Poststroke Apathy

Jan Willem van Dalen, MSc; Eric P. Moll van Charante, MD, PhD; Paul J. Nederkoorn, MD, PhD;
Willem A. van Gool, MD, PhD; Edo Richard, MD, PhD

I n addition to acute motor, sensory, and language impair-

ments, subacute and chronic neuropsychiatric disturbances
after stroke can have major impact on activities of daily liv-
ing.1 Cognitive impairment and depression are the most com-
monly reported neuropsychiatric symptoms, both occurring
in approximately one third of patients after stroke.2,3 Apathy,
most commonly defined as a syndrome of diminished goal-
directed behavior, emotion, and cognition,4 is far less stud-
ied but has also been reported as a frequent consequence of
stroke. Apathy can have negative impact on functional recov-
ery, activities of daily living, general health, and quality of
life.5–7 It can also lead to significant burden for caregivers.8,9
Apathy can occur as an independent syndrome, although it
may also occur as a symptom of depression or dementia.10,11
Patients present with loss of motivation, concern, interest, and
emotional response, resulting in a loss of initiative, decreased
interaction with their environment, and a reduced interest in
social life.11–14 Despite its potentially pervasive and negative
consequences, the importance of poststroke apathy is difficult
to interpret. Differences in study design, results, and interpre-
tation have lead to a wide variety in reported characteristics,
Downloaded from http://ahajournals.org by on November 28, 2022
last updated in February 21, 2012. Titles, abstracts, and articles were
reviewed by 2 independent observers (J.W.D. and E.R.) to assess in-
clusion criteria. If necessary, full text copies of articles were obtained.
Discrepancies of the 2 separate selections were compared and were
resolved by discussion. A third investigator (P.J.N.) was available for
appeal if disagreements persisted. In addition, references of all in-
cluded articles and reviews, and key publications were searched for
studies that met inclusion criteria.
Inclusion criteria were based on recommendations by the Center
for Reviews and Dissemination.17 Studies were included if they (1)
were on patients with symptomatic stroke, (2) included at least 25
patients, (3) clearly specified a definition of apathy, (4) reported on
patient characteristics, selection process, and method of inclusion,
(5) were not restricted to specific stroke localizations, (6) were writ-
ten in a European national language, Chinese, or Japanese. If there
was >1 publication on the same patient cohort, data were taken from
the publication on the most comprehensive stroke-patient group.
Because of a lack of large studies on treatment of poststroke apa-
thy, our inclusion criteria for this research question were less strict.
Articles on the effect of pharmacological treatment of apathy were
included if they were (1) on patients with symptomatic stroke and (2)
written in English.
Data Extraction
Full text articles of selected studies were obtained for further evalua-

prevalence, and clinical impact.15,16
In this systematic review and meta-analysis, we aim to
establish the impact of poststroke apathy by assessing the
prevalence and the association with disability, depression, and
cognitive impairment. In addition, the influence of lesion loca-
tion on the occurrence of apathy and the possibilities for phar-
macological treatment are systematically reviewed.
tion. Data from each study were extracted by 2 observers (J.W.D. and
E.R.), using a predefined data extraction form (Appendix SII in the
online-only Data Supplement). Authors were contacted if published
results lacked information necessary for the meta-analyses. Risk of
bias was assessed using an assessment form based on the Newcastle–
Ottawa quality assessment scale for cohort studies, and rated selec-
tion, confounding, and information bias subitems (Appendix SIII in
the online-only Data Supplement).18

Methods Statistical Analysis

Search Strategy
We conducted a comprehensive literature search of the Medline,
PsycINFO, and Embase (from 1980 onward) databases. Methods
were predetermined in a research protocol. Key search terms for
stroke were cross-referenced to apathy, closely related, or descrip-
tive terms for apathy and psychometric instruments to assess apathy.
The full search strategy, including all search terms, is specified in
Appendix SI in the online-only Data Supplement. The search was
Analysis of statistical heterogeneity of apathy rate between studies
was done with I2 tests in every meta-analysis. Risk of publication
bias was assessed by visual interpretation of the funnel plot. The
pooled estimate of the prevalence of apathy in a stroke population
was obtained using the DerSimonian and Laird random effect binary
model. For each proportional characteristic, 95% confidence intervals
(95% CIs) were estimated using binomial distribution. When a study
provided >1 apathy rate in a single cohort (eg, at a different time since
stroke or with a different method of assessment used), we calculated

Received August 22, 2012; final revision received November 21, 2012; accepted November 28, 2012.
From the Department of Neurology (J.W.v.D., P.J.N., W.A.v.G., E.R.) and Department of General Practice (E.P.M.v.C.), Academic Medical Centre,
University of Amsterdam, Amsterdam, the Netherlands.
J. van Dalen contributed to study design, literature search, data extraction, data synthesis, data interpretation, statistical analysis, and writing; E.P. Moll
van Charante for data interpretation and writing; P.J. Nederkoorn for data synthesis, data interpretation, and writing; W.A. Gool for data interpretation and
writing; and E. Richard contributed to study design, literature search, data extraction, data interpretation, and writing.
The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA.
112.674614/-/DC1.
Correspondence to Jan Willem van Dalen, MSc, Department of Neurology, Academic Medical Centre, University of Amsterdam, Meibergdreef 15, 1105
AZ, Amsterdam, the Netherlands. E-mail j.vandalen@amc.nl
(Stroke. 2013;44:851-860.)
© 2013 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.112.674614

851
 852  Stroke  March 2013

one average apathy rate per study to include in the meta-analysis.
To identify variables associated with poststroke apathy, separate
meta-analyses were performed for age, sex, mini-mental state
examination (MMSE) score, depression, and disability at assessment.
These factors were derived from the literature. We used a binary
random effects model for analysis of the relative risk of apathy for
depressed and female patients. A continuous random effects model
with unequal within-study variance was used to estimate associations
with age, MMSE score, and disability. Because of the different scales
used to assess disability, we standardized the disability scores using
the Hedges’ G method.19 When multiple values for these factors at
different time points were provided in 1 single cohort, we calculated
one average value and standard deviation for meta-analysis. The
relationship of apathy with functional recovery and with lesion
location was assessed qualitatively.
A prespecified sensitivity analysis was designed to assess the in-
fluence of the definition of apathy used and that of suspected con-
founding variables. This analysis only included studies reporting on
all proposed explanatory variables and used methods of apathy as-
sessment recommended in an extensive review of the psychometric
evidence on the validity of available apathy measures.15 Two addi-
tional analyses were performed to explore heterogeneity of studies
in our main analysis. In the first, to determine the individual effect
of each study on the overall estimate, a range of overall apathy rates
were estimated by leaving out one study at the time, for all stud-
ies (jackknife analysis). The second analysis only included studies,
which we estimated to have a relatively low risk of confounding and
selection bias (for criteria and selected studies, see Appendix SIII
in the online-only Data Supplement). To this analysis, we added a
sensitivity analysis in which we excluded studies with an average
age below 60 years because these may not be representative for the
general stroke population.
Several further exploratory subgroup analyses were performed
on the type of assessment instrument used, source of information
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(patient-based, informant-based, or clinician-based apathy rating
scale), setting, time passed since stroke, exclusion criteria, history of
stroke, and type of stroke included. These subgroup analyses were not
prespecified but were defined during analysis to explore potential rea-
sons for large differences between study results. Univariate inverse-
varience–weighted meta-regression was used to estimate the effect
of age, depression rates, and MMSE scores on reported apathy rate.
Microsoft Office Excel 2003, PASW Statistics 18, and Meta-analyst
beta 3.13 were used for the statistical analysis.20
Results
Our search yielded 5463 articles, of which 4328 remained
after duplicate removal (Figure 1). In total, 49 research arti-
cles were selected for full text analysis. Eight full articles and
2 abstracts of case reports on treatment could be obtained.
For reference search, 27 reviews were selected of which 19
could be obtained. Searching the references yielded 1 addi-
tional article on treatment and none on prevalence (Figure 1).
After further evaluation, 24 articles on prevalence and 11 on
treatment were included in our review. Two articles reported
on apathy prevalence in the same cohort at different time
points.23,44 Results reported in these articles were combined
using size weighted averages for all analyses except for those
regarding time since stroke and population age.
Reasons for exclusion of studies are listed in Appendix SI
in the online-only Data Supplement. After quality assessment,
we included 24 articles on the prevalence of apathy.5,6,21–42
Table 1 shows the study design and demographic details of all
24 selected studies.

5463 references from electronic search

1942 from Medline
2011 from Embase
1510 from PsycINFO

1135 duplicates removed

4328 abstracts

88 selected articles
49 on prevalence
27 reviews
11 on treatment 17 articles unavailable
8 reviews
8 conference/dissertation abstracts
Treatment: Figure 1. Article selection.
1 case report
74 selected articles
41 on prevalence
19 reviews
10 on treatment

36 articles excluded after full review

1 article from references 19 reviews
1 on treatment 7 not concerning apathy
6 same cohort
4 cohort restricted to subcategory

35 articles included in review:

24 articles on prevalence
11 articles on treatment

To supplement data, 22 authors were contacted, of whom 9
were able to complement the data of 10 studies.33–42 Assessment
of the risk of bias per study is provided in Appendix SIII in the
online-only Data Supplement.
Patient characteristics and reported apathy rates can be
found in Figure 2. The total number of patients included was
2706 with a median number of 88 per study (range, 30–408
patients). The median time since stroke was 120 days (range,
2–850). The median reported average age was 65.1 years
(range, 49.6–76.6). All but 4 studies concerned prospectively
collected cohorts of stroke patients. Nine studies assessed
patients in a subacute setting within 30 days after stroke. Six
studies were done in a mixed population of in- and outpa-
tients, 4 studies were done exclusively among rehabilitating
inpatients and another 4 exclusively among outpatients. Four
articles provided longitudinal data with the length of follow-
up ranging from 6 to 16 months.6,21,31,36
The estimate for the mean prevalence of apathy across stud-
ies was 34.6% (95% CI, 29.5–40.2). Heterogeneity was mod-
erate (I2=46.4%). The funnel plot was roughly symmetrical
(Appendix SIV in the online-only Data Supplement).19 The
predefined sensitivity analysis of studies using recommended
measurement instruments (n=9),5,21,23,28,29,31,36,37,42 resulted
in an estimated prevalence of 26.3% (95% CI, 20.5–33.1;
I2=42.8%). Excluding the study identified by the funnel plot
as a major source of heterogeneity42 reduced heterogeneity
(24.2%; 95% CI, 20.4%–28.4%; I2=25.2%) (Appendix SV
in the online-only Data Supplement). Jackknife sensitivity
analysis resulted in estimates ranging from 33.2% (95% CI,
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28.5–38.3) to 35.7% (95% CI, 30.6–41.2). Sensitivity analy-
sis, including studies with low risk of selection and confound-
ing bias (n=10), resulted in a mean prevalence of 41.4% (95%
CI, 33.3–50.0) but did not reduce heterogeneity (I2=47.0%).
Excluding studies with an average patient age under 60 years
from this analysis had no significant effect (38.0%; 95% CI,
29.9–47.9; I2=46.0%; n=5).
The reported prevalence of apathy seemed to vary with
different methods of assessment used. The pooled prevalence
based on studies using informant-based assessment
instruments was lower than that of studies using patient-based
instruments, whereas that of the studies using clinician-based
instruments exceeded both (Figure 2). In studies using the
NeuroPsychiatric Inventory (NPI), a lower prevalence was
reported compared with studies using other informant-based
scales (23.0%; 95% CI, 18.4–28.2; I2=30.0% versus 39.4;
95% CI, 30.0%–49.5%; I2=45.5%). In addition, the analysis
stratified for most commonly used assessment instruments
showed significantly lower prevalence when apathy was
assessed with the NPI compared with apathy-specific
assessment instruments (Figure 2). Studies which excluded
patients with history of stroke had a lower combined estimate
compared with those including patients regardless of stroke
history (24.1%; 95% CI, 19.5–29.5; I2=22.1% versus 38.9; 95%
CI, 38.9%–44.9%; I2=46.2%) (Appendix SVI in the online-
only Data Supplement). Stratification according to study
setting revealed a relatively low prevalence and heterogeneity
in the subgroup of studies, which only included outpatients
(25.6%; 95% CI, 19.6–32.6; I2=26.9%) (Appendix SVI in the
online-only Data Supplement). Additional subgroup analyses
van Dalen et al   Poststroke Apathy   853
did not improve heterogeneity (Appendix SVI in the online-
only Data Supplement). Finally, meta-regression with age,
depression rates, and MMSE scores did not have significant
impact on the overall apathy rate (P>0.1). Associations
between apathy and its clinical correlates are reported in
Table 2. Apathetic patients were on average 3.8 years older
(95% CI, 2.1–4.7; I2=0%). Women had a slightly higher
chance of being apathetic than men (relative risk, 1.2; 95% CI,
>1.0–1.5; I2=6.6%). Other associations that are less commonly
reported are listed in Table 3.
The mean MMSE score of apathetic patients (n=10 studies)
was 2.7 points lower (95% CI, 1.6–3.8; I2=60.2%). Excluding
2 outliers identified in the funnel plot somewhat reduced
these results (2.1; 95% CI, 1.3–2.9), but significantly reduced
heterogeneity (I2=0%) (Appendix SVII in the online-only
Data Supplement).30,33 In 7 studies, a significant association
between the presence of apathy and reduced performance on
different tests of cognitive function was found.
The estimated relative risk of depression among apathetic
patients (n=11 studies) was 1.8 (95% CI, 1.3–2.4) (Table 2).
Depression occurred in 40.1% of patients with apathy (95%
CI, 29.9%–51.1%) and in 46.7% vice versa (95% CI, 36.4%–
56.3%). The prevalence of depression in the nonapathetic
patients was estimated at 23.6% (95% CI, 17.1%–31.6%). Six
studies reported a significant association between the presence
of poststroke apathy and poststroke depression.
Assessment of the relationship between apathy and disabil-
ity using Hedges’ G analysis was hampered by high heteroge-
neity (I2=81.6%). Visual assessment of the funnel plot did not
identify any single obvious cause and dichotomous stratifica-
tion based on time because stroke did not substantially improve
heterogeneity. In total, a significant association of apathy with
increased disability was reported in 9 of 11 studies. In 7 of
these, apathy was associated with concurrent increased dis-
ability (Table 1). In 2, apathy at baseline was associated with
decreased functional status at follow-up,6,33 and in another 2,
with decreased functional recovery over time.5,32
Information regarding lesion location and treatment was
assessed qualitatively. Of the 9 studies that assessed the rela-
tionship between lesion location and presence of poststroke
apathy, 6 reported on a significant association between spe-
cific lesion locations and an increased risk of apathy, although
in 1 study all significant associations disappeared after the
appropriate Bonferroni correction (Tables 4–7).23 No sig-
nificant difference was found between lacunar and cortical
infarctions.
Two clinical trials assessing the effect of pharmacological
treatment on poststroke apathy were identified, both using
apathy as secondary outcome (Tables 8 and 9). In 1 phase II
trial, significantly reduced apathy scores were found in the
group treated with 900 mg of the nootropic agent nefirace-
tam (n=22) compared with groups receiving 600 mg (n=26)
or placebo (n=22).43 In another small (n=22) open study, the
acetylcholinesterase inhibitor donepezil had a modest benefi-
cial effect on functional status, which was also associated with
a reduction in apathy score.44 In 5 case reports, a favorable
effect of treatment with bromocriptine was reported,14,45–48 and
in 3 with methylphenidate.14,49,50 Ropinirole, zolpidem, and
selegiline were reportedly beneficial in one case each.14,51,52
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Table 1. Study Characteristic Design

Major Exclusion Criteria Excluded Stroke Severity Disability at Assesment

Author Year Design Age Disab. Cog. I. Major Depr. Com. Dis. % Setting Recruitment Period Type of Stroke Apathy Criterion Depression Measure Cognition Measure Measure Mean Score Measure Mean Score

Starkstein30 1993 PC … … Yes … … 17 Subacute <1993 First IH AS > 13 (s) HDSa MMSEb … … JHFIc 6/27 (i)*
Marin28 1994 RC 45–85 Yes … … … n.r. Outpatients <1991 I AES > 38 (c) HRSD MMSE … … … …
Andersson22 1999 CC … … Yes History Yes n.a. Inpatient rehabilitation n.r. IH AES > 33 (c) MADRSa … … … … …
854  Stroke  March 2013

Angelelli21 2004 CS … Yes Yes … Yes n.r. In- and outpatients 1999–2002 First I NPI > 95 p of control (c) NPI Raven test … … FIM 85.7/10 (d)
Piamarta27 2004 PC <60 Yes … History Yes n.r. Subacute n.r. First IH Expanded PSDRS (s, i) PSDRS SPSMQ NIHSS 2.9/42 (i) BIc 79.7/100 (d)
23 a b
Brodaty 2007 PC >85 … Yes … Yes 34 In- and outpatients 1997–2000 I AES > 37 (i) SCID-1 MMSE ESS 93.5/100 (d) IADLc, ADLc 7/8, 5/6 (i)*
Carota35 2005 PC … Yes … … … 16 Inpatient 1995–1999 I EBIF nurse > 0 (c) Subjective yes or no … … … BI 80/100 (d)
Hochstenbach24 2005 PC >69 Yes … <10 years … n.r. Outpatients 1992–1996 IH Questionnaire (s, i) Questionnaire (s) … … … IADL n.r.
Caeiro33 2006 PC … … … … Yes 18 Subacute n.r. IH PSDRS (c) MADRSa MMSE NIHSS n.r. mRS n.r.
Kaji25 2006 PC … … Yes … Yes 0 Subacute 2004–2005 IH AS > 15 (s) HAM-D17a + MINI … … … … …
Hama5 2007 PC … … … History Yes 40 Inpatient rehabilitation 2002–2006 IH AS > 15 (s), NPI > 0 (i) SDS MMSE … … FIMd 77/126 (d)
Jarzebska26 2007 PC … … … … Yes 18 Subacute 2004–2005 I AS > 13 (s) HAM-D MMSEb … … … …
32
Santa 2008 PC 45–90 … Yes … Yes n.r. Inpatient rehabilitation 1999–2001 First IH AS > 15 (s) SDS MMSE NIHSS 9.2/42 (i) NIHSSd 9/42 (i)*
Greenop37 2009 PC … Yes … … Yes 90 In- and outpatients 2003–2005 IH NPI > 0 (i) NPI-i CAMCOGb … … MFAQ-IADL 2.8/8 (i)
Mayo6 2009 PC … Yes … … … 40 In- and outpatients 2003–2004 IH WBIBS (i) SF-36 MMSE telephoneb CNS 8.3/1.5 (d) SIS-physc, d 65.6/100 (d)
Hoffmann38 2010 PC 18–90 Yes Yes Current Yes 96 Inpatients 2003–2006 IH FRSBE > 65 (s, i) excluded FRSBE, CCN, WCST NIHSS 3.3/42 (i) NIHSS 3.3/42 (i)*
Onoda40 2011 PC … … … History Yes n.r. In- and outpatients 2005–2009 I AS > 15 (s) SDSa MMSEb … … mRSc 3/6 (i)
Rush29 2010 CC … … Yes … … n.a. Outpatient replicants 2005–2007 I NPI > 0 (i) BDI-II > 13 MMSE NIHSS 3.0/42 (i) BI 97/100 (d)
Sagen42 2010 PC … … Yes … Yes 43 In- and outpatients 2003–2005 IH AES > 33 (s) HADS-D MMSE (sus) … … BI 87/100 (d)
Caeiro34 2012 PC … Yes Yes … Yes 20 Subacute 2000–2002 IH AES-10 (c) MADRS MMSE NIHSS n.r. mRSd n.r.
Castellanos36 2011 PC … … Yes … … n.r. In- and outpatients 2007–2008 I NPI > 0 (i) HAM-D MMSE CNS 7.4/11.5 (d) mRSc, BI 2.0/6 (i), 79/100 (d)*

Marasco39 2011 PC … … Yes History Yes 22 Subacute 2009 First I PSDRS > 0 (c) PSDRS MMSE NIHSS 2.9/42 (i) mRS 2.8/6 (i)*
Withall31 2011 PC >85 … Yes … Yes 48 In- and outpatients 1997–2000 I AESi >37 (i) SCID-1 MMSEb ESS 89/100 (d) IADLc, ADLc 7/8, 5/6 (d)
Planton41 2012 PC 18–80 … Yes History Yes 80 Outpatients with good recovery 2007–2009 First I AS > 13 (s) BDI-II > 13 Broad cognitive testing NIHSS 2.6/42 (i) mRS 0.7/6 (i)*
CC indicates case–control; CS, cross-section; Com. Dis, communication disorder; Cog. I., cognitive impairment; Depr., depression; Disab., major disability and severe disease; First, no history of stroke; H, hemorrhage; I, infarction; n.a., not applicable; n.r., not reported; PC, prospective cohort; RC,
retrospective cohort; Apathy measures: (s), self-assessment; (c), clinician assessment; (i), informant assessment; AS, apathy scale; AES, Apathy Evaluation Scale; NPI, Neuropsychiatric Inverntory; EBIF, Emotion Behavior Index Form; PSDRS, PostStroke Depression Rating Scale; WBIBS, modified apathy items
from the Williams Brain Impairment Behavior Scale; AES-10, Apathy Evaluation Scale modified to 10 items; Depression measures: articles may have used multiple measures, the measure reported is the one used to assess the prevalence of depression used in this review: HDS, HRSD, HAM-D17, HAM-D,
Hamilton Rating Scale for Depression; MADRS, Montgomery and Asberg Depression Rating Scale; SCID, Structural Clinical Interview for DSM-IV; SDS, Zung’s Self-Rating Scale for Depression; SF-36, short form health survey; BDI-II, Beck Depression Inventory II; cognition measures: MMSE, Mini-Mental State
Examination, SPSMQ: CAMCOG, cognitive section of the Cambrdige Examination for Mental Disorders of the Elderly Revised; CCN, Coconuts neurological test; WCST, Wisconsin Card Scoring Test; MMSE (sus), MMSE taken only when patients were suspected to have cognitive impairment; stroke severity:
NIHSS, National Institutes of Health Stroke Scale; ESS, European Stroke Scale; mean, mean/maximum score; (d), score decreases with increased disability; (i), score increases with increased disability; Disability measures: (d), score decreases with disability; (i), score increases with disability; JHFI, John
Hopkins Functional Inventory; FIM, functional independence measure; IADL, Lawton Instrumental Activities of Daily Living Scale; ADL, Katz Activities of Daily Living Scale; BI, Barthel Index; mRS, modified Rankin Scale; NIHSS, National Institute of Health Stroke Score; MFAQ-IADL, Instrumental Activities of
Daily Living scale from the Multi-Dimensional Functional Assessment Questionnaire; SIS-phys, physical component of the Stroke Impact Scale; Disability score: underlined: study provided enough information for separate meta-analysis on the association between apathy and disability.
a
Significant association between apathy and depression; bsignificant association between apathy and a decrease in performance on cognitive test; csignificant association between apathy and increased disability; and dsignificant association between apathy and worse functional recovery.
 van Dalen et al   Poststroke Apathy   855

Discussion including prevalence, associated symptoms, lesion localiza-

We found that apathy occurs in every third patient after stroke.
This estimate was not importantly affected by selection and
confounding bias, time since stroke, or inclusion criteria apart
from history of stroke. Concomitant depression was present
in only 40% of apathetic patients, confirming the occurrence
of apathy as a distinct entity. Poststroke apathy is associated
with worse cognitive function. There is considerable evidence
for an association of poststroke apathy with disability and
worse outcome of rehabilitation. No clear association between
poststroke apathy and specific stroke lesion locations could be
established. Systematic trials on treatment of poststroke apathy
have not been conducted and there is currently insufficient
evidence to start any medical treatment of apathy after stroke.
Strengths and Limitations
To our knowledge, this is the first systematic review and quan-
titative analysis covering several aspects of poststroke apathy,
tion, and treatment. Several of the included studies had a high
risk of selection bias and information bias. Confounding bias
was generally low. The 3 factors that we hypothesized to be
the most influential (depression, age, and cognitive function)
were reported in all but 1 study.
Because apathy is mostly assessed as a secondary outcome,
there might be overreporting of higher prevalence rates. In
addition, significantly associated factors are more likely to
be reported, also increasing the risk of publication bias. To
minimize these shortcomings, we included all studies, includ-
ing a formal instrument to assess apathy, and tried to acquire
unpublished data by contacting the authors.
Studies differed widely in design and patient characteris-
tics. Heterogeneity was moderately high. Subgroup analy-
ses on type of stroke, method of assessment used, source
of information, and time since stroke did not substantially
consistently reduce heterogeneity. In the sensitivity analysis

Study N % Apathy 95% CI Weight Scale Age (SD) TSS (SD) Dep % Fem % MMSE

Greenop (2009) 51 11.8% 5.4-23.8 0.077 NPI i 65.7 (11.0) 90~ 45.1 33.3 26.6 (3.5)
Piamarta (2004) 33 15.2% 6.5-31.6 0.061 Apathy Q s 76.6 (7.7) 13.3 (6.8) 57.6 39.4 n.m.
Marasco (2011) 54 18.5% 10.3-31.1 0.118 PSDRS c 65.3 (10.5) 7~ 41.0 27.8 22.7 (6.8)
Rush (2010) 53 20.8% 11.9-33.7 0.126 NPI i 70 (12.0) 854 (488) 13.2 38.0 27.4 (2.4)
Santa (2008) 67 20.9% 12.8-32.3 0.16 AS s 65.4 (1.7) 49.4 (3.0) 37.3 43.3 21.9 (0.9)
Hochstenbach (2005)* 157.5 21.9% 16.1-29.0 0.39 Q i, Q s 55.3 (10.9) 300 (60) 47.0 39.5 n.m.
Starkstein (1993) 80 22.5% 14.7-32.9 0.202 AS s 59.5 (13.5) 6.2 (4.0) 33.8 46.3 22.3 (6.3)
Angelelli (2004) 124 26.6% 19.6-35.1 0.351 NPI i 60.1 (12.9) 200~ 61.3 40.4 n.m.
Marin (1994) 40 27.5% 15.9-43.2 0.115 AES c 68.3 608~ 32.5 45,0 26 (3.5)
Brodaty/Withall (2007)** 120.5 28.2% 20.9-36.9 0.353 AES i 72.2 (8.8) 280.5~ 13.7 39.3 27.3 (2.4)
Castellanos (2011)* 75.25 28.6% 19.5-39.7 0.222 NPI i 70.0 (11.9) 61.1 45.8 48.3 22.9 (8.8)
Planton (2012) 60 35,0% 24.1-47.8 0.198 AS s, NPI i 59.7 (14) 109 (20) 3.3 35.0 n.m.
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Onoda (2011) 102 36.3% 27.5-46.0 0.341 AS s 73.0 (11.6) 11.75 12.7 44,0 23.7 (4.4)
Caeiro (2012) 94 38.3% 29.1-48.5 0.322 AES-10 c 55.7 (12.9) 2.4 (1.1) 19.1 35.1 25.3 (4.0)
Kaji (2006) 92 40.2% 30.7-50.5 0.32 AS s 64.9 (11.9) 25~ 25.0 39.0 n.m.
Hama (2007)*** 243 40.3% 34.3-46.6 0.847 AS s, NPI i 65.2 (11.3) 40.7 (19.6) 32.5 34.2 24.3 (5.4)
Mayo (2009) 408 45.8% 41.1-50.7 1,466 WBIBS i 67.0 (14.6) 180~ 23 40.9 n.m.
Carota (2005) 273 47.6% 41.8-53.5 0.986 EBIF c 64.4 (15.9) 3.5 (0.7) 43.6 47.0 n.m.
Hoffmann (2010)** 75.5 47.7% 36.7-58.9 0.273 FRSBE s, i 49.9 (13.7) 30 excluded 42.3 n.m.
Sagen (2009) 85 48.2% 37.8-58.8 0.307 AES s 64.5 (13.6) 134.6 (18.4) 21.2 48.2 n.m.
Caeiro (2006) 178 51.7% 44.4-58.9 0.644 PSDRS c 56.8 (13) 2.4 (1.1) 46.1 40.4 25 (4.6)
Andersson (1999) 30 56.7% 38.8-72.9 0.107 AES c n.r. 390~ n.r. n.r. n.m.
Jarzebska (2007) 90 71.1% 60.9-79.5 0.268 AS s 53 6~ 43.3 46.7 n.m.

Subgroup: measure^ N Proportion 95% CI N studies I^2 Age TSS Dep % Fem % MMSE
NPI 577 23,0% 18.4-28.2 6 30.0% 65.2 237.9 46.3 40.7 25.3
Other 1178 36.1% 27.3-46.0 7 47.2% 62.4 106.2 34.8 341.5 24.5
AS 734 37.7% 27.3-49.3 7 46.9% 63.7 33.07 28.3 39.9 23.5
AES 369 38.8% 29.3-49.4 5 42.1% 65.2 220.5 19.3 37.7 26.4
Subgroup: source^^ N Proportion 95% CI N studies I^2 Age TSS Dep % Fem % MMSE
Informant 1314 28.6% 21.5-35.8 10 46.9% 65.9 180.5 33,0 40.6 26.1
Patient 1103 34.8% 26.2-44.6 11 47.2% 61.8 81.4 31.4 40.7 23.5
Clinician 669 40.3% 31.2-50.2 6 44.5% 61.3 56.8 39.8 39.8 24.8
Subgroup: TSS^^^ N Proportion 95% CI N studies I^2 Age TSS Dep % Fem % MMSE
TSS: < 10 858 39.7% 26.7-54.3 6 48.2% 60.9 3.7 39.8 43.2 23.8
TSS: 10<50 696 35.7% 29.6-42.3 5 40.3% 65.8 31.1 29.4 40,0 23.4
TSS :50<181 807 33.9% 24.9-44.3 6 45.9% 67.1 146.1 22.7 40.4 27,0
TSS: 181 =< 566 28.7% 21.8-36.8 6 39,0% 61.6 379.8 40,0 40.2 26,0

N Proportion 95% CI N studies I^2 Age TSS Dep % Fem %

Pooled 2586 34.6% 29.5-40.2 23 46.4% 63,5 120 31,9 40,4

0 10 20 30 40 50 60 70 80 90 100

Figure 2. Clinical characteristics. AES-10 c indicates Apathy Evaluation Scale modified to 10 items clinician assessment; AES c, Apathy Evalua-
tion Scale clinician assessment; AES i, Apathy Evaluation Scale informant assessment; AS s, apathy scale self-assessment; CI, confidence interval;
Dep, depression; EBIF c, Emotion Behavior Index Form clinician assessment; Fem, female; MMSE, Mini-Mental State Examination; n.r., measured
but not reported fully; n.m., not measured; NPI i, Neuropsychiatric Inverntory informant assessment; PSDRS c, PostStroke Depression Rating Scale
clinician assessment; Qi, questionnaire informant assessment; Qs, questionnaire self assessment; TSS, time since stroke in days; and WBIBS i,
modified apathy items from the Williams Brain Impairment Behavior Scale informant assessment. *denotes values averaged between assessments
within article; **denotes values averaged between article on baseline and article on follow-up; ***denotes assessment with the most additional infor-
mation used. Underlined: Studies provided information for separate meta-analysis on the clinical factor; Italic: additional information supplied by
author. ≈ denotes estimated value; ^ denotes multiple apathy rates allowed per study when measured with different measures; ^^ denotes multiple
rates allowed per study when measured with different sources; ^^^ denotes multiple rates allowed when measured at different time since stroke.
 856  Stroke  March 2013

Table 2. Associations With Apathy Identified by Meta-analysis

Factor Effect of Apathy No. of Studies N PSA No PSA Estimate 95% CI I 2 (%)
Poststroke apathy vs no poststroke apathy
MMSE Mean difference 10 808 268 540 −2.7 points −3.8, −1.6 60.2
Age Mean difference 13 1290 470 820 3.8 y 2.1, 4.7 0.0
Disability Hedges G (SMD) 9 627 194 433 −0.3 −0.7, 0.1 81.6
Women Relative risk 8 681 96/203 180/478 1.2 1.0, 1.5 6.6
Poststroke apathy vs poststroke depression
PSD Relative risk 14 1240 179/442 185/798 1.8 1.4–2.4 52.0
PSD in PSA Proportion 14 442 179 … 40.1% 0.3. 0.5 42.7
PSD in pop. Proportion 14 1240 179 185 28.1% 0.2. 0.4 46.1
CI indicates confidence interval; MMSE, Mini-Mental State Examination; pop., population on which information on depression in apathetic patients was available; PSA,
poststroke apathy; PSD, poststroke depression; and SMD, standardized mean difference.

regarding recommended measurement instruments, heteroge-
neity improved after exclusion of the main outlier. However,
of the 6 remaining studies, 4 used the NPI as measurement
instrument, making this result difficult to interpret. Other
sensitivity analyses, using stricter criteria, hardly affected
our results. The persistence of heterogeneity implies that sev-
eral other factors are involved that have not been taken into
consideration.
Therefore, it seems that many aspects of poststroke apa-
thy remain to be elucidated. Different methods of assessment
may lack convergent validity, measuring slightly different
conditions.15 Also, the specific range of symptoms of post-
stroke apathy may differ from what is regarded apathetic
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Studies have tried to correct for these factors by asking
patients and caregivers to score their behavior relative to
their behavior before the stroke occurred. In 3 studies, the
association between apathy and other concurrent neuropsy-
chiatric symptoms was assessed, but none were found.27,36,42
In one study, personality before stroke was assessed, and no
association with apathy was found.37 More research on the
interplay between other factors, such as fatigue and apathy,
is needed to further elucidate the nosological position of
poststroke apathy.
The heterogeneity of the results has some implications for
the generalizability of our findings. Although the weighted
average age and depression rates (Figure 2) seem representa-

behavior in other conditions (eg, Parkinson or Alzheimer tive of the general stroke population, this is only an indica-
disease). In addition, high scores on apathy scales may be tion. Apathy rates in our subgroup analyses may only differ
caused by several other factors and conditions that were not slightly from each other, but the real difference between
measured in the studies included in our review, such as post- these subgroups may be confounded by other factors that
stroke fatigue, prestroke personality traits, and cultural fac- are still unknown. Our study provides a clear example of
tors. These aspects of poststroke apathy may all be important this ecological fallacy. Although analyses of the difference
sources of the substantial heterogeneity that was found in between apathetic and nonapathetic patient groups within
this review. studies show clear relations with age, MMSE scores, and
depression rates, these results could not be significantly con-
Table 3. Significant Associations With Apathy
firmed by meta-regression or subgroup analyses. Therefore,
results gained at a group level need to be interpreted
Other Associations with caution.
Study With Apathy Association (95% CI) Test
Angelelli21 TSS > 2 mo P<0.01 ANOVA Prevalence
Castellanos 36
TSS > 4 wk P<0.05 t With a prevalence of 34.6%, poststroke apathy occurs as
Caeiro 34
Education < 10 y OR, 4.2 (1.3–13.6) Log. reg. frequently as poststroke depression (33%)2 and poststroke
Hama5 CT-defined lesion P<0.02 Mann–Whitney U dementia (21.0%–41.3%).3 Whereas these neuropsychiat-
volume ric syndromes are frequently studied and treatments often
Hochstenbach24 Low agreement κ=0.5 Kappa coefficient initiated, poststroke apathy has so far been largely ignored.
between patients and Because the prevalence of apathy in the general population
care givers is largely unknown, it is difficult to establish to which degree
Mayo6 High comorbidity on OR, 2.1 (1.0–4.3) Ord. reg. poststroke apathy should be attributed to the stroke. In healthy
Charlson Index volunteers of comparable age, apathy was found in 6.0% and
Sagen42 Comorbidity OR, 3.0 (1.0–8.3) Log. reg.
Withall31 Apathy at baseline OR, 7.2 (2.2–24.1) Log. reg.
Table 4. Association Between Apathy and Type of Stroke
with depression at
follow-up Author Type of Stroke P Test
CI indicates confidence interval; κ, kappa value; Log. reg., logistical Santa 32
Nonhemorrhagic stroke <0.05 χ2
regression; MSE, Mini-Mental State Examination; OR, odds ratio; Ord. reg.,
Caeiro34 Hemorrhagic stroke <0.03 χ2
ordinal regression; and TSS, time since stroke.
 van Dalen et al   Poststroke Apathy   857

Table 5. Association Between Apathy and Laterality of Stroke Table 6. Association Between Apathy and Region of Stroke
Lesion Lesion
Author Laterality P Test Author Region P Test
Right Subcortical
Brodaty23 Right hemisphere <0.02* t Starkstein30 Posterior internal capsule <0.05 χ2 Yates
Right frontal subcortical circuit <0.02* t Brodaty 23
Right frontal subcortical circuit <0.02* t
Left Basal ganglia
Santa32 Left basal ganglia <0.05 χ2 Hama5 Bilateral basal ganglia > right <0.01 ANOVA
Onoda40 Left basal ganglia <0.01 χ2 hemisphere > left hemisphere
> none
Bilateral
Bilateral basal ganglia > no basal <0.01 Fisher
Hama5 Bilateral basal ganglia > right <0.01 ANOVA ganglia damage
hemisphere > left hemisphere
> none Santa32 Left basal ganglia <0.05 χ2

Bilateral basal ganglia > left <0.001 Fisher Onoda40 Left basal ganglia <0.01 χ2
basal ganglia Reduced rCBF basal ganglia <0.001** ANCOVA
Onoda40 Reduced regional cerebral blood <0.001** ANCOVA FAB indicates frontal assessment battery; HDS-R, Hamilton Depression
flow in basal ganglia Rating Scale; MMSE, Mini-Mental State Examination; rCBF indicates regional
FAB indicates frontal assessment battery; HDS-R, Hamilton Depression cerebral blood flow; and SDS, Zung’s Self-Rating Scale for Depression.
Rating Scale; MMSE, Mini-Mental State Examination; rCBF, regional cerebral *Corrected for age, no longer significant when Bonferroni correction was
blood flow; and SDS, Zungs Self-rating Depression Scale. applied; **corrected for age, sex, MMSE, HDS-R, FAB, SDS, and false discovery
*Corrected for age, no longer significant when Bonferroni correction was applied; ratio.
**corrected for age, sex, MMSE, HDS-R, FAB, SDS, and false discovery ratio.
may importantly contribute to the decrease in reported apathy
in 15.8% 5 years later.53 In another study, a community-based prevalence over time.
sample of elderly, a prevalence of 19.9% was found.54 This
suggests that not all cases of poststroke apathy are directly Associated Symptoms
attributable to the stroke, although its prevalence is higher in The association between apathy and age has also been
patients with a history of multiple strokes. reported in the general population.53,55 Possibly, poststroke
apathy occurs more frequently in patients with reduced
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The average estimate of studies using informant-based

assessment instruments seems to be lower and that of studies
using clinician-based instruments higher than the average esti-
mate of studies using patient-based assessment instruments.
Use of the NPI leads to a lower estimated apathy prevalence
compared with other scales. Results of a study that estimated
the prevalence of apathy at 19.2% using the NPI and at 41.4%
using the AS in the same cohort confirm this finding.5 The
relatively low apathy rate found in studies using informant-
based instruments may be explained by the NPI being the
most used informant-based instrument. Studies using a dif-
ferent informant-based instrument found a relatively high
apathy rate (39.4% versus 23.0%) (Figure 2).6,23,24,31 The
NPI uses 1 to 3 dichotomous (yes/no) screening questions
to establish the presence of apathy, which may increase the
threshold of its diagnosis (ie, through reluctance to describe
oneself or someone else as being apathetic). Apathy rates are
reported to be rather stable over time in longitudinal stud-
ies,6,31 sometimes after a significantly lower prevalence in
the first months after stroke.21,36 There were insufficient data
for pooling the results of longitudinal studies separately.
Stratification of studies according to the average time since
stroke shows that reported apathy rates were generally lower
in studies with assessment later after stroke. This is probably
owing to differences in study design. In studies with assess-
ment early after stroke, clinician-based instruments, which
estimate higher apathy rates, were used relatively often. In
contrast, studies in which patients were assessed longer after
stroke predominantly used informant-based instruments,
which estimate relatively low apathy rates. This difference
cognitive function, which is more common in older indi-
viduals in both the general and the poststroke population.3,55
The difference we observed in MMSE scores between apa-
thetic and nonapathetic patients after stroke supports this
hypothesis.
The association between apathy and reduced cognitive
function was also reported in studies that used more extensive
neuropsychological examination.6,37 This association could, in
turn, be confounded by age,3,55 for which the analysis was cor-
rected in only 1 study.6 The relationship between poststroke
apathy and cognitive impairment may be explained by several
factors. Incapability of goal-oriented thinking and behavior
may lead to loss of interest and lack of effort in cognitive test-
ing.56,57 Also, both apathy and cognitive impairment could be a
consequence of the same underlying brain damage. Lesions in
distant areas related to memory and learning and their projec-
tions may influence anterior cingulate circuit function, which
is associated with motivation.58,59
Apathetic patients have an almost 2-fold risk of concur-
rent poststroke depression. Apathy can occur as a symptom
of depression,10,11 and many instruments to assess depres-
sion also contain items that assess apathy. Therefore, when
Table 7. Studies that Did Not Identify any Relation Between
Apathy and the Location of the Stroke Lesion
Author Assessment P Test
Angelelli21
Laterality >0.05 ANOVA
Kaji25 Laterality 0.23 t
 858  Stroke  March 2013

Table 8. Trials Regarding Treatment of Poststroke Apathy

Author Year Design Main Outcome Setting Diagnosis NI ND Intervention Dose Follow-up, wk Outcome
Robinson 43
2009 RCT Depression Outpatient PSD Modified AS 26 69 Nefiracetam 600 mg 12 ITT ANOVA: 900 mg vs
22 900 mg placebo: 4 point decrease in
AS score (P=0·01), ARR 0.18
22 … Placebo … (95 CI, 0.02–0.34), more
frequent remissions
Whyte44 2008 OT + RC CI Inpatient PSCI AES 13 41 Donepezil 5–10 mg 12 PP ANOVA: Donepezil and
decrease of apathy both
13 Galantamine 4–12 mg independently associated
PS non-CI … 98 … Control: none … 20 with an increase in FIM-gain
over time
AES indicates Apathy Evaluation Scale; ARR, absolute risk reduction; AS, apathy scale; FIM, functional independence measure; ITT, intention to treat; ND, number of
drop-outs; NI, number for intervention; OT, open trial; PP, per protocol; PSCI, patients with poststroke cognitive impairment; PSD, patients with poststroke depression; PS
non-CI, matched stroke patients without cognitive impairment; RC, retrospective cohort; and RCT, randomized controlled trial.

in studies depression is defined by a cutoff score on a depres-
sion scale, high scores on the apathy items could contribute
to misclassification of apathy as depression. Misclassification
of apathetic patients as being depressed could contribute to
the reported lack of treatment effect in poststroke depression60
because symptoms of apathy do not to respond well to selec-
tive serotonin reuptake inhibitors.14,61,62 Distinction between
isolated poststroke apathy and apathy in the context of post-
stroke depression can, therefore, have important consequences
from a clinical point of view.
Quantitative assessment of the relationship between apathy
and disability is difficult owing to very high heterogeneity
between studies. Nevertheless, an association between apathy
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association with stroke severity or lesion volume on magnetic
resonance imaging. An association with subcortical lesions,
mainly the basal ganglia, is reported most consistently. Two
studies with high prevalence of poststroke apathy (50%–55%)
described patients with subcortical infarctions, often affecting
the basal ganglia.63,64 Apathy also occurs more frequently in
other neurological conditions involving the basal ganglia (eg,
progressive supranuclear palsy, Parkinson, and Huntington
disease).65,66 These findings are in line with the hypothesis
that apathy arises from defects in the frontal subcortical cir-
cuit, of which the anterior cingulate circuit is associated with
motivation.12,58

and increased disability was reported in most of the studies. Treatment

In 2 studies, an association between apathy and increased
disability remained significant after correction for the effect
of functional status at baseline.5,6 Another study reported sig-
nificantly worse functional outcome in apathetic patients com-
pared with nonapathetic patients with comparable functional
status at baseline.32 These findings suggest a detrimental effect
of poststroke apathy on functional recovery.
Lesion Location
We found no clear association either between apathy and a
specific lesion location or hemisphere. We also did not find an
There is currently insufficient evidence to support a phar-
macological approach to treat poststroke apathy. High doses
of the nootropic agent nefiracetam showed a positive effect
on apathy as a secondary outcome in a group of poststroke
depression patients in a small controlled trial with small
treatment groups,43 but results are difficult to translate to
other poststroke populations. Evidence for an advanta-
geous effect of the acetylcholinesterase inhibitor donepe-
zil in patients with acute poststroke cognitive impairment
compared with a retrospective control group is circumstan-
tial.44 A number of case reports describing a beneficial effect

Table 9. Case Reports and Series Regarding Treatment of Poststroke Apathy

Reported Successfully
Author Year Design Main Outcome Setting Diagnosis Patients Intervention Dose Follow-up Treated
Kohno51 2010 CR Apathy Inpatient Clinician 1 Ropinirole 0.75 mg/d … 1
Marin14 1995 CS Apathy Outpatient Clinician 2 MPH/BRC, 50/90 mg/d, 5 mg 1, >2 y 2
Selegiline
Watanabe49 1995 CR Apathy Inpatient Clinician 1 MPH 5 mg/d 9 mo 1
Spiegel50 2009 CS Apathy Inpatient Clinician 3 MPH 2.5–12.5 mg/d 1 mo 3
Fong46 2001 CR Apathy n.a. n.a. 1 BRC 10 mg n.a. 1
Catsman45 1988 CR CI, apathy n.a. n.a. 1 BRC n.a. n.a. 1
Parks47 1992 CR FLS Inpatient Clinician 1 BRC 5–60 mg/d 5 mo 1
Barett48 1991 CR Abulia Inpatient Clinician 1 BRC 5–55 mg/d … 1
Mathieu 52
2011 CR Apathy Outpatient AI 1 Zolpidem … … 1
AI indicates apathy inventory; ARR, absolute risk reduction; BRC, bromocriptine; CI, cognitive impairment; CR, case report; CS indicates case series; FLS, frontal lobe
syndrome; ITT, intention to treat; MPH, methylphenidate; n.a., full article not available; and PP, per protocol.

of dopamine agonists and methylphenidate may warrant
further study.14,45–51
Implications for Clinical Practice and Future
Research
Our findings on the prevalence and clinical characteristics
of poststroke apathy in a poststroke population are clinically
relevant for adequately informing patients, caregivers, and
clinicians. Poststroke apathy is a pervasive but insufficiently
recognized neuropsychiatric symptom. The wide array of
definitions and instruments to assess apathy may provide an
important barrier for its recognition after stroke.15 Consensus
on its construct and development of a gold standard of assess-
ment is of major importance.3,11,15 Poststroke apathy is consis-
tently associated with higher rates of cognitive impairment,
depression, and disability, regardless of method of assessment.
This renders it an important symptom to be studied. Although
no effective pharmacological therapy is currently available,
rehabilitation programs could be adapted to patients’ needs.
Inadequate treatment with antidepressant drugs might be pre-
vented through improved discrimination between depression
and apathy. Research into successful treatment and coping
strategies for poststroke apathy could increase rehabilita-
tion success rates. Given its potential impact, apathy should
be included as an outcome measure in future studies on
depression, cognitive impairment, and other neuropsychiatric
sequelae of stroke. Apathy may also be an important contribu-
tor to poststroke disability and should be taken into account
in studies with a long-term follow-up of functional recovery.
Downloaded from http://ahajournals.org by on November 28, 2022
Conclusions
Apathy occurs in every third patient after stroke, often with-
out concomitant depression. Poststroke apathy is associated
with reduced cognitive function, increased disability and may
have a negative effect on rehabilitation outcome. No specific
lesion location associated with apathy could be identified.
There is currently insufficient evidence to support any specific
pharmacological treatment of poststroke apathy. Better recog-
nition could potentially benefit rehabilitation programs and
prevent inadequate treatment of depression. Some promising
treatment strategies warrant further research in randomized
controlled trials.
Acknowledgments
We thank R. Spijker and J.G. Daams from the Academic Medical
Centre, Amsterdam medical library for their help with conducting our
search. We also thank all investigators who helped supply original
data, in particular L. Caeiro (Department of Neurosciences, Servico de
Neurologia, Hospital de Santa Maria, Portugal), A. Carota (Clinique
de Genolier, Neurocentre GSMN, Switzerland), F. Castellanos-Pinedo
(Department of Neurology, Hospital Virgen del Puerto, Spain), K.
Greenop (Telethon Institute for Child Health Research, Center for
Child Health Research, University of Western Australia, Australia);
S. Hama (Division of Rehabilitation, Hibino Hospital/Department of
Neurosurgery, Hiroshima University, Japan), M. Hoffmann, (James
A. Haley Veterans’ Hospital, Tampa), A. Iavarone (Neurological and
Stroke Unit, CTO Hospital, AORN Ospedali dei Colli, Italy), K.
Onoda (Department of Neurology, Shimane University, Japan), M.
Planton and J. Pariente (Service de Neurologie, Center Hospitalier
Universitaire de Toulouse, CHU Purpan, France), and U. Sagen
(Department of Psychiatry, Telemark Hospital, Norway).
van Dalen et al   Poststroke Apathy   859
Disclosure
None.
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Key Words: apathy ◼ behavioral neurology ◼ cognitive impairment
◼ depression ◼ epidemiology ◼ neuropsychology ◼ stroke ◼ stroke recovery