Evolution of Cognitive Impairment After Stroke and
Risk Factors for Delayed Progression
Teodoro del Ser, MD, PhD; Raquel Barba, MD, PhD; Maria M. Morin, MD; Julio Domingo, MD;
Carlos Cemillan, MD; Margarita Pondal, MD; Jose Vivancos, MD
Downloaded from http://stroke.ahajournals.org/ by guest on July 31, 2017
Background and Purpose—Cognitive decline occurs in ⬇30% of stroke patients. Acute risk factors have been identified,
but long-term risk has not been examined in large samples. The purpose of this research was to determine factors
associated with the progression of cognitive impairment after stroke.
Methods—Consecutive stroke patients (193) without previous dementia were assessed 3 months after stroke with an
extensive neuropsychological battery and diagnosed according to the Diagnostic and Statistical Manual of Mental
Disorders Fourth Edition criteria and the Clinical Dementia Rating as normal (139), cognitive decline without dementia
(18), or dementia (18 mild, 10 moderate, and 8 severe). After a 24-month follow-up, they were classified as stable,
progressing, or improving, according to change in Clinical Dementia Rating score. The determinants of progression of
cognitive decline were ascertained by logistic regression analysis of all clinical, neuroimaging, and complementary data.
Results—Cognitive status at 24 months was stable in most cases (151; 78.2%), decline progressed in 27 (14%; 6 demented
and 21 nondemented), and improved in 15 (7.8%; 7 demented and 8 nondemented). Seven nondemented patients became
demented at 24 months, and 5 demented became nondemented. The age (odds ratio [OR], 1.05; 95% CI, 1.01 to 1.1),
mental decline before stroke (OR, 1.14; 95% CI, 1.02 to 1.27), number of prescribed drugs (OR, 1.34; 95% CI, 1.05 to
1.72), diastolic blood pressure on admission (OR, 0.96; 95% CI, 0.93 to 0.99), and episodes of hypotension during
admission (OR, 7.61; 95% CI, 1.11 to 52.1) were significantly associated with cognitive deterioration.
Conclusions—Cognition is rather stable for 2 years after stroke. Both progression and improvement of cognitive
impairment are frequent in demented patients. Age, previous cognitive decline, polypharmacy, and hypotension during
admission are risk factors for progression. (Stroke. 2005;36:2670-2675.)
Key Words: vascular cognitive impairment 䡲 dementia 䡲 risk factor 䡲 longitudinal study
A
n emerging field of research over the last decade has
been vascular cognitive impairment and poststroke dementia,1,2 a condition that can be found in 20% to 30% of
stroke patients.1– 4 These studies have identified several risk
factors for dementia after stroke1,2 and have demonstrated
that poststroke dementia increases the risk for recurrent
stroke5 and mortality.4 – 6
Despite the aforementioned research, data about evolution
of cognition after stroke7 are quite scarce. Vascular cognitive
impairment is considered to progress in patients who do not
adequately control vascular diseases or are genetically predisposed to brain vessel damage. However, this reasonable
hypothesis has not been effectively tested. We do not know
how many stroke patients show progression or regression of
their cognitive impairment over several years, and we do not
have good prognostic clues to identify those more prone to
deterioration.
The search for markers of cognitive decline would provide
useful tools for preventive and therapeutic trials in vascular
dementia and vascular cognitive impairment. In this study we
evaluate the evolution of cognitive status in a group of stroke
patients during a 2-year follow-up.
Methods
Patients
We have previously described2 327 consecutive stroke patients and
their cognitive state after 3 months. A follow-up was proposed at
discharge, and all of the complying patients were reassessed after 3,
6, 12, and 24 months.
For this longitudinal study, we excluded 63 patients (19.2%) who
died before the third month after stroke, 32 (9.8%) who were
demented before stroke,6 and 39 (11.9%) who did not attend any of
the scheduled follow-up visits (29; 8.8%) or had an inadequate
baseline evaluation (10; 3%). The present prospective study included
193 patients.
Clinical Variables
During admission, every patient underwent a structured anamnesis
and a prospective protocol of neurological, functional, cognitive, and
ancillary exams.2 The following variables were obtained: demo-
Received June 13, 2005; final revision received September 1, 2005; accepted September 7, 2005.
From the Sección de Neurologı́a (T.d.S., M.M.M., J.D., C.C., M.P.), Hospital Severo Ochoa, Leganés; Servicio de Medicina Interna (R.B.), Hospital
de Alcorcón; and Servicio de Neurologı́a (J.V.), Hospital de la Princesa, Madrid, Spain.
Correspondence to Teodoro del Ser, MD, Sección de Neurologı́a, Hospital Severo Ochoa, Avda, Orellana s/n, Leganés, 28911 Madrid, Spain. E-mail
[email protected]
© 2005 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
DOI: 10.1161/01.STR.0000189626.71033.35
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del Ser et al
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graphics (age, sex, and education); previous habits (obesity, smoking, and drinking); and previous psychiatric (anxiety and depression), cardiovascular (hypertension, myocardial infarction, heart
failure, atrial fibrillation, other arrhythmia, mitral and aortic valve
disease, hypercholesterolemia, diabetes, and peripheral arterial disease), cerebrovascular (transient ischemic attacks and strokes), and
other diseases (renal, pulmonary, hepatic, cataracts, surgical procedures); number of prescribed drugs; prestroke functional status
(Barthel Index)8 and cognitive decline (shortened Spanish version of
the Informant Questionnaire on Cognitive Decline in the Elderly,
SS-IQCODE)9 according to a proxy relative.
Other variables included the following: clinical (systolic-diastolic
pressure and axilar temperature), neurological (Canadian Neurological Scale),10 functional (Barthel Index),8 and cognitive (Short
Portable Mental Status Questionnaire [SPMSQ])11 status on admission and at discharge; episodes of hypertension (systolic ⬎150 or
diastolic ⬎90 mm Hg) or hypotension (systolic ⬍100 or diastolic
⬍50 mm Hg) during admission; ECG (arrhythmia), chest roentgenogram (aortic arch calcification), hemogram, serum biochemistry,
and Quick’s index.
Cranial computed tomography (CT) performed between the first
and 30th day after stroke, available in 167 cases, was assessed by a
neuroradiologist, without clinical information, for cerebral atrophy
(0 to 3),12 leukoaraiosis (0 to 4), side, number, vascular territory,
critical site (interpeduncular, thalamus, lenticular, caudate head,
hippocampus, gyrus angularis, and anterior cingulum), and volume
(cm3) of vascular lesions, width of the third and lateral ventricles
(mm), and (in 102 patients) left and right medial temporal lobe
atrophy (0 to 3).13 The test-retest reliability in 54 CT scans was as
follows: cerebral atrophy, ␬⫽0.812; leukoaraiosis, ␬⫽0.867; medial
temporal atrophy, ␬⫽0.815; and total volume of vascular lesions,
r⫽0.944.
The mechanism of stroke was categorized as probably embolic
(presence of atrial fibrillation, mitral valve, or other embolic source)
or thrombotic, the type (according to CT) as ischemic (lacunar: ⬍2
cm3, nonlacunar), hemorrhagic, or indefinite (CT not performed), as
well as single or multiple lesion, and the clinicoradiologic location as
left or right carotid or vertebrobasilar.
Diagnosis of Poststroke Dementia and
Cognitive Status
Three months after stroke, all of the patients were diagnosed as
demented or nondemented2 based on the clinical interview of the
patient and of a close informant, the present SPMSQ score, the
SS-IQCODE assessing cognitive changes, an extensive neuropsychological battery described elsewhere,2 a questionnaire about activities of daily living, and the Center for Epidemiologic Studies
Depression Scale (CES-D) of depression.14
Dementia was diagnosed according to Diagnostic and Statistical
Manual of Mental Disorders–Fourth Edition criteria when scores in
tests of recent and late memory and of another cognitive function
were ⬍1 SD of the normative control group, relatives scored ⬎57 in
SS-IQCODE, and activities of daily living were impaired. The final
diagnosis was always reached by an experienced neurologist (T.d.S.)
after a thorough judgment of all clinical and neuropsychological
data, trying to control for the effects of sensory-motor defects. The
stage of overall cognitive function was established with the Clinical
Dementia Rating (CDR)15 as follows: 0, no cognitive decline; 0.5,
cognitive decline without dementia; 1, mild dementia; 2, moderate
dementia; or 3, severe dementia.
Follow-Up
Antiplatelet agents; anticoagulants; drugs to control blood pressure,
serum glucose, or cholesterol; and good dietary and life habits were
prescribed when indicated. These treatments and those of concomitant or intercurrent illnesses were mainly controlled by family
physicians under universal and homogeneous coverage of the Spanish Health System.
After informed consent, all of the patients were followed up on 3,
6, 12, and 24 months after stroke. In these visits, blood pressure,
Evolution of Cognitive Impairment After Stroke
2671
neurological status, presence of aphasia, intercurrent illnesses, and
vascular events (stroke recurrence, acute myocardial infarction, deep
venous thrombosis, and peripheral arterial disease) were recorded,
and the physical examination, SPMSQ, SS-IQCODE (on informant
availability), CES-D scale, neuropsychological battery, and CDR
stage were performed.
Groups
Patients were classified according to changes in their CDR scores
during the follow-up: stable, when they had the same score at 3 and
24 months visits; progressing, when they developed a higher CDR
score; and improving, when they dropped down to a lower CDR
score at the end of the study. Only the change between the first and
final visit was considered for classification independent of the
baseline score.
Statistical Analyses
All of the clinical variables listed before were compared among the
stable, progressing, and improving groups in a first series of
univariate analyses (␹2 test or ANOVA). The determinants of the
primary outcome measure, “progression of cognitive impairment”
(defined as increase in the CDR score), were ascertained by multiple
logistic regression analysis with a forward stepwise method. Progression versus no progression (stable or improving) was the
dependent variable, and independent variables were introduced in 2
blocks: age, sex, and literacy and then all of the variables with
statistical significance (P⬍0.05) in the univariate analyses. These
analyses were performed on the total sample (n⫽181; 2 demented
and 10 nondemented patients lacked the SS-IQCODE score before
stroke) and on nondemented (n⫽148) cases. Demented cases were
too few for a specific multivariate analysis.
Results
All of the 193 patients included in this study had clinical and
neuropsychological exams 3 and 6 months after stroke; 185
cases (95.8%) attended the 12-month follow-up visit, and 155
cases (80.3%) attended the 24-month visit. Sample attrition
was attributed to death in 14 cases (7%; 4 at 12 and 10 at 24
months; 8 demented and 6 nondemented) and refusal in 24
cases (12.5%; 4 at 12 and 20 at 24 months; 5 demented and
19 nondemented). The mean follow-up was 23.3⫾6.8 months
(21.1⫾8 for demented and 23.8⫾6.3 for nondemented).
Their mean age was 66.8⫾13.2 years (range, 20 to 96),
78 (40.4%) were women, 31 (16.1%) were illiterate, 113
(58.9%) had very low education, 35 (18.2%) had primary
school education, and 14 (7.3%) had high school or university
studies. The stroke was left carotid in 91 cases (47.2%), right
carotid in 66 (34.2%), vertebrobasilar in 34 (17.6%), indefinite in 2 (1%), ischemic in 169 cases (87.6%; 23 embolic and
83 lacunar), and hemorrhagic in 24 (12.4%; 20 hematoma and
4 hemorrhagic infarcts). Cerebrovascular lesions were multiple in 64 cases (33.1%).
At baseline, 3 months after stroke, 139 patients were cognitively normal (CDR⫽0, 72%), 18 had cognitive decline
without dementia (CRD⫽0.5, 9.3%), and 36 were demented
(CRD⫽1 to 3, 18.6%; 18 mild dementia, 10 moderate, and 8
severe). Eleven severely aphasic or motor-impaired patients
(5.7%) did not have a definite diagnosis at that time and were
classified several months later, when their language or motor
functions improved, as cognitive decline without dementia
(7 cases), mild dementia (3 cases), or severe dementia (1
case). Demented patients had gross infarcts or hemorrhages
(17 cases; 47.2%), small infarcts (6; 16.6%), or multiple
small vessel lesions (13; 38.1%).
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December 2005
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Big numerals indicate cases in every stage and follow-up time.
Arrows and small numerals indicate cases that transition from
each stage to other stages at the subsequent follow-up time.
Lost indicates cases examined at 6/12 months and lost at the
24-month follow-up.
The evolution of CDR scores throughout the follow-up is
shown in Figure. There were cases that improved or worsened at
every cognitive stage and evolutionary time point. However, by
the end of follow-up, the majority of patients were cognitively
stable (151; 78.2%); only 42 cases (21.8%) had worsened
(27; 14%) or improved (15; 7.8%). Six of 28 mild-moderate
demented cases (21.4%) and 21 nondemented (13.4%) cases
worsened (␹2: 1.24, not significant); 7 (19.4%) demented and
8 of 18 patients with cognitive decline without dementia
(44.4%) improved (␹2: 3.74, P⫽0.053). Five demented patients (13.9%) became nondemented (1 to normal, 4 to
cognitive decline without dementia); 7 nondemented patients
(4.5%; 4 normal and 3 cognitive decline without dementia)
became demented. A 1-stage change in the CDR was recorded in 38 patients (25 worsening and 13 improving) and a
2-stage change in 4 (1 stepwise progressive: stages 0.5 to 1 to
2; 3 fluctuant: 1 to 3 to 2, 1 to 0 to 0.5, and 1 to 0 to 0.5).
Univariate Analysis
Patients who improved during follow-up had more frequent
previous psychiatric disease, previous depression, hemorrhagic stroke, aphasia after stroke; and more left parietal, left
temporal, left hemispheric, and total volume of cerebrovascular lesion (Table 1). Patients who progressed were significantly older and more illiterate and had more frequent
cataracts, drug intake, cognitive impairment before stroke,
hypotensive episodes during admission, and third ventricle
width (Table 1). Stable patients had significantly higher
systolic and diastolic blood pressure during admission, better
SPMSQ scores during admission and 3 months after stroke,
better SS-IQCODE score 3 months after stroke, and less
mild-moderate left medial temporal atrophy (Table 1). All of
the other variables listed in the methods section, including
vascular risk factors, baseline depression, and intercurrent
illnesses did not differ between the groups; multiple strokes
had a nonsignificant relationship to progression.
When cases were sorted in only 2 groups: progressing (n⫽27)
and nonprogressing (both stable and improving, n⫽166), the
former were older (74.8⫾9.8 versus 65.5⫾13.2 years;
P⫽0.001), more illiterate (33.3% versus 12.6%; P⫽0.006),
treated with more drugs (2.6⫾2.0 versus 1.7⫾1.7; P⫽0.01),
more cognitively impaired before stroke (SS-IQCODE
55.5⫾5.0 versus 53⫾4.1; P⫽0.02), had lower systolic
(144.2⫾36.3 versus 159.5⫾32.1 mm Hg; P⫽0.02) and diastolic
(81.6⫾14.7 versus 92.2⫾17.3 mm Hg; P⫽0.003) blood pressure on admission, more episodes of hypotension during admission (11.1% versus 2.4%; P⫽0.02), worse SPMSQ score (during admission: 13.4⫾4.6 versus 15.9⫾3.9; P⫽0.01; 3 months
after stroke: 14.5⫾4.2 versus 17.3⫾3.5; P⫽0.004), more leukoaraiosis (56% versus 33.3%; P⫽0.03), third ventricle size
(7.2⫾1.9 versus 6⫾2.9 mm; P⫽0.01), total atrophy (92% versus
72%; P⫽0.03) and left hippocampal atrophy (53% versus 26%;
P⫽0.02).
Multivariate Analysis
Age, number of drugs, SS-IQCODE score before stroke,
diastolic blood pressure on admission, and hypotension during admission entered into the 2 logistic regression models
(with all of the sample and with only the nondemented cases
at baseline) as predictive factors for progression (Table 2).
These models accounted for 30% and 38.1% of the variance,
respectively, and correctly classified 86.2% and 72.8% of the
cases, respectively.
Discussion
The main objective of our longitudinal study was to determine the cognitive evolution over 2 years of an unselected
sample of registered stroke patients. Most losses were attributed to death, and the type of vascular lesions and the
frequency of dementia and cognitive decline without dementia were very similar to those of other previous series.1– 4
Therefore, our sample is rather representative of the stroke
surviving population.
A remarkable finding of this study is the evidence of
multiple evolutionary trends in the sample. There were
patients with stable, improving, or worsening cognitive status
at every evolutionary time frame and in every cognitive stage.
Moreover, cognitive changes in demented cases were as
frequent as in nondemented cases. Tham et al16 also found in
252 transient ischemic attacks or nondisabling strokes a 33%
overall rate of change from the cognitive baseline state after
a 1-year follow-up both by improving and deteriorating cases.
Several studies have reported that cognitive impairment
after stroke may improve over time,7,16 –18 although the
recovery rates were very diverse because of different basal
characteristics of the samples. Of our patients, 7.8% improved during the follow-up and, in contrast to previous
reports,17 demented cases had a high improvement rate with
5 (13.9%) conversions to nondementia. The reversion of
vascular dementia to a milder cognitive condition has been
documented in some case reports19 and small clinical series,20
but its frequency and circumstances are unknown.
del Ser et al
Evolution of Cognitive Impairment After Stroke
2673
TABLE 1. Demographic and Clinical Features of Study Subjects: Comparison of
the Groups of Patients
Variable
Improving
(n⫽15)
Stable
(n⫽151)
68.9⫾12.9
65.1⫾13.2
Progressing
(n⫽27)
P
Value
74.8ⴞ9.8
0.02*
Antecedents
Mean age, y (SD)
Illiterate
2 (13.3%)
9 (33.3%)
0.011†
Previous psychiatric disease
6 (40%)
9 (6%)
5 (18.5%)
⬍0.0001†
Previous depression
3 (20%)
6 (4%)
4 (14.8%)
0.01†
Cataracts
1 (6.7%)
2 (1.3%)
4 (14.8%)
0.002†
No. of drugs
SS-IQCODE before stroke
19 (12.7%)
1.5⫾1.1
1.7⫾1.8
2.6ⴞ2.1
0.03*
53.6⫾3.8
52.9⫾4.1
55.5ⴞ5.0
0.02*
Admission
Hemorrhagic stroke
6 (40.0%)
15 (10.1%)
3 (10.7%)
0.005†
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Systolic blood pressure
144.6⫾17.2
161.1ⴞ32.9
144.2⫾36.3
0.015*
Diastolic blood pressure
89.6⫾11.4
92.4ⴞ17.8
81.6⫾14.7
0.011*
SPMSQ
12.2⫾3.1
16.1ⴞ3.8
13.4⫾4.6
0.001*
Hypotension during
admission
1 (6.7%)
3 (2%)
3 (11.1%)
0.045†
3 (11.1%)
0.03†
After 3 months
Aphasia
6 (40%)
23 (15.2%)
Short Portable Questionnaire
13.2⫾4.7
17.7ⴞ3.1
14.5⫾4.2
⬍0.0001*
SS-IQCODE Questionnaire
68.6⫾7.8
58.9ⴞ8.8
62.6⫾9.6
⬍0.0001*
n⫽12
n⫽130
n⫽25
5.4⫾1.5
6.1⫾2.2
7.2ⴞ1.9
CT scan
Third ventricle width, mm
Medial temporal atrophy, in
102 cases
Left parietal lesion, cm3
3
Left temporal lesion, cm
3 (50%)
19 (24.1%)
11.2ⴞ25.9
1.8⫾7.0
0.031*
7 (53%)
0.035
1.1⫾4.6
0.003*
0.002*
6.1ⴞ11.9
0.6⫾4.8
0⫾0
Left hemispheric lesion, cm3
22.5ⴞ33.1
5.7⫾21.0
2.6⫾6.4
0.02*
Total lesion, cm3
33.9ⴞ34.0
12.3⫾29.0
7.9⫾11.4
0.023*
Bold font indicates the group differing in comparisons between-groups by Newman-Keuls test.
*ANOVA; †␹2.
Our patients who improved had more total and left hemispheric volume of lesion and more frequent aphasia, depression, and hemorrhagic stroke. Aphasia and left carotid stroke
have been described as risk factors for poststroke dementia in
some short-term crossover studies;3 however, great overall
cognitive improvement or the correction of a dementia
TABLE 2.
misdiagnosis may result when language defects related to
these dominant hemispheric syndromes clear up. Desmond et
al7 reported this finding in their longitudinal study of ischemic stroke, but Ballard et al18 found that the severity of
language expression defects 3 months after stroke was associated with delayed dementia. The association of cognitive
Predictors of Progression of Cognitive Decline in 2 Logistic Regression Models
Total Sample (n⫽181 cases*)
Variables
B
Odds Ratio (95% CI)
Nondemented Patients (n⫽147 cases*)
P Value
B
Odds Ratio (95% CI)
P Value
Age
0.052
1.05 (1.01 to 1.10)
0.03
0.067
1.07 (1.01 to 1.13)
0.021
No. of drugs
0.292
1.34 (1.05 to 1.72)
0.02
0.330
1.39 (1.05 to 1.85)
0.022
0.128
1.14 (1.02 to 1.27)
0.024
0.157
1.17 (1.01 to 1.36)
0.038
⫺0.040
0.96 (0.93 to 0.99)
0.021
⫺0.047
0.95 (0.92 to 0.99)
0.031
SS-IQCODE before stroke
Diastolic pressure on admission
Hypotension during admission
Constant
Explained variance
Correctly classified cases
2.029
⫺9.717
7.61 (1.11 to 52.10)
0.039
2.813
0.00
0.009
⫺11.826
16.67 (1.41 to 197.51)
0.026
0.00
0.011
30%
38.1%
86.2%
72.8%
*In 2 demented and 10 nondemented patients, the SS-IQCODE score was not available.
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December 2005
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improvement with previous depression may be attributed to
the recovery of mood disorder after treatment21 in some cases,
because depression itself can impair performance on many
cognitive function tests. Interestingly, depressive symptoms 3
months after stroke were not associated with cognitive
evolution.
Most of our demented and nondemented cases (78.2%)
had stable cognition during follow-up. This subgroup was
younger, had better cognitive performance before and after
stroke, and had less left medial temporal atrophy in their CT
scan, indicating that patients without previous cognitive decline2
and without neuroimaging signs of neurodegeneration22 are
prone to be stable over time. Several clinical trials have clearly
documented the nonprogressive evolution of vascular dementia23 in contrast with the progression of Alzheimer disease. A
stable cognitive pattern was also associated with higher blood
pressure, perhaps because this condition precludes hypoperfusion states24 and subclinical ischemic penumbra25 and is contrary
to the observed lowering of blood pressure over decades in
elderly individuals who develop dementia.26 However, both
progressing and improving patients have lower systolic and
diastolic pressure indicating that cognitive evolution may have a
complex relationship with blood pressure.27
Patients who progressed were more frequently illiterate,
had more cataracts, and showed more third ventricle width, in
accordance with population studies where low education,28
sensory deprivation, and brain atrophy29 are associated with
dementia.
All of the findings discussed in the previous paragraphs
come from a series of univariate analyses that were mainly an
intermediate tool to select the variables for the main multivariate analyses. A correction for multiple comparisons was
not used; consequently, these results have to be considered as
provisional and heuristic. By contrast, older age, previous
cognitive impairment, polypharmacy, low diastolic pressure,
and hypotensive episodes during admission were identified in
the final logistic regression analyses as the outstanding
features for patients who progressed. Old age and previous
cognitive impairment are well-known risk factors for both
neurodegenerative30 and vascular dementia.1–2 High-drug intake is a risk factor for delirium and cognitive impairment31 in
the elderly and may be a surrogate marker of higher comorbidity, as well as a determinant of vascular instability.
Low-blood pressure and hypotensive episodes during admission were not associated with short-term poststroke dementia in
our previous crossover study,2 but in the present longitudinal
study, they turned out to be important factors for the progression
of cognitive impairment between 3 and 24 months. Acute
episodes of hypotension have been described as determinants of
dementia in stroke patients,24 and there are some case reports of
vascular dementia resulting from systemic hypotension;32 nonetheless, this very delayed association of hypotensive conditions
with cognitive decline progression has not been described
previously. These effects may be related to arterial changes in
the ageing brain and increasing vulnerability to clinical or
subclinical hypoperfusion in periventricular regions, basal ganglia, or hippocampus.33 Low diastolic blood pressure is associated with cognitive impairment in elderly population samples,34
and a decline in blood pressure increases the risk of dementia in
older people with vascular disorders.35 Acute hypotension and
hypoperfusion probably explain the high risk for cognitive
impairment after congestive heart failure or surgical procedures
in older patients,33 and chronic brain hypoperfusion may trigger
hypometabolic and neurodegenerative changes,36 as well as
subcortical vascular dementia.33 Demented patients frequently
have neurocardiovascular instability, and repeated hypotensive
episodes may exaggerate their cognitive decline.37
The assumption that long-term cognitive evolution of stroke
patients depends mainly on recurrent cerebrovascular illness is
challenged by our data. Previous research has already shown that
recurrent stroke is no more frequent in cases with than without
cognitive deterioration,38 and poststroke cognitive impairment
with a 2-year delay is more associated with intercurrent medical
hypoxic or ischemic illnesses,24 brain atrophy,17,39 and multiple
ischemic lesions17,39 than to recurrent stroke. Our findings are
concordant with these data, although only a tendency for
multiple strokes was found, and they stress the importance of
poorly controlled hypotension, a condition easy to correct.
In conclusion, cognitive evolution 2 years after stroke is
rather heterogeneous, but a substantial number of patients
remain stable or even improve. Additional population-based
studies are required to reliably identify the individuals at risk
for cognitive decline who would be more suitable for pharmacological or other therapeutic interventions and those who
will probably spontaneously improve. The determinants of
progression of cognitive impairment are still poorly known.
Those found in our sample are age, previous cognitive
decline, polypharmacy, and low-blood pressure.
Acknowledgments
This work was supported by a grant (94/0022) from the “Fondo de
Investigaciones Sanitarias” from the Ministerio de Salud y Consumo
of Spain and a grant from Bayer S.A. We are indebted to many
people who worked in the follow-up of patients included in the
Stroke Registry of the Hospital Severo Ochoa.
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Teodoro del Ser, Raquel Barba, Maria M. Morin, Julio Domingo, Carlos Cemillan, Margarita
Pondal and Jose Vivancos
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Stroke. 2005;36:2670-2675; originally published online October 27, 2005;
doi: 10.1161/01.STR.0000189626.71033.35
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