From the Memory Research Unit and Stroke Unit, Department of Neurology,
University of Helsinki (Finland).
Methods—The study group comprised 337 of 486 consecutive patients
aged 55 to 85 years who 3 months after ischemic stroke
completed a comprehensive neuropsychological test battery and MRI,
including structured medical, neurological, and laboratory evaluations;
clinical mental status examination; interview of a knowledgeable
informant; detailed history of risk factors; and evaluation of stroke
type, localization, and syndrome. The DSM-III definition for dementia
was used.
Results—Frequency of any poststroke dementia was 31.8%
(107/337), that of stroke-related dementia (mixed Alzheimer's
disease plus vascular dementia excluded) was 28.4% (87/306), and that
of dementia after first-ever stroke was 28.9% (79/273). The patients
with poststroke dementia were older and more often had a low level of
education, history of prior cerebrovascular disease and stroke, left
hemispheric stroke (reflecting laterality), major dominant stroke
syndrome (reflecting laterality and size), dysphasia, gait impairment,
and urinary incontinence. The demented patients were also more
frequently current smokers, had lower arterial blood
pressure values, and more frequently had an orthostatic
reaction compared with the nondemented stroke patients. The correlates
of dementia in logistic regression analysis were dysphasia
(odds ratio [OR], 5.6), major dominant stroke syndrome (OR, 5.0),
history of prior cerebrovascular disease (OR, 2.0), and low educational
level (OR, 1.1). When we excluded those with cerebrovascular disease
plus Alzheimer's disease or those with recurrent stroke, the
order of correlates remained the same. When the patients with dysphasia
(n=30) were excluded, the correlates were major dominant syndrome (OR,
4.6) and low educational level (OR, 1.1).
Conclusions—Our data suggest that a single explanation for
poststroke dementia is not adequate; rather, multiple factors including
stroke features (dysphasia, major dominant stroke syndrome), host
characteristics (educational level), and prior cerebrovascular disease
each independently contribute to the risk.
The mechanisms related to poststroke dementia are still subject to
debate.14 15 To better understand the mechanisms of
dementia from CVD, one approach is to examine those factors that
increase the risk of dementia in patients with verified
ischemic stroke.
With the use of cross-sectional observations, the aim of this study was
to identify the clinical features that distinguish demented from
nondemented subjects in a large well-defined stroke cohort.
The subjects underwent a structured medical and neurological history
based on review of all available hospital charts, interview of the
subject and a knowledgeable informant, and a structured clinical and
neurological examination performed by board-certified neurologists
(T.P., R.V.). In addition, all the cases were reviewed by a senior
neurologist (T.E.). The neurological examination focused on factors and
features related to dementia and stroke similar to the method of the
Memory Research Unit, Department of Neurology, University of
Helsinki,16 and the National Stroke Data
Bank.17 The laboratory evaluations included hemoglobin,
hematocrit, white blood cell count, thrombocytes, sodium, potassium,
liver function tests, calcium, total and HDL cholesterol,
triglycerides, vitamin B12, erythrocyte folate,
thyroid function tests, fasting blood glucose, and
creatinine. History of main vascular risk factors was
obtained as described earlier.3 Types of ischemic
stroke were classified according to the TOAST criteria into
large-artery arteriosclerosis,
cardioembolism, small-vessel occlusion (lacune), and
stroke of undetermined etiology.18 Localization of the
stroke was divided into right hemispheric, left hemispheric, and
bilateral, as well as anterior (carotid), posterior (vertebrobasilar),
and anteroposterior (symptoms and signs from both carotid and
vertebrobasilar circulation).3 19 Furthermore, the stroke
syndromes assessed included major dominant and nondominant hemispheric,
minor dominant and nondominant hemispheric, deep/lacune, brain stem and
cerebellar, and unknown.17 Major dominant hemispheric
stroke syndrome included mixed aphasia with hemiparesis,
hemisensory, and hemianopia/neglect; major motor (Broca)
aphasia; sensory (Wernicke) aphasia; anterior cerebral artery syndrome
with aphasia; or right hemianopia with dysnomia and/or dysmnesia and
dyslexia. Stroke severity was assessed with the Scandinavian Stroke
Scale20 and the National Institutes of Health Stroke
Scale.21 Arterial blood pressure was measured
with the patient in the supine position, and orthostatic
reaction was defined as decrease of systolic blood pressure
over 20 mm Hg or diastolic over 10 mm Hg after
5 minutes with the patient in the upright position.22
Details of the clinical mental status examination, as well as
assessment of emotional and social functions, are given in previous
reports.3 19 Aphasia was assessed clinically and with the
Acute Aphasia Screening Protocol.23
The clinical criteria for dementia were those of the American
Psychiatric Association DSM-III.24 Instead of using the
more recent definitions for dementia,3 we chose the DSM-III
definition because it was used in a previous comparative stroke
cohort.2 4 6 The patients with any poststroke dementia were
further divided into those with stroke-related dementia (mixed AD+VD
excluded=no presence of prestroke cognitive decline)6 and
dementia after first-ever stroke.7
Cognitive domains of the DSM-III definition assessed by the
neuropsychological test battery included memory functions (short- and
long-term memory), abstract thinking, judgment, aphasia, apraxia,
agnosia, and constructional difficulty including visuospatial and
constructional functions. The norms were adjusted for age but not
education. The results were evaluated in different age groups.
Adjustment for education was not done because most of the individuals
in the age cohorts had completed grade school. In addition, personality
change, work, and social activities were assessed by the neurologist.
Abnormality in each domain was judged with the use of norms based on a
random healthy Finnish population (2 SD or, if more than one test was
used, 1 SD below the level of the norm on several tests indicated
abnormality).25 The diagnosis of abnormality in
neuropsychological domains was based not only on individual low scores
compared with normative data. In addition, we used the process
approach, in which qualitative functional features known to be
associated with distinct neuropsychological syndromes also guide the
diagnostic decision; for example, if impairment of
executive functions was the primary feature in the syndrome, the
perseverative errors and other executive difficulties in the Token test
were not regarded as primary dysphasia, but rather as secondary
language difficulty.
Short-term memory was assessed with the Fuld Object-Memory Evaluation
(learning curve over five trials, delayed recall, and
recognition)26 and the Logical Memory and Visual
Reproduction of the Wechsler Memory Scale, Revised (immediate
and delayed verbal and visual memory).27 Long-term semantic
memory and ability to recall previously learned knowledge was assessed
with the short form of Information Task (10 questions on general
knowledge and Finnish history) of the WAIS-R.28 Abstract
thinking (conceptualization/abstraction) was evaluated by the
Similarities Subtest of the WAIS-R. Judgment was evaluated by
analysis of four questions in the comprehension portion of the
WAIS-R.28 Aphasia was assessed by the short version of the
Token test (comprehension; parts 4 and 6, total count of correct
responses)29 and the Boston naming test (15
items).30 Verbal fluency was evaluated in both semantic
category (animal naming in 1 minute) and letter generation (letter
k in 1 minute).31 Overall evaluation of speech
function was based on the modified Boston Diagnostic
Aphasia Examination.29 32 Motor control and praxis were
evaluated with items from the D test,30 32 including
reciprocal coordination and serial and spatial organization of hand
movements. Agnosia (perceptual functions) was assessed with the
recognition tasks from the D test battery and Poppelreuters
pictures.33 34 Constructional functions were assessed by
the block design section of the WAIS-R,28 by the clock test
(recognizing and setting time),33 and by copying a
triangle, a flag, a three-dimensional cube, and a Greek
cross.33 34 According to the neuropsychologist's best
judgment, all the patients included in the study were able to complete
the tests to arrive at clinical decisions of normality and abnormality
in abstract thinking, judgment, agnosia, and apraxia.
The patients clinically scored as having dysphasia had only mild
symptoms: the mean (SD) score of the Acute Aphasia Screening Protocol
was 45.1 (4.3) in those with and 49.1 (3.1) in those without dysphasia
(P<.001).
Education was divided into two categories: low with 0 to 6 years and
high with more than 6 years of formal education.
Data Analysis and Statistics
Among vascular risk factors, only current smoking and cardiac failure
were associated with dementia, and high total cholesterol
was more frequent in the nondemented group (Table 2
Characteristics of ischemic stroke associated with dementia
were left hemispheric localization (P=.0366) and major
dominant hemispheric stroke syndrome (P=.0002), but not
stroke type. The nondemented patients more often had stroke located in
the right hemisphere (P=.0482) or had minor nondominant
stroke syndrome (P=.0140) compared with the demented
patients (Table 3
Dysphasia in the clinical neurological examination was more frequent in
the demented group (20.6% versus 3.5%; P<.001) (Table 4
Of the main neurological signs, gait impairment (43.9% versus 25.7%;
P=.001) and urinary incontinence (14.0% versus 3.5%;
P<.001) were more frequent in the demented group (Table 4
We used a logistic regression model to identify the correlates of
dementia in the whole series of the aforementioned variables. The
following correlates were found (n=337, demented n=107, model A):
dysphasia (OR, 5.64; 95% CI,2.26 to 15.5), major dominant stroke
syndrome (OR, 5.0; 95% CI, 1.92 to 14.1), any prior CVD (OR, 2.01;
95% CI, 1.073 to 3.74), and low level of education (OR, 1.13; 95% CI,
1.05 to 1.22) (Table 5
In the second approach, when those with mixed AD+VD (n=306, demented
n=87, model B) were excluded, the correlates of dementia remained the
same. Furthermore, in the third approach in which only the patients
with first-ever stroke were included (n=273, demented n=79, model C)
dysphasia, major dominant stroke syndrome and education were the
correlates of dementia. Finally, in the fourth approach in which
patients with dysphasia were excluded (n=307, demented n=85, model D),
major dominant stroke syndrome and education remained correlates of
dementia.
The correlates of dementia in logistic regression analysis were
dysphasia, major dominant stroke syndrome, history of previous CVD, and
low level of education. When those with CVD+AD or those with recurrent
stroke were excluded, the order of correlates remained the same. When
the patients with dysphasia (n=30) were excluded from the logistic
model, the correlates were major dominant syndrome and education.
In our series, presence of dysphasia in the clinical examination was
associated with dementia in the whole series, in those with
stroke-related dementia (mixed AD+VD excluded), and in those with
first-ever stroke. From the series, we had excluded patients with
severe aphasia after attempting to test everyone and included only
those who could be tested, as suggested in recent
guidelines.37 In a similar stroke cohort using the DSM-III
definition of dementia (n=251, demented n=61), Tatemichi et
al6 did not find an association. In both series the
frequency of dysphasia was close (8.9% versus 9.7%), but in our study
the percentage of demented patients with dysphasia was higher (20.6%
versus 12.6%). In the series of Ladurner et al8 (n=71,
demented n=41), dysphasia was also more frequent in the demented
subjects. Furthermore, in a smaller series (n=110, demented n=15)
focused on dementia after first-ever stroke, dysphasia was also
independently associated with dementia.7 The use of
different criteria for judging aphasia to be severe enough to
necessitate exclusion from a study may explain differences between the
cited studies.
Major dominant stroke syndrome was also a predictor of dementia
independent of the effect of dysphasia in the present study, which
agrees with the findings of Tatemichi et al6 and Ladurner
et al.8 Left hemispheric stroke localization was also more
common in demented patients, as shown previously.6 9 In the
series of Censori et al,7 dominant hemisphere stroke was
more frequent among the demented than nondemented patients (80.0%
versus 50.6%), but the independent correlates were total anterior
circulation stroke and frontal lesions. Because the focus of this
report was on clinical factors, we did not examine quantitative brain
imaging features. Although dysphasia is closely connected to the
concept of major dominant stroke syndrome, in the present series
69% of the patients with major dominant stroke syndrome had dysmnesia
and 31% dysphasia. In the series of Tatemichi et al,6
major dominant stroke syndrome was found in 12% of the patients, and
of these it was reported that 10 (40.0%) did not have cognitive
impairment, including language impairment.
Major stroke syndrome relates to left-sided lesions and reflects both
language and verbal and nonverbal memory disturbance that may
occur from unilateral left-sided damage.6 38 39 Memory and
language deficits are essential domains in definitions used for
dementia3 and are also known to be potential consequences
of stroke. Language impairment seems to also have an independent
correlation with dementia that is not explained by the consequences of
major dominant hemispheric stroke, partly because nondominant stroke
syndromes can also affect language and other cognitive domains.
In the present series, none of the stroke types were associated
with dementia. In the series of Tatemichi et al,6
small-vessel occlusion (lacunae) was an independent predictor of
poststroke dementia. This may well reflect selection since lacunar
lesions predominate in patients with small-vessel disease and
subcortical ischemic lesions.40 However, possible
selection and small sample size may have underpowered this study to
detect a possible association. In our series, including an older random
population, the frequency of stroke of undetermined etiology was 60%.
Originally TOAST was designed for clinical drug trials, in which the
frequency of undetermined stroke has been more than 40%.41
Our higher figure is mainly due to the strict classification system,
including clinical definition of lacunar syndromes, lack of repeated
brain images early in the course, and the absence of systematic cardiac
assessments. Accordingly, both stroke due to small-vessel occlusion
(lacunar) and cardioembolism are likely underestimated
in our series.18 In addition to our series, the only other
stroke cohort examining both the frequency of dementia and types of
stroke thus far is that of Tatemichi et al.6 In that series
the frequency of lacunar stroke was 29.7% among the nondemented and
36.4% in the demented subgroups, and the frequency of DSM-III dementia
was 26.3%. Whether difference in distribution of lacunar stroke (8%
in the study presented here) could have had an effect on the difference
in frequency of dementia compared with our series (31.8%) cannot be
confirmed.
Only completed previous strokes seemed to be a risk factor for VD
(26.2% versus 15.7%; P=.0220), not the history of TIAs,
which actually seemed to occur less often (5.6% versus 16.5%;
P=.0056) in patients with dementia in our series. In the
series of Tatemichi et al,6 demented patients did not
differ from nondemented patients in regard the history of prior TIA
(17.2% versus 19.1%; P=.732), but demented subjects more
often had a history of stroke (31.8% versus 20.0%;
P=.064). A history of TIA increases the risk of subsequent
stroke,42 but a history of TIA at the time of
ischemic stroke did not influence outcome in 3 years of
follow-up.43
Low level of education was a correlate of dementia, as shown in two
previous poststroke series,6 9 as well as in
population-based series on dementia.44 The norms on
cognitive tests were not adjusted for education because so few subjects
were highly educated in this cohort. However, this may have slightly
influenced the diagnosis of dementia. Higher education likely relates
to larger functional cognitive reserve45 and also to
differences in lifestyle and risk factor profile.46
Of the vascular risk factors, current smoking was associated with
dementia in the present series, as in the series of Gorelic et
al,9 where it was an independent correlate of dementia
poststroke. Previously diabetes,6 7 myocardial
infarction,9 and arterial
hypertension8 have been related to poststroke dementia,
which could not be confirmed in the present series.
In epidemiological studies, risk factors of VD have included
arterial hypertension,10 12 13 cardiac
disorders,10 11 12 diabetes,10 11 prior
stroke,11 13 high hematocrit level,12 and
alcohol abuse13 in different combinations. Recently, Skoog
et al47 related high midlife blood pressure to a higher
risk of dementia later in life. In the present study mean
arterial blood pressure was lower in the demented group. In
addition, in the series of Guo et al48 the demented
patients showed lower arterial blood pressure values at the
time of diagnosis, which was not the case in the series of Skoog et
al.47 Low blood pressure has been related to the severity
of dementia,48 which may be a factor in explaining these
differences. The demented patients in our series more frequently had
abnormal orthostatic reaction. Thus far the association
between postural hypotension and dementia is still controversial. In a
general aged population, postural hypotension was not associated with
dementia.49 On the other hand, the presence of more
frequent orthostatic reaction among patients with
poststroke dementia may reflect changes in autoregulation due to
small-vessel changes or other ischemic brain
lesions.47
Our data suggest that a single explanation for poststroke dementia is
not adequate and that multiple factors, including stroke features, host
characteristics, and prior CVD, each independently contribute to the
risk. In addition to ischemic brain changes, coexisting AD-type
pathology may also be a factor, as indicated by the number of patients
with prestroke cognitive decline and presumed coexisting AD.
Received May 27, 1997;
revision received October 20, 1997;
accepted October 20, 1997.
© 1998 American Heart Association, Inc.
Original Contributions
Clinical Determinants of Poststroke Dementia
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and Purpose—Frequency of
poststroke dementia is high, and stroke considerably increases the risk
of dementia. The risk factors for dementia related to stroke are still
incompletely understood. We sought to examine clinical determinants of
poststroke dementia in a large well-defined stroke cohort.
Key Words: cerebral ischemia • dementia • diagnosis • Finland
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The frequency of
VD1 and that of poststroke dementia2 3 are
higher than previously expected, and stroke considerably increases the
risk of dementia.2 4 5 The risk factors for dementia
related to stroke are still incompletely understood. In addition to age
and low level of education, different combinations of risk factors and
stroke features have been associated with poststroke dementia in
previous stroke cohorts6 7 8 9 and follow-up
studies.5 Studies on risk factors for VD have also shown
inconsistent findings.10 11 12 13
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Procedures of the Helsinki Stroke Aging Memory Study cohort were
detailed in a report on methods and baseline findings.3
Briefly, 486 consecutive patients aged 55 to 85 years were evaluated 3
months after ischemic stroke. Of these, 451 completed a
clinical neurological and mental status examination.3 The
excluded patients included 1 who refused, 1 with reduced level of
consciousness, 1 with severe hearing impairment, and 32 with severe
aphasia. Of the 451 patients, 337 (74.7%) completed MRI of the head
and a comprehensive neuropsychological examination. The 114 patients
not included were 59 in whom MRI was not performed (contraindication in
27, refusal in 18, claustrophobia in 2, severe illness in 11, obesity
in 1) and 55 who did not complete in detail the cognitive test battery
(lack of sufficient cooperation in 23, refusal in 14, nonfluency in
Finnish language in 5, severe aphasia in 5, severe neglect in 3,
hearing or visual impairment in 3, illiteracy in 2). The 114 patients
excluded were older (mean age, 73.5 versus 70.2 years;
P<.001), less often had small-vessel occlusion (1/114
versus 27/337; P=.0064), and more often stroke of
undetermined etiology (82/114 versus 202/337; P=.0219), but
they did not differ in terms of main demographic and clinical features
including sex, education, and number, side, and site of stroke).
We compared nondemented and demented patients. A
2 test was used for categorical data and pooled
t test for continuous data. All the variables that
significantly differentiated the nondemented and demented groups were
set to a logistic regression model to determine the correlates of
dementia in four different patient groups: model A, poststroke dementia
(n=337); model B, stroke-related dementia (mixed AD+VD excluded)
(n=306); model C, dementia after first-ever stroke (n=273); and model
D, patients with dysphasia excluded (n=307). Statistics were calculated
with the use of the BMDP and SAS programs.35 36
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Of the 377 patients with ischemic stroke, dementia was
present in 107 (31.8%). The patients with dementia were older and
more often had less than 6 years of education (Table 1
).
View this table:
[in a new window]
Table 1. Characteristics of Nondemented and Demented Patients
in the Helsinki Stroke Aging Memory (SAM) Study Cohort (n=337) ). History of any prior CVD (28.0%
versus 17.4%; P=.0295) and prior ischemic stroke
(26.2% versus 15.7%; P=.0220), but not that of TIA (5.6%
versus 16.5%; P=.0056), were more frequent in the demented
than in the nondemented group.
View this table:
[in a new window]
Table 2. Risk Factors of Stroke and Prior (CVD) in
Nondemented and Demented Patients in the Helsinki Stroke Aging Memory
Study Cohort (n=337) ).
View this table:
[in a new window]
Table 3. Characteristics of Ischemic Stroke in
Nondemented and Demented Patients in the Helsinki Stroke Aging Memory
Study Cohort (n=337) ). Of the 30 patients with dysphasia, 22
(73.3%) had dementia. Compared with the nondemented dysphasic
patients, the demented patients did not differ significantly in regard
to stroke localization on the left side (87.5% versus 81.8%),
presence of major stroke syndrome (12.5% versus 36.4%), history of
previous stoke (25.0% versus 18.2%), or presence of cognitive decline
before index stroke (25.0% versus 31.8%). Of the 30 patients with
dysphasia, 9 (30%) had major dominant stroke syndrome, 17 (56.7%)
minor dominant stroke syndrome, and 4 (13.3%) another stroke syndrome.
Of the 29 patients with major dominant stroke syndrome, 9 (31%) had
dysphasia and 20 (69%) had hemianopia and dysmnesia.
View this table:
[in a new window]
Table 4. Neurological Signs and Clinical Findings in
Nondemented and Demented Patients in the Helsinki Stroke Aging Memory
Study Cohort (n=337) 
).
The demented patients had lower mean values of systolic
(P=.0338) and diastolic (P=.0075)
arterial blood pressure when supine and had more frequently
an orthostatic reaction (21.5% versus 14.3%,
P=.045). None of the laboratory measures showed differences
between the two groups (data not shown). ).
View this table:
[in a new window]
Table 5. Correlates of Dementia in the Logistic Regression
Analysis 3 Months After Ischemic Stroke Using Multiple
Logistic Models in the Helsinki Stroke Aging Memory Study Stroke Cohort
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
We report here the largest well-defined stroke cohort thus far to
examine cross-sectional features related to risk of dementia. The
patients with poststroke dementia in the present series were more
often older and had a lower level of education, history of prior CVD
and stroke, history of current smoking, cardiac failure, left
hemispheric stroke (reflecting laterality), a major dominant stroke
syndrome (reflecting laterality and size), dysphasia, gait impairment,
urinary incontinence, lower arterial blood pressure values,
and more frequently had an orthostatic reaction compared
with the nondemented stroke patients.
Selected Abbreviations and Acronyms
AD
=
Alzheimer's disease
CI
=
confidence interval
CVD
=
cerebrovascular disease
DSM-III
=
Diagnostic and Statistical Manual of Mental
Disorders, edition 3
OR
=
odds ratio
TIA
=
transient ischemic attack
TOAST
=
Trial of Org 10172 in Acute Stroke Treatment
VD
=
vascular dementia
WAIS-R
=
Wechsler Adult Intelligence Scale, Revised
Acknowledgments
This study was supported in part by grants from the Medical
Council of the Academy of Finland, Helsinki (T.E.); the Clinical
Research Institute, Helsinki University Central Hospital (T.P., R.V.);
and the Finnish Alzheimer Foundation for Research, Helsinki
(T.P., T.E.). We thank Vesa Kuusela, senior research officer,
Statistics Finland, Helsinki, for statistical support and
review.
Footnotes
Reprint requests to Dr T. Erkinjuntti, Memory Research Unit, Department of Neurology, University of Helsinki, Haartmaninkatu 4, 00290 Helsinki, Finland.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
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W. K. Tang, S. S.M. Chan, H. F.K. Chiu, G. S. Ungvari, K. S. Wong, T. C.Y. Kwok, V. Mok, K.T. Wong, P. S. Richards, and A.T. Ahuja Frequency and Determinants of Poststroke Dementia in Chinese Stroke, April 1, 2004; 35(4): 930 - 935. [Abstract] [Full Text] [PDF]
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J. G. Merino and K. M. Heilman Editorial Comment--Measurement of Cognitive Deficits in Acute Stroke Stroke, October 1, 2003; 34(10): 2396 - 2398. [Full Text] [PDF]
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A. Cherubini and U. Senin Editorial Comment--Elderly Stroke Patient at Risk for Dementia: In Search of a Profile Stroke, October 1, 2003; 34(10): 2445 - 2445. [Full Text] [PDF]
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J.-H. Lin, R.-T. Lin, C.-T. Tai, C.-L. Hsieh, S.-F. Hsiao, and C.-K. Liu Prediction of poststroke dementia Neurology, August 12, 2003; 61(3): 343 - 348. [Abstract] [Full Text] [PDF]
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 K. Narushima, K.-L. Chan, J. T. Kosier, and R. G. Robinson Does Cognitive Recovery After Treatment of Poststroke Depression Last? A 2-Year Follow-Up of Cognitive Function Associated With Poststroke Depression Am J Psychiatry, June 1, 2003; 160(6): 1157 - 1162. [Abstract] [Full Text] [PDF]
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M.-A. Cordoliani-Mackowiak, H. Henon, J.-P. Pruvo, F. Pasquier, and D. Leys Poststroke Dementia: Influence of Hippocampal Atrophy Arch Neurol, April 1, 2003; 60(4): 585 - 590. [Abstract] [Full Text] [PDF]
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 S. E. Vermeer, N. D. Prins, T. den Heijer, A. Hofman, P. J. Koudstaal, and M. M.B. Breteler Silent Brain Infarcts and the Risk of Dementia and Cognitive Decline N. Engl. J. Med., March 27, 2003; 348(13): 1215 - 1222. [Abstract] [Full Text] [PDF]
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R. Barba, M.-d.-M. Morin, C. Cemillan, C. Delgado, J. Domingo, and T. Del Ser Previous and Incident Dementia as Risk Factors for Mortality in Stroke Patients Stroke, August 1, 2002; 33(8): 1993 - 1998. [Abstract] [Full Text] [PDF]
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O. Godefroy, C. Dubois, B. Debachy, M. Leclerc, and A. Kreisler Vascular Aphasias: Main Characteristics of Patients Hospitalized in Acute Stroke Units Stroke, March 1, 2002; 33(3): 702 - 705. [Abstract] [Full Text] [PDF]
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H. Henon, I. Durieu, D. Guerouaou, F. Lebert, F. Pasquier, and D. Leys Poststroke dementia: Incidence and rela |