288.2010.511415.
2007.45. 95. Beekman AT, Smit F, Stek ML, Reynolds CF 3rd, Cuijpers PC. Preventing
87. Mitchell PH, Veith RC, Becker KJ, Buzaitis A, Cain KC, Fruin M, depression in high-risk groups. Curr Opin Psychiatry. 2010;23:8–11.
Tirschwell D, Teri L. Brief psychosocial-behavioral intervention doi: 10.1097/YCO.0b013e328333e17f.
with antidepressant reduces poststroke depression significantly more 96. Salter KL, Foley NC, Zhu L, Jutai JW, Teasell RW. Prevention of
than usual care with antidepressant: living well with stroke: ran- poststroke depression: does prophylactic pharmacotherapy work?
domized, controlled trial. Stroke. 2009;40:3073–3078. doi: 10.1161/ J Stroke Cerebrovasc Dis. 2013;22:1243–1251. doi: 10.1016/j.
STROKEAHA.109.549808. jstrokecerebrovasdis.2012.03.013.
88. Kirkness CJ, Becker KJ, Cain KC, Kohen R, Tirschwell DL, Teri L, 97. Hackett ML, Anderson CS, House A, Halteh C. Interventions for
Veith RR and Mitchell PH. Telephone versus in-person psychosocial preventing depression after stroke. Cochrane Database Syst Rev.
behavioral treatment in post-stroke depression. Stroke. 2015;46(suppl 1): 2008:CD003689.
AWP125. 98. Tsai CS, Wu CL, Chou SY, Tsang HY, Hung TH, Su JA. Prevention
89. Thomas SA, Walker MF, Macniven JA, Haworth H, Lincoln NB. of poststroke depression with milnacipran in patients with acute
Communication and Low Mood (CALM): a randomized controlled trial ischemic stroke: a double-blind randomized placebo-controlled
of behavioural therapy for stroke patients with aphasia. Clin Rehabil. trial. Int Clin Psychopharmacol. 2011;26:263–267. doi: 10.1097/
2013;27:398–408. doi: 10.1177/0269215512462227. YIC.0b013e32834a5c64.
90. Alexopoulos GS, Wilkins VM, Marino P, Kanellopoulos D, Reding 99. Robinson RG, Jorge RE, Moser DJ, Acion L, Solodkin A, Small SL,
M, Sirey JA, Raue PJ, Ghosh S, O’Dell MW, Kiosses DN. Ecosystem Fonzetti P, Hegel M, Arndt S. Escitalopram and problem-solving therapy
focused therapy in poststroke depression: a preliminary study. Int J for prevention of poststroke depression: a randomized controlled trial.
Geriatr Psychiatry. 2012;27:1053–1060. doi: 10.1002/gps.2822. JAMA. 2008;299:2391–2400. doi: 10.1001/jama.299.20.2391.
91. Ellis G, Mant J, Langhorne P, Dennis M, Winner S. Stroke liaison work- 100. Xu J, Wang J, Liu J. Preventive effects of antidepressants on post-stroke
ers for stroke patients and carers: an individual patient data meta-analy- depression. Chin Ment Health J. 2006;20:186–188.
sis. Cochrane Database Syst Rev. 2010:CD005066. 101. Watkins CL, Wathan JV, Leathley MJ, Auton MF, Deans CF, Dickinson
92. Smith J, Forster A, Young J; Cochrane Group for information provi- HA, Jack CI, Sutton CJ, van den Broek MD, Lightbody CE. The
sion after stroke. Cochrane review: information provision for stroke 12-month effects of early motivational interviewing after acute stroke:
patients and their caregivers. Clin Rehabil. 2009;23:195–206. doi: a randomized controlled trial. Stroke. 2011;42:1956–1961. doi: 10.1161/
10.1177/0269215508092820. STROKEAHA.110.602227.
93. Parke HL, Epiphaniou E, Pearce G, Taylor SJ, Sheikh A, Griffiths 102. Mikami K, Jorge RE, Moser DJ, Arndt S, Jang M, Solodkin A, Small SL,
CJ, Greenhalgh T, Pinnock H. Self-management support interven- Fonzetti P, Hegel MT, Robinson RG. Increased frequency of first-epi-
tions for stroke survivors: A systematic meta-review. PLoS One. sode poststroke depression after discontinuation of escitalopram. Stroke.
2015;10:e0131448. doi: 10.1371/journal.pone.0131448. 2011;42:3281–3283. doi: 10.1161/STROKEAHA.111.626507.

Guideline AVC 2

Uploaded by

Copyright:

Available Formats

Guideline AVC 2

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Guideline AVC 2

Uploaded by

Copyright:

Available Formats

AHA/ASA Scientific Statement

clinical practice. (Stroke. 2017;48:e30-e43. DOI: 10.1161/STR.0000000000000113.)

D epression occurs in approximately one third of stroke

poststroke depression (PSD) is one of the most common Methods

tion based). The studies included in Hackett’s and Ayerbe’s

Table. Summary of Findings

pressant medication to treat PSD (n=1121). Given the limi-

depressants in individuals with PSD have shown a benefi-

You might also like