Prevalence of Poststroke Cognitive Impairment

South London Stroke Register 1995–2010

Abdel Douiri, PhD; Anthony G. Rudd, FRCP; Charles D.A. Wolfe, MD

Background and Purpose—Stroke is a common long-term condition with an increasing incidence as the population ages.
This study evaluates temporal changes in the prevalence of cognitive impairment after first-ever stroke stratified by
sociodemography, vascular risk factors, and stroke subtypes, up to 15 years after stroke.
Methods—Data were collected between 1995 and 2010 (n=4212) from the community-based South London Stroke Register
covering an inner-city multiethnic population of 271 817 inhabitants. Patients were assessed for cognitive function using
Abbreviated Mental Test or Mini-Mental State Examination at the onset, 3 months, and annually thereafter. All estimates
were age adjusted to the European standard.
Results—The overall prevalence of cognitive impairment 3 months after stroke and at annual follow-up remained relatively
unchanged at 22% (24% [95% CI, 21.2–27.8] at 3 months; 22% [17.4–26.8] at 5 years to 21% [3.6–63.8] at 14 years).
In multivariate analyses, the poststroke prevalence ratio of cognitive impairment increased with older age (2% [1–3] for
each year of age), ethnicity (2.2 [1.65–2.89]-fold higher among black group) and socioeconomic status (42% [8–86]
increased among manual workers). A significant, progressive trend of cognitive impairment was observed among patients
with small vessel occlusion and lacunar infarction (average annual percentage change: 10% [7.9–12.8] and 2% [0.3–2.7],
respectively, up to 5 years after stroke).
Conclusions—The prevalence of cognitive impairment after stroke remains persistently high over time, with variations
being predominantly explained by sociodemographic characteristics. Given population growth and ageing
demographics, effective preventive strategies and poststroke surveillance are needed to manage survivors with cognitive
impairment. (Stroke. 2013;44:138-145.)
Key Words: cognitive impairment ■ long-term outcome ■ poststroke ■ prevalence ■ stroke ■ trend
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S troke is the second leading cause of death after ischemic

heart disease globally and a major cause of long-term dis-
ability.1 The nonstroke literature indicates that both cognitive
and physical disabilities have significant impacts not only on
patients, but also on families and informal caregivers.2
Patients who have had a stroke have an increased likelihood
of cognitive impairment than people who have not had a stroke.3
The short-term prevalence of poststroke dementia, including
cognitive impairment, has been reported in many studies.4–7
Most studies have used various standardized diagnostic mea-
sures, Diagnostic and Statistical Manuals of Mental Disorders
IV, or a Mini-Mental State Examination (MMSE) score of <24
as an outcome. In a systematic review of 73 articles including 21
hospital-based and 8 population-based cohorts (7511 patients),8
it was reported that the overall rates of dementia in the first year
after first-ever stroke were highly heterogeneous. Ninety-three
percent of the variance was explained by study methods and
case mix, with rates of poststroke dementia ranging from 7%
in population cohorts (2 studies, 1045 patients) in which pre-
stroke dementia has been excluded, to 41% in hospital-based
studies (4 studies, 409 patients) in which recurrent stroke and
prestroke dementia had not been excluded. However, most stud-
ies included in this review had short follow-up durations and
included small numbers of patients. Furthermore, the system-
atic review showed the limitations of the available longitudinal
studies to identify accurate prevalence in the overall population
as well as in high-risk groups9 of cognitive impairment and
dementia in poststroke survivors.
The objective of the current study is to evaluate temporal
changes and trends in the prevalence of cognitive impairment
after first-ever stroke by sociodemography, past medical his-
tory of vascular risk factors, and stroke subtypes up to 15
years of follow-up in population sample, the South London
Stroke Register (SLSR) (1995–2010).
Materials and Methods
Study Population
The SLSR is a prospective population-based stroke register set up in
January 1995, recording all first-ever strokes in patients of all ages
for an inner area of South London based on 22 electoral wards in
Lambeth and Southwark. Data collected between 1995 and 2010
were used in this analysis. The total source population of the SLSR

Received August 8, 2012; final revision received September 21, 2012; accepted September 26, 2012.
From the Division of Health and Social Care, King’s College London, London, United Kingdom; and National Institute for Health Research
Comprehensive Biomedical Research Centre, Guy’s and St Thomas’ NHS Trust and King’s College London, London, United Kingdom.
Correspondence to Abdel Douiri, PhD, Division of Health and Social Care Research, King’s College London, Capital House, 42 Weston St, London SE1
3QD, United Kingdom. E-mail abdel.douiri@kcl.ac.uk
© 2013 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.112.670844

138
 Douiri et al   Poststroke Cognitive Impairment   139
area was 271 817 individuals, self-reported as 63% white, 28% black
(9% black Caribbean, 15% black African, and 4% black other), and
9% of other ethnic group in the 2001 census.10
Case Ascertainment
Standardized criteria were applied to ensure completeness of case as-
certainment, including multiple overlapping sources of notification.
All patients with a suspected diagnosis of stroke or transient isch-
emic attack documented in different hospital and community-based
information sources were investigated for study eligibility. Patients
admitted to hospitals serving the study area were identified by regular
reviews of acute wards admitting stroke patients, weekly checks of
brain imaging referrals, and monthly reviews of bereavement offi-
cer and bed manager records. Additionally, national data on patients
admitted to any hospital in England and Wales with a diagnosis of
stroke were also screened for additional patients. To identify patients
not admitted to hospital, all general practitioners within and on the
borders of the study area were contacted regularly and asked to notify
the SLSR of stroke patients. Regular communication with general
practitioners was achieved by telephone contact and quarterly news-
letters. Referral of nonhospitalized stroke patients to a neurovascular
outpatient clinic (from 2003) or domiciliary visit to patients by the
study team was also available to general practitioners. Community
therapists were contacted every 3 months. Death certificates were
checked regularly. Completeness of case ascertainment has been esti-
mated at 88% by a multinomial-logit capture-recapture model using
the methods described elsewhere.10,11
Data Collection
Special trained study nurses and field workers collected all data pro-
spectively. A study clinician verified stroke diagnosis. The following
sociodemographic characteristics were collected at initial assessment:
self-definition of ethnic origin (census question), stratified into white,
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black (black Caribbean, black African, and black other), and other
ethnic group. Socioeconomic status was categorized as nonmanual,
manual, and economically inactive (retired and no information on
previous employment), according to the patient’s current or most re-
cent employment using the UK General Register Office occupational
codes.
Stroke was defined according to World Health Organization crite-
ria. Pathological stroke subtypes were classified using neuroradiol-
ogy or necropsy results into ischemic stroke, primary intracerebral
hemorrhage or subarachnoid hemorrhage. Ischemic strokes were
further investigated according to 2 stroke subtypes: The Oxfordshire
Community Stroke Project12 classification and the modified Trial of
Org 10172 in Acute Stroke Treatment classification. The Oxfordshire
Community Stroke Project contains 4 subtypes according to clinical
features: lacunar infarct, total anterior circulation infarcts, partial an-
terior circulation infarcts, and posterior circulation infarcts. Modified
Trial of Org 10172 in Acute Stroke Treatment denotes 5 pathogenetic
subtypes: large artery atherosclerosis, cardioembolism, small vessel
occlusion (SVO), other determined pathogenesis and no pathogenesis
identified. Data with modified Trial of Org 10172 in Acute Stroke
Treatment classification were collected only after the year 1999.
Past medical history of vascular risk factors for stroke (either self-
reported or from medical notes) were collected including smoking,
hypertension, diabetes mellitus, atrial fibrillation, ischemic heart dis-
ease (history of angina pectoris or myocardial infarction), and tran-
sient ischemic attack. Before stroke treatment of these risk factors
were also collected (antihypertensives, anticoagulants, antiplatelets,
diabetes control treatments, and cholesterol-lowering medications).
Barthel Index13 scores with a cutoff of 15 was used before and
after stroke to identify patients with moderate-to-severe disability
and Glasgow Coma Score14 dichotomized to <13 or ≥13 was used to
measure stroke severity at onset. Other case-mix indicators used for
initial stroke severity included urinary incontinence, aphasia, dyspha-
gia, visual field defects, visuospatial neglect, dysphasia, dysarthria,
hemiparesis, and cerebellar symptoms.
Cognitive state was assessed using the MMSE15 or Abbreviated
Mental Test16 in the acute phase as well as at follow-ups. Before
January 1, 2000, all assessments were conducted using the MMSE;
after January 1, 2000, the Abbreviated Mental Test was administered.
Subjects were defined as cognitively impaired according to pre-
defined cutoff points (MMSE, 24 or Abbreviated Mental Test, 8).10
Subjects who could not undergo the cognitive test, because of severe
aphasia or dysphasia or dysarthria, deafness, or visual impairment
were excluded from the study. Patients were assessed at the stroke
onset, 3 months, and annually after stroke. All follow-up assessments
included in the present study were completed by August 31, 2010.
Statistical Analysis
The prevalence of cognitive impairment was stratified by sociode-
mography, past medical history of vascular risk factor, and stroke
subtypes. Prevalence ratios (PRs) between patient groups were used
for comparison. All estimates were applied to the standard European
population using the direct method with 4 age groups 0 to 64, 65 to
74, 75 to 84, and 85+. Ninety-five percent confidence intervals of
age-standardized rates and ratios were calculated using the percentile
bootstrap technique with 10 000 replications. Multivariate analyses,
using a European age-standardized Poisson regression model with a
robust error variance, were used to assess whether changes in preva-
lence ratios at each time point could be explained by differences in
sociodemographic, past medical history, case-mix stroke severity, or
stroke subtype.
Trends in the prevalence rates of cognitive impairment were analyzed
using joinpoint regression. The joinpoint permutation test was used to
select the optimal model that best fitted the data and tests of significance
use a Monte Carlo permutation method. The average annual percentage
change was used to quantify the change in prevalence rates over time.
Kaplan–Meier estimates were used to model survival and to measure
the cumulative survival and 95% CI at 1, 5, 10, and 15 years after stroke
according to the cognitive status at 3 month after stroke. Differences in
survival according to cognitive status were compared with the multivari-
ate Cox proportional hazards model. The assumption for proportionality
of the mortality hazards was assessed by visual inspection of cumula-
tive hazard logarithm plots. All multivariate models were adjusted for
sociodemographic, past medical history, disability, stroke severity, and
Oxfordshire Community Stroke Project stoke subtype.
To assess the robustness of the results, we conducted sensitivity
analyses with imputation of missing data as described in our previous
study for stroke outcomes on SLSR (1995–2005).10 Similarly, when
assessing trends over time of all imputation methods, although over-
all rates were altered, the trends over time closely followed those in
the observed and complete case analysis. The observed data analysis
was used for the present study. Statistical analyses and graphics were
performed using STATA17 and JoinPoint program.18
Ethics
All patients and their relatives gave written informed consent to par-
ticipate in the study, and over the study period very few patients have
declined to be registered. The design of the study was approved by the
ethics committees of Guy’s and St Thomas’ NHS Foundation Trust,
King’s College Hospital Foundation Trust, St George’s University
Hospital, National Hospital for Nervous Diseases, and Westminster
Hospital.
Results
A total of 4212 patients with their first-ever stroke between
January 1, 1995 and December 31, 2010 were registered in
the SLSR, of whom 1101 were dead within 3 months, 534
were not eligible because of late registration, and 570 subjects
were unable to undergo a cognitive assessment because of
severe verbal, visual, or hearing impairment. Of the 2007
remaining subjects, a cognitive test was conducted in 1618 at
3 months and 389 were lost to follow-up by 3 months. Three
months poststroke characteristics of these patients including
sociodemographic, past medical history, case mix, and stroke
subtypes are presented in Table.
 140  Stroke  January 2013

Table. Three Months Poststroke Characteristics of SLSR (1995–2010) Patients

Cognitive Impairment
Characteristics (N=1618) Yes (N=518) No (N=1100) Crude Rates
Age, mean (SD) 73 (12.7) 67 (13.8) …
Sex
Female 264 (51.0%) 491 (44.6%) 35% (31.6–38.5)
Male 254 (49.0%) 609 (55.4%) 29% (26.4–32.6)
Ethnicity
White 328 (63.3%) 826 (75.1%) 28% (25.8–31.1)
Black 150 (29.0%) 218 (19.8%) 41% (35.7–46.0)
Socioeconomic status
Manual 352 (68.0%) 611 (55.5%) 37% (33.5–39.7)
Nonmanual 107 (20.7%) 323 (29.4%) 25% (20.9–29.3)
Economically inactive 46 (8.9%) 133 (12.1%) 26% (19.5–32.8)
Premorbid disability 39 (7.5%) 14 (1.3%) 74% (59.7–84.7)
Prestroke vascular risk factors
Transient ischemic attack 82 (15.8%) 141 (12.8%) 37% (30.4–43.5)
Atrial fibrillation 84 (16.2%) 125 (11.4%) 40% (33.5–47.2)
Ischemic heart disease 87 (16.8%) 181 (16.5%) 33% (26.9–38.4)
Hypertension 360 (69.5%) 726 (66.0%) 33% (30.4–36.0)
Diabetes mellitus 114 (22.0%) 181 (16.5%) 39% (33.1–44.5)
Hypercholesterolemia 83 (16.0%) 244 (22.2%) 25% (20.8–30.5)
Smoking (current smoker) 148 (28.6%) 390 (35.5%) 28% (23.8–31.5)
Case-mix severity
Loss of consciousness 84 (16.2%) 80 (7.3%) 51% (43.3–59.1)
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Urinary incontinence 230 (44.4%) 230 (20.9%) 50% (45.3–54.7)

Aphasia 84 (16.2%) 103 (9.4%) 45% (37.7–52.4)
Dysphagia 175 (33.8%) 185 (16.8%) 49% (43.3–53.9)
Visual field defects 143 (27.6%) 144 (13.1%) 50% (43.9–55.8)
Visuospatial neglect 129 (24.9%) 164 (14.9%) 44% (38.3–49.9)
Dysphasia 145 (28.0%) 159 (14.5%) 48% (42.0–53.5)
Dysarthria 225 (43.4%) 377 (34.3%) 37% (33.5–41.4)
Hemiparesis 390 (75.3%) 707 (64.3%) 36% (32.7–38.5)
Cerebellar symptoms 48 (9.3%) 193 (17.5%) 20% (15.1–25.5)
Pathological stroke subtypes
Ischemic stroke 418 (80.7%) 891 (81.0%) 32% (29.4–34.5)
Primary intracerebral hemorrhage 68 (13.1%) 101 (9.2%) 40% (32.8–48.0)
Subarachnoid hemorrhage 11 (2.1%) 42 (3.8%) 21% (10.8–34.1)
OCSP subtypes
Total anterior circulation infarcts 69 (13.3%) 46 (4.2%) 60% (50.5–69.0)
Partial anterior circulation infarcts 153 (29.5%) 273 (24.8%) 36% (31.4–40.7)
Posterior circulation infarcts 53 (10.2%) 166 (15.1%) 24% (18.7–30.4)
Lacunar infarct 143 (27.6%) 403 (36.6%) 26% (22.6–30.1)
TOAST subtypes (data collected after 1999)
Large artery atherosclerosis 34 (6.6%) 60 (5.5%) 36% (26.5–46.7)
Cardioembolism 58 (11.2%) 109 (9.9%) 35% (27.5–42.5)
Small vessel occlusion 61 (11.8%) 224 (20.4%) 21% (16.8–26.6)
Undetermined pathogenesis 58 (11.2%) 122 (11.1%) 32% (25.5–39.6)
OCSP indicates Oxfordshire Community Stroke Project; TOAST, Trial of Org 10172 in Acute Stroke Treatment.
 Douiri et al   Poststroke Cognitive Impairment   141

The cognitive impairment rate in stroke survivors was
strongly associated with age at all time points and it pro-
gressively increased after 5 years of stroke for patients aged
65 to 85 years old (Figure 1). Among stroke survivors, the
age-standardized prevalence of cognitive impairment ranged
from 24% (95% CI, 21.2–27.8) at 3 months, 22% (95% CI,
17.4–26.8) at 5 years, and 18% (95% CI, 8.9–26.6) at 10 years
to 21% (95% CI, 3.6–63.8) at 14 years after stroke. On aver-
age, the overall prevalence of cognitive impairment 3 months
after stroke and annually between 1995 and 2010 was similar
and remained relatively unchanged at around 22% up to 15
years after stroke (Figure 1). No significant differences were
found between males and females, and no significant trends of
cognitive impairment rates over the period 1995–2010 were
observed (Figures 1 and 2).
In analyses adjusted for sociodemography, prestroke risk
factors, case mix, and stroke subtypes, the age-standardized
prevalence ratio after stroke increased on average by 2% for
each year of chronological age (PR=1.02; 95% CI, 0.01–0.03
at 3 months, PR=1.01; 95% CI, 0.1–0.03 at 3 years, and
PR=1.03; 95% CI, 0.01–0.05 at 5 years).
Higher cognitive impairment rates were observed within
first 7 days, particularly for stroke survivors aged >65. At
3 months, cognitive function improved but then remained
stable with little variation up to 15 years (Figure 1). Among
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patients who were cognitively impaired in the acute stage
(up to 7 days after stroke) function was regained by nearly
a quarter of patients at 3 months (24%; 95% CI, 20.8, 26.6).
After 3 months, cognitive impairment was significantly
higher among the black ethnic group (26%) compared with
the white ethnic group (17%) and the manual socioeconomic
group (24%) compared with the nonmanual (20%) (Figure 2).
Black-to-white and manual-to-nonmanual prevalence ratios
of cognitive impairment were higher up to 7 years after
stroke. PR of cognitive impairment among high-risk groups
are presented in Figure 3. In a multivariate analysis control-
ling for sociodemography, prestroke risk factors, case mix,
and stroke subtypes, black-to-white adjusted PR were 2.2,
95% CI, 1.65–2.89 at 3 months, 2.3, 95% CI, 1.64–3.19 at 3
years, and 1.6, 95% CI, 1.02–2.38 at 7 years; and manual-to-
nonmanual adjusted PR were 1.42, 95% CI, 1.08–1.86 at 3
months, 1.6, 95% CI, 1.11–2.23 at 3 years, and 1.7, 95% CI,
1.05–2.76 at 7 years.
Cognitive impairment rates were also high in total ante-
rior circulation infarct (49%) and large artery atherosclerosis
(40%) subtypes up to 5 years after stroke (Figure 2). Cognitive
impairment in lacunar infarct and SVO strokes was increas-
ingly prevalent during the first 3 to 4 years after stroke and
decreased slightly thereafter (Figure 2). Using joinpoint
regression, the estimated average annual percentage change

Figure 1. Age-specific and overall age-standardized prevalence of cognitive impairment according to the year of stroke (left) and according
to time after stroke (right) of SLSR (1995–2010) patients, with 95% CIs.
 142  Stroke  January 2013
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Figure 2. Age-standardized prevalence of cognitive impairment according to time after stroke, with 95% CIs. TACI indicates total ante-
rior circulation infarct; PACI, partial anterior circulation infarct; POCI, posterior circulation infarct; LACI, lacunar infarct; LAA, large artery
­atherosclerosis; CE, cardioembolism; SVO, small vessel occlusion; UND, no pathogenesis identified.

of cognitive impairment was even greater for SVO compared
with lacunar infarct up to 5 years after stroke (10% [95% CI,
7.9–12.8] for SVO and 2% [95% CI, 0.3–2.7] for lacunar
infarct). Similarly, a progressive trend of cognitive impair-
ment was also observed for patients with no prestroke vascular
risk factor with an average annual percentage change of 6%
(95% CI, 5.3–7.5) in the first 5 years after stroke. However,
a negative trend of cognitive impairment was observed in
patients with prestroke vascular risk factors (average annual
percentage change of −6% (95% CI, −11.0 to −0.3).
Cumulative survival up to 15 years after stroke stratified by
3 months cognitive status is illustrated in Figure 4. Patients
cognitively impaired at 3 months had the worst survival,
with 53% (95% CI, 48.2–56.8), 37% (95% CI, 32.4–40.7),
and 34% (95% CI, 29.6–37.7) surviving up to 5, 10, and 15
years, respectively, after stroke. After fitting the Cox propor-
tional hazards model adjusted for sociodemographic, previous
vascular risk factors, case mix, and stroke subtypes, stroke
survivors with cognitive impairment at 3 months experienced
a 53% increased risk of death compared with those with no
 Douiri et al   Poststroke Cognitive Impairment   143
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Figure 3. Age-standardized prevalence ratios of cognitive impairment according to time after stroke, with 95% CIs. TACI indicates total
anterior circulation infarct; PACI, partial anterior circulation infarct; POCI, posterior circulation infarct; LACI, lacunar infarct; LAA, large artery
atherosclerosis; CE, cardioembolism; SVO, small vessel occlusion; UND, no pathogenesis identified.

known cognitive impairment at the same time point (hazard Discussion

ratio: 1.53, 95% CI, 1.30–1.80). Moreover, the prevalence
ratio of disability at each year after stroke was on average
twice as high for cognitively impaired patients. Using the
Poisson regression model with robust error variance adjusted
for sociodemographic, prestroke vascular risk factors, case
mix, and stroke subtypes the relative risk of d­ isability progres-
sion among patients with cognitive impairment at 3 months
were 2.4 (95% CI, 1.93–3.08) at 1 year, 1.9 (95% CI, 1.38–
2.60) at 3 years, and 1.8 (95% CI, 1.27–2.55) at 5 years.
This study estimates the prevalence of cognitive impairment
up to 15 years after stroke using practical and commonly
administered psychometric screening questionnaires for mod-
erate cognitive deficits or dementia in stroke.19–21 It not only
provides population estimates, to our knowledge for the first
time, on the longer term cognitive outcomes in a diverse inner-
city population, but it also highlights the long-term impacts of
stroke in subgroups of the population and illustrates the risk of
cognitive impairment long term. It is rare that population-based
studies estimate this range of outcomes in such a prospective
 144  Stroke  January 2013
manner, with up to 15 years of follow-up.8 Furthermore, the
use of these year-on-year prevalence estimates provides more
precise estimates of temporal changes of poststroke cognitive
impairment based on population observations.
The overall prevalence of poststroke cognitive impairment
seemed to be stable after 3 months after stroke and during the
1995–2010 period. A major observation is that there are some
differences in the cognitive impairment rates among groups
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when stratified by sociodemography, past medical history of
vascular risk factors, and stroke subtypes. These differences
in prevalence of cognitive impairment by group and by time
after stroke bear witness to the heterogeneity of this condition.
Although age could be linked to accumulated lifetime expo-
sures affecting cognitive function and socioeconomic status
could be a proxy for education level, the effect of ethnicity
is largely unexplained. Given population growth and ageing
demographics, these could prove to be some of the main chal-
lenges of our time.
A prevalence of cognitive impairment of almost half the
patients up to 5 years after stroke was found in patients having
a total anterior circulation infarct stroke. However, a stepwise
progression of cognitive impairment frequencies was observed
among stroke survivors with SVO and lacunar infarct stroke,
which may represent progressive vascular dementia associated
with stroke.3 Other studies have shown that the progressive
cognitive decline of these groups could be related to vascular
dementia (where the prevalence of cognitive impairment could
double every 5 years)22,23 or Alzheimer disease.3 A similar but
unexplained progressive pattern was observed among patients
with no known prestroke vascular risk factors.
This population-based study has produced estimates of
cognitive status over time in stroke survivors, but with no
comparison to the nonstroke population. The group-specific
estimates and temporal trends confirm the dynamic process
and heterogeneous nature of poststroke cognitive impairment.
Further longitudinal analyses of predictors in various sociode-
mographic, vascular risk factors, stroke subtype, and case-mix
groups are thus needed to develop a useful predictive tool for
Figure 4. Kaplan–Meier survival estimates
stratified by cognitive impairment status at 3
months, with 95% CIs.
patient management. Furthermore, the psychometric screen-
ing tools used in this study may underestimate the impact of
cognitive impairments, particularly mild cognitive impair-
ment. It has been shown that MMSE or Abbreviated Mental
Test are insensitive to mild cognitive impairment and execu-
tive ­function.19,24,25 Although these are limitations in detecting
mild cases, this study has shown high prevalence of cognitive
impairments. Similar large l­ong-term studies of poststroke
cognitive function using sensitive tools to detect all cases,
including mild cognitive impairments, will be of benefit to
reconfirm the burden of this condition.
The loss to follow-up rates in this study, once deaths are
accounted for, are <20% at each time point except at 3 months.
One might have expected the highest participation rate at 3
months. However, some of subjects were unable to complete
the cognitive assessments because of language difficulties,
visual or hearing impairment, and a proportion of patients are
registered retrospectively for whom a 3-month assessment is
not possible. Owing to late registrations and latter improve-
ment in some patients who were originally severely impaired,
there were subjects who had a cognitive test done at their
annual assessments, but not at 3 months.
This loss to follow-up may introduce bias, yet estimates
from analyses of the patients with complete data did not dif-
fer significantly from those presented here. Loss to follow-up
may be an issue in certain sociodemographic groups, although
we have not been able to identify such groups in this analy-
sis. The healthier participants and those from higher socio-
economic groups may be more likely to engage in research
follow-up. In other cohort and stroke register studies, loss to
follow-up rates are not often presented. Inner-city populations
are mobile, with large numbers of migrant families. Although
we acknowledge this as a potential factor in loss to follow-up,
efforts were made for all patients’ changes of address to be
recorded from hospital, general practice, or family sources.
To conclude, cognitive impairment is one of the indicators
of long-term impact of stroke. The overall prevalence of cogni-
tive impairment remains persistently high over time in stroke
 Douiri et al   Poststroke Cognitive Impairment   145
patients after their first stroke. Variations in poststroke cognitive
impairment rates could be explained by subgroup differences
and temporal changes after stroke. Age, ethnicity, socioeco-
nomic characteristics, and stroke subtypes are the most pre-
dominant factors that are associated with poststroke cognitive
impairment. Given the predicted global population growth and
ageing demographics, this study shows that effective preventive
intervention and strategic planning are needed for health sys-
tems to identify and to manage stroke survivors with cognitive
impairment.
Acknowledgments
We wish to thank all the patients and their families and the healthcare
professionals involved. Particular thanks to all the fieldworkers and
the whole team who have collected data since 1995 for the South
London Stroke Register. We are also very thankful for the anonymous
reviewers for their helpful comments.
Sources of Funding
The study was funded by the Northern & Yorkshire NHS R&D
Programme in Cardiovascular Disease and Stroke, Guy’s and St
Thomas’ Hospital Charity, Stanley Thomas Johnson Foundation,
The Stroke Association, Department of Health HQIP grant, National
Institute for Health Research Programme Grant (RP-PG-0407-10184).
The authors acknowledge financial support from the National Institute
for Health Research (NIHR) Biomedical Research Centre based at
Guy’s and St Thomas’ NHS Foundation Trust and King’s College,
London. The views expressed in this article are those of the authors
and not necessarily those of the National Health Service, the NIHR,
or the Department of Health.
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Disclosures
None.
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