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Abstract

Background: Vascular dementia is extremely common and contributes to stroke-associated morbidity and mortality. The study of vascular dementia may help to plan preventive interventions. Aims: To study the frequency of cognitive impairment after stroke in a series of consecutive patients with acute stroke, along with factors which influence it. Methods: Fifty adults with acute infarct or hemorrhage (as seen on computed tomography of the brain) were included in the study. The National Institute of Health Stroke Scale (NIHSS) and Barthel’s Index scores were done. Cognitive testing was done by PGI Battery of Brain Dysfunction (PGI-BBD) and Short Form of the Informant Questionnaire on Cognitive Decline in the Elderly (SIQCODE). Statistical analysis was by Student’s t-test, Chi-square test, Fisher’s exact test, and Mann-Whitney U test. Results: Mean age of patients was 61.82 years; males and ischemic strokes predominated. Dementia was seen in 30%, cognitive impairment no dementia (CIND) in 42%, and normal cognition in 28% patients. Factors associated with vascular cognitive impairment included old age, male sex, low education, hemorrhages, recurrent or severe stroke, silent infarcts, severe cortical atrophy, and left hemispheric or subcortical involvement. Conclusions: Up to 72% of patients have some form of cognitive impairment after a stroke. Secondary stroke prevention could reduce the incidence of vascular dementia.
Received 07/18/2015
Review began 09/09/2015
Review ended 09/15/2015
Published 09/29/2015
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Cognitive Impairment After Stroke
Pushpendra Nath Renjen , Charu Gauba , Dinesh Chaudhari
1. Neurosciences, Indraprastha Apollo Hospital 2. Neurosciences, Indraprastha Apollo Hospitals 3.
Internal Medicine / Neurosciences, Indraprastha Apollo Hospital
Corresponding author: Pushpendra Nath Renjen, pnrenjen@hotmail.com
Disclosures can be found in Additional Information at the end of the article
Abstract
Background: Vascular dementia is extremely common and contributes to stroke-associated
morbidity and mortality. The study of vascular dementia may help to plan preventive
interventions.
Aims: To study the frequency of cognitive impairment after stroke in a series of consecutive
patients with acute stroke, along with factors which influence it.
Methods: Fifty adults with acute infarct or hemorrhage (as seen on computed tomography of the
brain) were included in the study. The National Institute of Health Stroke Scale (NIHSS) and
Barthel's Index scores were done. Cognitive testing was done by PGI Battery of Brain Dysfunction
(PGI-BBD) and Short Form of the Informant Questionnaire on Cognitive Decline in the Elderly
(SIQCODE). Statistical analysis was by Student's t-test, Chi-square test, Fisher's exact test, and
Mann-Whitney U test.
Results: Mean age of patients was 61.82 years; males and ischemic strokes predominated.
Dementia was seen in 30%, cognitive impairment no dementia (CIND) in 42%, and normal
cognition in 28% patients. Factors associated with vascular cognitive impairment included old
age, male sex, low education, hemorrhages, recurrent or severe stroke, silent infarcts, severe
cortical atrophy, and left hemispheric or subcortical involvement.
Conclusions: Up to 72% of patients have some form of cognitive impairment after a stroke.
Secondary stroke prevention could reduce the incidence of vascular dementia.
Categories: Internal Medicine, Physical Medicine & Rehabilitation, Neurology
Keywords: cognitive impairment, stroke, vascular dementia, cind, psd, nihss, iqcode, barthel index
Introduction
Vascular dementia is one of the two most prevalent forms of dementia. Studies have
demonstrated that post-stroke dementia (PSD) increases the risk for recurrent stroke and
mortality [1]. Post-stroke dementia (PSD) is defined as the presence of dementia identified at
three months after an acute, either recurrent or first-ever, stroke. A stroke increases the risk of
dementia four to 12 times. The prevalence of PSD among stroke patients varies from 6% to 55%
and may decline years after stroke [2]. Some patients may have cognitive impairment that does
not meet the criteria for dementia but nevertheless have an increased risk of cognitive
deterioration, institutionalization, and death. These patients may have more opportunities for
treatment and prevention [3]. The study of predictors of dementia after a stroke may assist in
planning interventions to prevent vascular dementia [4].
1 2 3
Open Access Original
Article DOI: 10.7759/cureus.335
How to cite this article
Renjen P, Gauba C, Chaudhari D (September 29, 2015) Cognitive Impairment After Stroke. Cureus 7(9):
e335. DOI 10.7759/cureus.335
Materials And Methods
This was a prospective study of 50 consecutive patients of stroke attending the emergency or
outpatient department. The Scientific Review Committee of Indraprastha Apollo Hospital
approved this study. No approval number was required for this project. Patients included were
those aged 45 years or above who had a stroke within one week of the first visit, irrespective of
their previous cerebrovascular or cognitive status. Patients with transient ischemic attack, stroke
associated with other brain lesions (e.g., tumour or trauma), other neurodegenerative disorders
which may lead to dementia (e.g., Parkinsonism), and patients with persistent moderate to
severe aphasia (score ≥ 1 on the language component of the National Institute of Health Stroke
Scale, NIHSS) were excluded. Patients were evaluated on the first visit, at three months, and at
12 months. On the first visit, the diagnosis and type of stroke were established. Demographic
details, handedness, education, past family and medication history, and risk factors for stroke
were noted along with the BP on admission and any hypotensive episodes (BP < 105 systolic)
during the hospital stay. Physical examination was done, including NIHSS scoring to assess
stroke severity. A non-contrast computerised tomography (NCCT) of the head was performed to
document the site and size of the infarct or haemorrhage and to look for strokes in strategic
locations and silent infarcts [5].
The severity of white matter changes (WMC) was graded as 0, 1 or 2. In Grade 1, the abnormality
was restricted to the region adjoining the ventricles. In Grade 2, the abnormality involved the
entire region from lateral ventricle to the cortex. The grades given to the regions were added to
give an overall value between 0 and 4 [6]. The measurements for cortical atrophy were taken from
the CT slice that best depicted the third ventricle [7].
Atrophy was classified as absent if the maximal third ventricle width was less than 5 mm, mild if
5 to 6 mm, moderate if 6 to 7 mm, and severe if 7 mm and above. Pre-stroke cognitive status was
assessed by means of the Short Form of the Informant Questionnaire on Cognitive Decline in the
Elderly (Short IQCODE) and the functional status by the Barthel index. These were administered
to the patient’s primary caregiver on all visits. The PGI battery of brain dysfunction (PGI BBD)
was applied to all patients at three and 12 months after stroke. This is a battery of
neuropsychological tests specifically designed for Indian patients keeping cultural factors in
mind. Worsening in IQCODE scores between the first visit and the third-month examination
would, therefore, imply deterioration mainly produced by the stroke. The third month was taken
as a post-stroke baseline to assure stable cognition. Changes between three months and 12
months would reflect cognitive evolution after the acute phase of the stroke. Fresh vascular
events were reassessed on the three and 12-month visits, and demographic, neurological, and
functional data were compared among all patients.
Vascular dementia was defined as per the Diagnostic and Statistical Manual of Mental Disorders
criteria. These were assessed by the IQCODE, neuropsychological test battery, and the activities
of daily living on the Barthel index. PGI BBD scores less than 17 was taken as normal, 18 to 29 as
cognitive impairment no dementia (CIND), and more than 30 as dementia [8-9]. The results were
statistically analysed and an attempt was made to draw inferences about the presence of post-
stroke cognitive impairment with and without dementia, factors influencing its development,
whether it is more often cortical or subcortical, and the evolution of cognitive impairment over
time.
Results
The study group comprised of 50 patients of whom 32 were males and 18 were females with a
mean age of 61.82 years. Eighty percent had studied up to grade 10 or more. Infarcts were seen in
37 and haemorrhages in 13 patients. Of the 50 patients, 14 (28%) had normal cognition, 15 (30%)
had dementia, and 21 (42%) had CIND as per the PGI BBD score (Figure 1). Thus, 36 (72%) had
2015 Renjen et al. Cureus 7(9): e335. DOI 10.7759/cureus.335 2 of 9
some form of cognitive impairment following a stroke. The domains that were commonly
involved were retention for dissimilar pairs, visual retention, attention, and recognition.
FIGURE 1: Post-Stroke Dementia
The prevalence of cognitive impairment was higher with increasing age (100% in the age group
80 - 89 years), P = 0.695, and in male subjects (75% vs. 66.6% in females), P = 0.473. Of all the
patients who studied until grade 10, 80% had cognitive impairment while only 70 % of all the
patients who studied beyond grade 10 had cognitive impairment, P = 0.100. More patients with
hemorrhagic strokes (84.6%) had cognitive impairment compared to those with ischemic strokes
(67.5%), P = 0.077. Five of 50 patients had a recurrence of stroke, and of those patients, four
(80%) had cognitive impairment (2 CIND, 2 dementia). Of the remaining 45 patients with no
stroke recurrence, 32 (71.1%) had cognitive impairment (19 CIND, 13 dementia).
Of the 50 study patients, only one had CIND before stroke (SIQCODE 3.31). No relation of
2015 Renjen et al. Cureus 7(9): e335. DOI 10.7759/cureus.335 3 of 9
cognitive impairment was found with the level of glycemic control. Only four patients had
hypotensive episodes in the post-stroke period, of whom two had CIND and two normal
cognition. No particular vascular risk factor was associated with a greater risk of cognitive
decline. Patients with dementia had a higher median NIHSS score of 6 (a greater disability at the
time of stroke) and a lower median Barthel index of 12 (a greater dependency for activities of
daily living). No obvious correlation was found with the size of the lesion or the degree of WMC
on CT scan. The mean WMC score was 1.42 for patients with normal cognition, 1.42 for patients
with CIND, and 1.26 for patients with dementia, P = 1.00.
Cognitive impairment was more frequent in patients with left-sided lesions (80.7%), P = 0.176,
silent infarcts (88.8%), P = 0.694, and cortical atrophy (100% in severe atrophy), P = 0.337. Of the
36 patients with some form of cognitive impairment, the location of the lesion was subcortical in
25 and cortical in 11 subjects. Of the 14 patients with normal cognition, the location of the lesion
was subcortical in seven and cortical in the other seven subjects (Figure 2). Of the 32 patients
with subcortical distribution of the infarct or haemorrhage, 25 (78.1%) had some form of vascular
cognitive impairment. Of the 18 patients with cortical distribution of the infarct or haemorrhage,
11 (61.1%) had some form of vascular cognitive impairment. There were 24 patients with lesions
in strategic locations, 17 (70.8%) of whom had some form of cognitive impairment. Of the 26
patients with lesions in non-strategic locations, 19 (73%) had some form of cognitive
impairment. Statistical tests applied were Student’s t-test, Mann-Whitney U test, Fisher’s exact
test, and Chi-square test but none of the associations were statistically significant.
2015 Renjen et al. Cureus 7(9): e335. DOI 10.7759/cureus.335 4 of 9
FIGURE 2: Cognitive impairment association with the location of
lesion
Discussion
The distribution of infarcts and haemorrhages in this study reflected the usual pattern seen in
stroke patients [2]. The mean age of the study subjects was 61.82 years, which was lower than
that seen in most other studies [1, 10-12]. The mean age of Indian patients with stroke ranges
from 63 - 65 years for men and 57 - 68 years for women. In this study, the ratio of men to women
with stroke was 2:1. The male/female sex ratio for stroke patients in India is 7:1, which may be
due to smoking and drinking being more prevalent among men than women [13]. These risk
factors, however, are also common among urban, rich women, which may explain why strokes
were common in women in this study.
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Sundar, et al. studied 164 patients with stroke and concluded that 31.7% patients had cognitive
impairment at three months post-ischemic stroke, either on the Mini-Mental State Examination
(MMSE) or the frontal assessment battery (FAB) [14]. Of the study subjects, 17.07% were impaired
on frontal executive functions only. Single and multiple infarcts were not significantly different
with respect to post-stroke cognitive impairment, the main difference being that memory
affection was significantly more common in the latter; hence, the importance of the need to be
aware of disorders of these specialized functions, which directly impact the quality of life post-
stroke, cannot be over-emphasized [14].
Das, et al. studied 960 patients and concluded that an overall prevalence of mild cognitive
impairment (MCI) detected based on neuropsychological testing was 14.89% (95% CI: 12.19 to
17.95) [15]. Prevalence of the amnestic type was 6.04% (95% CI: 4.40 to 8.1) and that of the
multiple domain type was 8.85% (95% CI: 6.81 to 11.32). Adjusted for age, education, and gender,
the amnestic type was more common among men and the multiple domain types among women
with the advancement of age. Rates differed considerably with educational attainment.
Hypertension and diabetes mellitus were the major risk factors for both types of MCI [15].
Mukhopadhyay, et al. studied the prevalence of stroke and post-stroke cognitive impairment in
the elderly and concluded that prevalence rates of stroke from their study were found to be
comparable to rates from contemporary Indian studies and higher than older studies [16]. The
rates are lower than those in more developed countries, which may be due to higher mortality in
this particular low-income group. The continuous population ageing process in India, in
conjunction with the increasing incidence of diabetes and hypertension, can cause an alarming
rise in the incidence and prevalence of stroke, besides adversely affecting post-stroke residual
disability and cognitive function. There is a pressing need for population-based awareness
initiatives on healthy lifestyles. Existing treatment and rehabilitation facilities require
upgrading, together with early diagnosis and adequate treatment of risk factors, especially for
the underprivileged sections of society [16].
In the present study, vascular cognitive impairment was present in 36 (72%) of our patients, of
whom 15 (30%) had dementia and 21 (42%) had CIND. The prevalence of PSD among recurrent or
first-ever stroke patients varies from 6% to 55% [2, 10-12]. The difference of the prevalence of
PSD among various studies depends on the study design (e.g., non-prospective or non-
consecutive samples), the demographic characteristics of the population studied (e.g., age,
gender, and ethnicity), criteria used for the diagnosis of dementia, the pre-existing cognitive
level, lesion-related and radiological-associated factors (like exclusion of haemorrhage or
recurrent stroke, white matter changes, and the presence of cerebral atrophy), vascular risk
factors, the time interval between the stroke and the neuropsychological assessment, and length
of follow-up [2].
Although our study group included more females and a relatively younger population as
compared to other studies, the prevalence of dementia was not low. This may have been due to
the fact that haemorrhages and recurrent strokes were also included in this study. Moreover,
the incidence of dementia in hospital-based studies like this one are much higher than
the incidence reported from the community-based Framingham Study in which the rate of
dementia was 19.3% in stroke patients compared to 11.0% in controls over a 10-year period [10].
This compares with an up to nine-fold increase reported in some cross-sectional studies. It is
possible that strokes in the community sample were less severe. Cognitive dysfunction does not
follow a linear time course after stroke. Short-term studies may over-diagnose cognitive post-
stroke dysfunction. Further follow-up in this study may have revealed a decline in the prevalence
of cognitive impairment [17]. The definition of vascular dementia used is an important
consideration in the interpretation of prevalence rates. In our study, the presence of an infarct
was not considered necessary for the diagnosis if the subject had extensive white matter
pathology. This may have contributed to the high prevalence of vascular cognitive impairment.
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In this study, the prevalence of cognitive impairment was higher with increasing age (100% in
the age group 80 - 89 years) and in male subjects (75% vs. 66.6% in females). A lower level of
education also appeared to be associated with a greater chance of cognitive impairment (80% in
patients having studied till class 10 vs. 70% in those having studied further). More patients with
hemorrhagic strokes (84.6%) had cognitive impairment compared to those with ischemic strokes
(67.5%). There were no previous comparative studies that compared the prevalence of cognitive
impairment in ischemic and hemorrhagic strokes. On the other hand, increasing age (> 60 years)
and low education have consistently emerged as risk factors for cognitive impairment after
stroke [2, 10]. This was considered to be due to the additional cerebrovascular pathology in older
patients, which may be due to previous infarctions and non-infarct ischemic changes.
The role of Alzheimer’s disease (AD) type pathology in older patients is another important
factor. Patients with higher educational attainment have a larger functional cognitive reserve
and differences in lifestyle and risk factor profile, which are protective against cognitive decline.
Although patients with stroke recurrence tended to have a higher chance of cognitive
impairment (80% vs. 71% in those without stroke recurrence), no particular vascular risk factor
was associated with a greater risk of cognitive decline, in our study group. Patients with
cognitive impairment had a higher median NIHSS score (a greater disability at the time of stroke)
and a lower median Barthel index (a greater dependency for activities of daily living), as in other
studies. However, stroke recurrence did not predispose to cognitive impairment in all studies and
neither did any particular risk factor, although cognitively impaired patients had a higher overall
number of risk factors in comparison to non-impaired patients [10].
In our study, left-sided lesions (80.7%), the presence of silent infarcts (88.8%), and cortical
atrophy (100% in severe atrophy) correlated with a greater risk of cognitive impairment but the
size or volume of the lesion and degree of white matter change had no correlation. The strategic
location of the lesion did not appear to be associated with a higher incidence of cognitive
impairment either (70.8% in strategic lesions vs. 73% in non-strategic lesions). Other studies
have found a correlation with size or volume and strategic location of the lesion [10]. The classic
concept implies that dementia of vascular origin is the result of a critical volume of infarcted
brain tissue. Large-sized infarctions are expected to produce more cognitive impairment
compared to small-sized infarctions unless the small infarcts are in strategic locations (e.g.,
thalamus, internal capsule, basal ganglia, corpus callosum, and hippocampus) [18]. In other
studies as well, left-sided strokes had a greater association with cognitive impairment even when
patients with severe dysphasia were excluded. This is presumably because most memory tasks
rely on intact language function. In most studies, no significant differences were found in the
prevalence of dementia between patients with mild, moderate, and severe WMCs. The
subcortical syndrome with executive deficits and mental slowing are the most prominent
cognitive characteristics associated with severe WMCs, and these characteristics may lead to
secondary impairments of memory and visuospatial functions [19]. Studies have shown that
cortical atrophy predicts subsequent cognitive decline in both AD and PSD. Preventing strokes
should thus be considered complementary to therapies for AD, and the two therapeutic strategies
may produce synergistic effects [20].
In our study of the 36 patients with cognitive impairment, 25 (70%) cases had a subcortical
location of the lesion. CIND was found more often than dementia in these patients. In contrast,
the remaining patients with a cortical location of the lesion had an equal distribution of CIND
and dementia. Patients with a subcortical location of a lesion were more likely to have cognitive
impairment (78.1%) than those with a cortical location of a lesion (61.1%). Basal ganglia and
thalamic lesions were especially associated with cognitive impairment. The cognitive profile of
subcortical vascular disease can be distinguished from that of AD principally by milder memory
impairment but more pronounced impairment of executive function and a slowing of motor and
psychomotor speed. Because most studies have not included measures of motor speed in their
test battery, the prevalence of subcortical dementia has been found to be low [18].
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The main limitation of this study was that the number of subjects was small, and hence, none of
the results achieved statistical significance. The results reflect the incidence in a predominantly
urban population in a tertiary care hospital. Ischemic and hemorrhagic strokes should have been
studied separately as the evolution of cognition may be different in both. The neuropsychological
test battery did not effectively identify frontal lobe dysfunction or differentiate between cortical
and subcortical dementia. MRI scans of the brain would have been a better imaging modality
than CT to pick up radiological evidence of vascular brain damage. However, this was not done
due to cost concerns. Further evolution of cognition over time and the effect of treatment could
not be studied as no patients were available for follow-up. The strengths of the study were that it
was a prospective study and one of the few such studies done in India. The neuropsychological
test battery used was one that was validated in Indian patients and was performed by a single
observer so there was no observer bias.
Conclusions
In our study, we found that up to 72% of patients have some form of cognitive impairment after a
stroke of which 30% had dementia and 42% had CIND. Neuropsychological assessment should be
an important part of the clinical evaluation in stroke patients but is best done after about three
months once the stroke has stabilised. Secondary stroke prevention could reduce the incidence of
vascular dementia. This can be done by aiming at the modifiable risk factors for stroke, such as
hypertension, diabetes, dyslipidemia, hyperhomocysteinemia, and smoking.
Additional Information
Disclosures
Animal subjects: This study did not involve animal subjects or tissue. Human subjects: The
Institutional Ethics cum Scientific Review Committee of Indraprastha Apollo Hospital issued
approval N/A.
Acknowledgements
I would like to thank Mr Rahul Raut for his generous contribution and secretarial help in the
study.
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... Studies included: ischemic and hemorrhagic strokes (12 studies), [12][13][14]17,[19][20][21][22]25,32,36,38 ischemic stroke and TIA (one study), 33 ischemic strokes only (10 studies), 11,16,18,23,26,[29][30][31]35,37 hemorrhagic strokes only (two studies) 15,. Two studies only recruited lacunar infarcts 24,27 and one study only recruited supratentorial infarcts. ...
... Two studies only recruited lacunar infarcts 24,27 and one study only recruited supratentorial infarcts. 34 CT scans were performed: at admission/as soon as possible (10 studies), 11,17,19,21,24,28,30,35,37,38 within 48 h (six studies), 15,16,22,29,31,33 within one week (eight studies), 13,18,20,23,26,32,34,36 within two weeks (three studies), 12,25,27 within 0-30 days (one study). 14 ...
... Length of follow-up for PSD and/or PSCI ranged from three months to six years after stroke (Supplement 5). The primary cognitive outcomes were PSD (10 studies; prevalence ranging from 11 to 50%), [14][15][16][22][23][24][25]27,28,36 PSCI (17 studies; prevalence ranging from 8 to 80%), [11][12][13][17][18][19][20][21]26,29,30,[32][33][34][35]37,38 and one study analyzed both PSD and PSCI separately (prevalence 10% and 59%, respectively). 31 A variety of measures were used for diagnosing dementia and assessing cognition (Supplement 5). ...
Article
Full-text available
Background: Identifying whether acute stroke patients are at risk of cognitive decline could improve prognostic discussions and management. Structural computed tomography (CT) neuroimaging is routine in acute stroke, and may, identify those at risk of post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI). Aim: To systematically review the literature to identify which stroke or pre-stroke features on brain CT scans, performed at the time of stroke, are associated with PSD or PSCI. Summary of review: We searched electronic databases to December 2020. We included studies reporting acute stroke brain CT, and later diagnosis of a cognitive syndrome. We created summary estimates of size of unadjusted association between CT features and cognition. Of 9536 citations, twenty-eight studies (41 papers) were eligible (N=7078, mean age 59.8-78.6 years). Cognitive outcomes were PSD (10 studies), PSCI (17 studies), and one study analysed both. Fifteen studies (N=2952) reported data suitable for meta-analyses. White matter lesions (WML) (6 studies, N=1054, OR=2.46, 95% CI=1.25-4.84), cerebral atrophy (4 studies, N=558, OR=2.80, 95% CI=1.21-6.51), and pre-existing stroke lesions (3 studies, N=352, OR=2.38, 95% CI=1.06-5.32) were associated with PSD. WML (4 studies, N=473, OR=3.46, 95% CI=2.17-5.52) were associated with PSCI. Other CT features were either not associated with cognitive outcome, or there were insufficient data. Conclusions: Cognitive impairment following stroke is of great concern to patients and carers. Features seen on visual assessment of acute stroke CT brain scans are strongly associated with cognitive outcomes. Clinicians should consider when and how this information should be discussed with stroke survivors.
... Our literature review found 13 studies examining associations between CT-brain imaging variables and post-stroke dementia or PSCI ascertained at least 12 months after stroke (Table 12 and Appendices S1 and S2) [165][166][167][168][169][170][171][172][173][174][175][176][177]. Six studies reported on poststroke dementia [167,168,170,172,174,175] and six reported PSCI. ...
... unadjusted) [175], but relationships between WMH and PSCI were less certain. Severity of WMH was associated with dementia in three [167,170,175] of five studies [172,177] (e.g. RR 2.09, 95% CI 1.05-4.13). ...
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Background and purpose The optimal management of post-stroke cognitive impairment (PSCI) remains controversial. These joint European Stroke Organisation (ESO) and European Academy of Neurology (EAN) guidelines provide evidence-based recommendations to assist clinicians in decision making regarding prevention, diagnosis, treatment and prognosis. Methods Guidelines were developed according to the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) methodology. The working group identified relevant clinical questions, performed systematic reviews, assessed the quality of the available evidence, and made specific recommendations. Expert consensus statements were provided where insufficient evidence was available to provide recommendations. Results There was limited randomized controlled trial (RCT) evidence regarding single or multicomponent interventions to prevent post-stroke cognitive decline. Lifestyle interventions and treating vascular risk factors have many health benefits, but a cognitive effect is not proven. We found no evidence regarding routine cognitive screening following stroke, but recognize the importance of targeted cognitive assessment. We describe the accuracy of various cognitive screening tests, but found no clearly superior approach to testing. There was insufficient evidence to make a recommendation for use of cholinesterase inhibitors, memantine nootropics or cognitive rehabilitation. There was limited evidence on the use of prediction tools for post-stroke cognition. The association between PSCI and acute structural brain imaging features was unclear, although the presence of substantial white matter hyperintensities of presumed vascular origin on brain magnetic resonance imaging may help predict cognitive outcomes. Conclusions These guidelines highlight fundamental areas where robust evidence is lacking. Further definitive RCTs are needed, and we suggest priority areas for future research.
... Our literature review found 13 studies examining associations between CT-brain imaging variables and post-stroke dementia or PSCI ascertained at least 12 months after stroke (Table 12 and Appendices S1 and S2) [165][166][167][168][169][170][171][172][173][174][175][176][177]. Six studies reported on poststroke dementia [167,168,170,172,174,175] and six reported PSCI. ...
... unadjusted) [175], but relationships between WMH and PSCI were less certain. Severity of WMH was associated with dementia in three [167,170,175] of five studies [172,177] (e.g. RR 2.09, 95% CI 1.05-4.13). ...
Article
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Introduction: The optimal management of post stroke cognitive impairment remains controversial. These joint European Stroke Organisation (ESO) and European Academy of Neurology (EAN) guidelines provide evidence-based recommendations to assist clinicians in decision making around prevention, diagnosis, treatment, and prognosis. Methods: These guidelines were developed according to ESO standard operating procedure and the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) methodology. The working group identified relevant clinical questions, performed systematic reviews and, where possible, meta-analyses of the literature, assessed the quality of the available evidence, and made specific recommendations. Expert consensus statements were provided where insufficient evidence was available to provide recommendations based on the GRADE approach. Results: There was limited randomised controlled trial evidence regarding single or multicomponent interventions to prevent post stroke cognitive decline. Interventions to improve lifestyle and treat vascular risk factors may have many health benefits but a beneficial effect on cognition is not proven. We found no evidence around routine cognitive screening following stroke but recognise the importance of targeted cognitive assessment. We described the accuracy of various cognitive screening tests but found no clearly superior approach to testing. There was insufficient evidence to make a recommendation for use of cholinesterase inhibitors, memantine or cognitive rehabilitation for post stroke dementia. We made a weak recommendation against using the nootropics actovegin and cerebrolysin, but quality of evidence was very low. There was limited evidence on the use of prediction tools for post stroke cognitive syndromes (cognitive impairment, dementia and delirium). The association between post stroke cognitive impairment and most acute structural brain imaging features was unclear. Conclusions: These guidelines have highlighted fundamental areas where robust evidence is lacking. Further randomised controlled trials are needed and we suggest priority areas for future research.
... 95%CI 1.67-10.3). This is in accordance with the results of Arauz et al., 26 and Renjen et al., 27 who found that vascular dementia risk increases with left-sided ischemic lesions by 5 folds (OR=5.0, 95%CI 1.92-14.1). ...
... Despite various studies confirm our result, 21,23,[31][32][33][34] Renjen et al. did not find a statically significant difference between strategic and non-strategic infarction as risk factor of post stroke cognitive impairment (8 versus 73%). 27 About the relation between stroke subtypes and dementia, in this study, there was significantly higher percentage of large vessel ischemic stroke patients in PSD group in comparison to the non-demented group (45.0 versus 17.5%), while more patients with small vessel stroke were found in the non-demented group (77.5 versus 45.0%). However, large vessel stroke did not reach to be a predictor for dementia in our sample and we could not say that stroke subtype is an independent predictor for dementia after fist stroke. ...
Article
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Various mechanisms contribute to dementia after first ischemic stroke as lesions on strategic areas of cognition and stroke premorbidity. Objectives: Assessing clinical and neuroimaging predictors of dementia after first ischemic stroke and its relation to stroke location, subtypes and severity. Methods: Eighty first ischemic stroke patients were included. Forty patients with dementia after first stroke and forty patients without dementia according to DSM-IV diagnostic criteria of vascular dementia. All patients were subjected to general and neurological assessment, National Institute Health Stroke Scale (NIHSS) for stroke severity, Montreal Cognitive Assessment (MoCA) scale for cognition assessment, MRI brain and Trial of Org 10172 in acute stroke treatment (TOAST) classification for stroke subtypes. Results: Left hemispheric ischemic stroke, strategic infarctions, diabetes mellitus and stroke of anterior circulation were found to be independent risk factors for dementia after first ischemic stroke (OR=3.09, 95%CI 1.67-10.3, OR=2.33, 95%CI 1.87-8.77, OR=1.88, 95%CI 1.44-4.55, OR=1.86, 95%CI 1.45-6.54, respectively). Hypertension, dyslipidemia, smoking, ischemic heart disease, high NIHSS score and large vessel infarction were significantly higher among post stroke dementia patients. However, on binary logistic regression, they did not reach to be independent risk factors. Conclusion: Stroke location (left stroke, strategic infarction, anterior circulation stroke) and diabetes mellitus could be predictors of dementia after first ischemic stroke, but stroke severity, stroke subtypes, hypertension, dyslipidemia, smoking and ischemic heart could not.
... Many studies have shown that the severity of infarction and low score for activities of daily living are effective in predicting PSCI. 17,27 Patients with PSCI have a higher NIHSS score and a lower Barthel index. This study included the NIHSS score and mRS score, which were significantly different in single-factor analysis. ...
Article
Objective: Type 2 diabetes mellitus (T2DM) and ischemic stroke, which are common diseases among older people, are closely related to cognitive impairment. This study aims to investigate the influencing factors of post-stroke cognitive impairment (PSCI) in patients with T2DM. Methods: We enrolled 161 patients with T2DM who experienced acute ischemic stroke and were hospitalized in the Department of Neurology, Jinan Central Hospital, Shandong, China. Cognitive function was evaluated with the Montreal Cognitive Assessment scale. According to the results, patients were divided into three groups-the cognitively normal group, mild cognitive impairment group, and severe cognitive impairment group. We analyzed general demographic data, laboratory information, imaging data, the results of neuropsychological evaluation, and clinical features as well as influencing factors of PSCI in these patients and established a prediction model. Results: The three groups of patients were significantly different in terms of age, education level, course of diabetes mellitus (DM), recurrent cerebral infarction (RCI), and other factors. RCI, course of DM, and glycated hemoglobin (HbA1c) were independent risk factors of PSCI in patients with T2DM, with odds ratio (95% confidence interval): 7.17 (2.09, 30.37), 5.39 (2.40, 14.59), and 3.89 (1.66, 10.04), respectively, whereas female, senior high school, serum albumin were protective factors: 0.28 (0.07, 0.95), 0.05 (0.01, 0.21), 0.20 (0.08, 0.42), respectively. Furthermore, we constructed a prediction model using sex, age, education level, RCI, DM course, HbA1c and serum albumin and obtained a receiver operating characteristic (ROC) curve. The area under the ROC curve is 0.966, suggesting the significant association of these influencing factors with PSCI in patients with T2DM. Conclusion: In this study, the occurrence of PSCI in patients with T2DM was related to RCI, course of DM, and HbA1c, among other factors. Attention to influencing factors is needed in these patients for early diagnosis and timely intervention of cognitive impairment.
... In many ways, the high level of disability in stroke patients is mediated by damage to the hippocampus and development of cognitive impairment, combined with post-stroke dementia (PSD). Renjen et al. showed that ischemic stroke increases the risk of developing dementia by 4-12 times, and PSD per se is observed in a fairly wide range-from 6% to 55% of cases and, which is very important, PSD increases the probability of re-stroke almost twice as much (4). In this regard, numerous attempts have been made to reduce the risk of developing PSD by developing and implementing appropriate pharmaco-therapeutic strategies in clinical practice. ...
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Objectives: Ischemic stroke is a disease with complex pathogenesis that requires timely and rational pharmacological intervention. One possible treatment for this condition may be to improve mitochondrial function as part of neuroprotective therapy. Materials and methods: Cerebral ischemic damage was reproduced by middle cerebral artery permanent occlusion in Wistar male rats. 4-hydroxy-3,5-di-tretbutyl cinnamic acid was injected intraperitoneally in dose range of 25 mg/kg, 50 mg/kg, and 100 mg/kg. The time of administration was 3 days from the ischemia modeling. Further, changes in the rats' cognitive functions in the Morris water maze test were evaluated, and the state of mitochondrial function in the hippocampal tissue was studied. Results: The study showed that the use of the studied compound dose-dependently improved mitochondrial function in the rat hippocampus. At doses of 20 mg/kg and 50 mg/kg, administration of the test substance increased citrate synthase activity by 55.1% (P<0.05) and 43.4% (P<0.05), respectively and ATP content by 25.7% (P<0.05) and 23.9% (P<0.05). Also, the intensity of oxidative stress (activity of antioxidant enzymes increase whereas the concentration of TBARS reduces) and apoptosis (calcium content, concentration of apoptosis-inducing factor, and caspase-3 activity decrease; latent time of mitochondrial transition permeability pore opening increase) decreased against the background of administration of the test compound. At a dose of 100 mg/kg, the studied compound showed less effectiveness. Conclusion: Administration of 25 mg/kg and 50 mg/kg 4-hydroxy-3,5-di-tretbutyl cinnamic acid demonstrated neuroprotection action on hippocampal cells under the conditions of irreversible brain ischemia.
... Lower SES, lower levels of education and lower cognitive reserve (e.g. resistance to damage of the brain, related to SES and education) are associated with a higher risk of cognitive impairments after nTBI (Hardy et al., 2018;Marshall et al., 2015;Renjen et al., 2015;Sun et al., 2014). Moreover, mental health problems, such as depression or anxiety, have been associated with cognitive impairments after all nTBI types (Pinho et al., 2019;Tang et al., 2018). ...
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Het huidige onderzoek was drieledig: 1) Literatuuroverzicht van de effectiviteit van interventies gericht op het verminderen van gevolgen van NAH in forensische populaties en van risicofactoren voor NAH en behandelmogelijkheden, 2) Inzicht verkrijgen in de huidige kennis, en beperkingen daarin, over NAH bij behandelaars en hoe de behandeling wordt aangepast bij (een vermoeden van) NAH en 3) Uitvoeren van validatieonderzoek naar de sensitiviteit van een NAH-screener. Voor doel 1 zijn twee reviews uitgevoerd, waaruit een hogere prevalentie van NAH in de forensische dan in de algemene populatie bleek, 50% versus 12%. Om inzicht in NAH-gerelateerde beperkingen te vergroten bleek psycho-educatie zinvol. Daarbij was er matig bewijs voor verbeteringen in cognitie en gedrag middels interventies die sociale vaardigheden verbeterden en cognitieve vervormingen verminderden. De uitkomsten suggereren dat NAH een risicofactor is voor recidive, maar ook de behandeleffectiviteit kan belemmeren in termen van responsiviteit. Er blijkt veel winst te behalen binnen wetenschappelijk onderzoek en de verbetering van diagnostiek en behandeling van NAH in de forensische populatie. Voor doel 2 waren de bevindingen van het veldonderzoek onder behandelaars en patiënten grotendeels in lijn met doel 1. Het screenen op (gevolgen van) NAH is geen standaard onderdeel van het zorgtraject: slechts de helft van de behandelaars gaf aan wel eens een neuropsychologische test te hebben gebruikt en rekening te hebben gehouden met de klinische implicaties. Voor een deel lijkt de kennis en kunde op het gebied van NAH dan ook nog onvoldoende om NAH tijdig en adequaat te herkennen, evenals om er de behandeling op te kunnen aanpassen. Cliënten rapporteerden dat er in eerdere behandelingen onvoldoende aandacht was voor NAH, maar dat dit in de huidige behandeling beter was. De in huidig onderzoek ontwikkelde handreiking had een duidelijke meerwaarde voor de behandelaars. Zij werden bewust gemaakt op, en kregen (blijvend) aandacht voor, NAH. De handvatten omtrent hoe in de behandeling om te gaan met de gevolgen van NAH werden als zeer waardevol ervaren. Voor doel 3 bleek uit het validatieonderzoek naar de positieve uitslagen dat de screener in de huidige vorm geen valide methode is om adequaat (een vermoeden van) NAH in kaart te brengen. Een positieve uitslag, dus (vermoeden van) NAH, werd niet bevestigd middels objectivering op neuropsychologisch onderzoek of MRI. Mogelijke verklaringen, waaronder een beperkte steekproef, worden in het betreffende hoofdstuk besproken. Wel kan de screener aanleiding geven tot verder onderzoek bij de cliënt en zorgt het voor bewustwording omtrent NAH.
... Stroke is one of the global leading causes of death and may cause long-term disability for many stroke survivors (Mendis, 2013;Andrew et al., 2014). Up to three-quarters of patients with poststroke experienced ongoing cognitive impairment (Pasi et al., 2012;Jokinen et al., 2015;Renjen et al., 2015). Cognitive impairment and functional disability are often associated with the following stroke. ...
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Background: The efficacy of virtual reality (VR)-based intervention for improving cognition in patients with the chronic stage of stroke is controversial. The aims of this meta-analysis were to evaluate the effect of VR-based training combined with traditional rehabilitation on cognition, motor function, mood, and activities of daily living (ADL) after chronic stroke. Methods: The search was performed in the Cochrane Library (CENTRAL), EBSCO, EMBASE, Medline (OVID), Web of Science databases, PubMed, CINAHL Ovid, and Scopus from inception to May 31, 2021. All included studies were randomized controlled trials (RCTs) examining VR-based intervention combined with traditional rehabilitation for chronic stroke. The main outcomes of this study were cognition, including overall cognition (combined with all cognitive measurement results), global cognition (measured by the Montreal Cognitive Assessment, MoCA, and/or Mini-Mental State Examination, MMSE), and attention/execution. The additional outcomes were motor function, mood, and ADL. Subgroup analyses were conducted to verify the potential factors for heterogeneity. Results: Six RCTs including 209 participants were included for systematic review, and five studies of 177 participants were included in meta-analyses. Main outcome analyses showed large and significant effect size (ES) of VR-based training on overall cognition ( g = 0.642; 95% CI = 0.134–1.149; and P = 0.013) and attention/execution ( g = 0.695; 95% CI = 0.052–1.339; and P = 0.034). Non-significant result was found for VR-based intervention on global cognition ( g = 0.553; 95% CI = −0.273–1.379; and P = 0.189). Additional outcome analyses showed no superiority of VR-based intervention over traditional rehabilitation on motor function and ADL. The ES of VR-based intervention on mood ( g = 1.421; 95% CI = 0.448–2.393; and P = 0.004) was large and significant. In the subgroup analysis, large effects for higher daily intensity, higher weekly frequency, or greater dose of VR intervention were found. Conclusion: Our findings indicate that VR-based intervention combined with traditional rehabilitation showed better outcomes for overall cognition, attention/execution, and depressive mood in individuals with chronic stroke. However, VR-based training combined with traditional rehabilitation showed a non-significant effect for global cognition, motor function, and ADL in individuals with chronic stroke.
... 164 Our literature review found 13 studies examining associations between CT-brain imaging variables and post-stroke dementia or post stroke cognitive impairment (PSCI) ascertained at least 12 months after stroke (Table 12 and Supplementary Materials). [165][166][167][168][169][170][171][172][173][174][175][176][177] Six studies reported on post-stroke dementia 167,168,170,172,174,175 and 6 reported PSCI, one study reported both 176 . All seven dementia studies excluded patients with prior dementia/cognitive impairment and three excluded patients with prior stroke. ...
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Introduction The optimal management of post stroke cognitive impairment remains controversial. These joint European Stroke Organisation (ESO) and European Academy of Neurology (EAN) guidelines provide evidence-based recommendations to assist clinicians in decision making around prevention, diagnosis, treatment, and prognosis. Methods Guidelines were developed according to the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) methodology. The working group identified relevant clinical questions, performed systematic reviews, assessed the quality of the available evidence, and made specific recommendations. Expert consensus statements were provided where insufficient evidence was available to provide recommendations. Results There was limited randomised controlled trial evidence regarding single or multicomponent interventions to prevent post stroke cognitive decline. Lifestyle interventions and treating vascular risk factors have many health benefits but a cognitive effect is not proven. We found no evidence around routine cognitive screening following stroke but recognise the importance of targeted cognitive assessment. We described the accuracy of various cognitive screening tests but found no clearly superior approach to testing. There was insufficient evidence to make a recommendation for use of cholinesterase inhibitors, memantine nootropics or cognitive rehabilitation. There was limited evidence on the use of prediction tools for post stroke cognition. The association between post stroke cognitive impairment and acute structural brain imaging features was unclear, although the presence of substantial white matter hyperintensities of presumed vascular origin on MRI brain may help predict cognitive outcomes. Conclusions These guidelines highlight fundamental areas where robust evidence is lacking. Further, definitive randomised controlled trials are needed, and we suggest priority areas for future research.
Article
BACKGROUND: Falls are a significant patient safety concern in hospital. Adult patients with stroke, and those with communication disability, are at an increased risk of falls during their hospital admission compared to patients without stroke or communication disability. OBJECTIVE: The aim of this review is to determine the circumstances and outcomes of falls in hospitalised patients with communication disability following stroke. METHOD: A qualitative synthesis of 16 papers according to the Generic Reference Model of patient safety. This is a secondary analysis of studies in a systematic review of the association between communication disability after stroke and falls in hospitalised patients. RESULTS: In studies including participants with communication disability, falls commonly occurred at the patient bedside, during the day, and in transfers. However, no studies provided individual or group specifically detailing the circumstances and outcomes of falls of the included participants with communication disability. CONCLUSION: Research to date provides scant evidence on the circumstances and outcomes of falls in hospital patients with communication disability after stroke. This review performs a useful function in highlighting a glaring gap in the literature and the urgent need to enrich hospital falls prevention research that includes patients with communication disability following stroke. Findings of this review are discussed in relation to providing a framework for analysis of for future research.
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Cognitive decline after cerebrovascular stroke has adverse outcome consequences. Since some vascular causes can be prevented and treated, the identification of stroke-related cognitive impairment is a challenge. Patients with cognitive impairment and vascular diseases exhibit higher homocysteine (Hcy) concentrations. Whether Hcy is an independent risk factor for cognitive impairment after stoke is still in question. The objectives of this study were to determine: 1) the relative frequency of first-ever post-stroke dementia (PSD) (three months after onset) in a consecutive sample of our population, 2) the risk factors associated with PSD, and 3) the relationship between Hcy levels and PSD. Eighty-one inpatients with first-ever stroke were prospectively evaluated with a neuropsychological battery and event-related evoked potentials (P300) at onset and then after three months. A wide range of demographic, clinical, radiological and laboratory variables were examined. PSD was diagnosed if the clinical presentation fulfilled DSM-IV criteria of vascular dementia, the patient scored </=21 on Mini Mental State Examination (MMSE) and </=67 points on Cognitive Abilities Screening Instruments (CASI). PSD was diagnosed in 21%. PSD was significantly associated with increasing age, low levels of education, large sized and lacunar infarctions, severity of stroke, prolonged P300 latency, smoking, hypertension, and elevated Hcy levels. High Hcy levels increased the odds ratio of PSD after adjustment of significantly relevant variables including age, smoking, size of infarction, and carotid stenosis. Cognitive decline is common after stroke. The results of this study indicate that PSD may result from stroke and its related risk factors including possible direct association with high Hcy levels. Better knowledge of the risk factors for PSD should increase the effectiveness of preventive strategies in patients with this condition.
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Cognitive function was examined in 227 patients three months after admission to hospital for ischaemic stroke, and in 240 stroke-free controls, using 17 scored items that assessed memory, orientation, verbal skills, visuospatial ability, abstract reasoning, and attentional skills. After adjusting for demographic factors with standardised residual scores in all subjects, the fifth percentile was used for controls as the criterion for failure on each item. The mean (SD) number of failed items was 3.4 (3.6) for patients with stroke and 0.8 (1.3) for controls (p < 0.001). Cognitive impairment, defined as failure on any four or more items, occurred in 35.2% of patients with stroke and 3.8% of controls (p < 0.001). Cognitive domains most likely to be defective in stroke compared with control subjects were memory, orientation, language, and attention. Among patients with stroke, cognitive impairment was most frequently associated with major cortical syndromes and with infarctions in the left anterior and posterior cerebral artery territories. Functional impairment was greater with cognitive impairment, and dependent living after discharge either at home or nursing home was more likely (55.0% with, v 32.7% without cognitive impairment, p = 0.001). In a logistic model examining the risks related to dependent living after stroke, cognitive impairment was a significant independent correlate (odds ratio, OR = 2.4), after adjusting for age (OR = 5.2, 80 + v 60-70 years) and physical impairment (OR = 3.7, Barthel index < or = 40 v > 40). It is concluded that cognitive impairment occurs frequently after stroke, commonly involving memory, orientation, language, and attention. The presence of cognitive impairment in patients with strike has important functional consequences, independent of the effects of physical impairment. Studies of stroke outcome and intervention should take into account both cognitive and physical impairments.
Article
Lack of information is a major hurdle in combating stroke mortality and morbidity in India. This survey was undertaken in a slum area in Dharavi, Mumbai, to study the prevalence of stroke and post-stroke cognitive impairment in the elderly aged 60 years and above. Participants selected using systematic random sampling of households, were interviewed using a modified version of the World Health Organization Protocol for Screening of Neurological Diseases. Stroke was confirmed through clinical examination, medical records review and interviews with caregivers. Cognitive impairment was assessed using Addenbrooke's scale and Mini mental status examination. Participants comprised 730 men and 996 women. Confirmed stroke in 66 individuals yielded a crude prevalence rate of 3.82% (95% CI 3.01 - 4.84); the prevalence standardized to WHO world population was 4.87% (95% CI 3.76 - 6.23). Prevalence rates increased with age and were higher in men than in women. Out of 27 stroke survivors evaluated for cognitive dysfunction, 18 (66.66%) had MMSE scores of less than 24. Stroke prevalence in slum-dwellers is comparable to that of other sections of society. Prevalence rates in this study are higher than rates seen in previous Indian studies, possibly due to the combined effects of population ageing with increased incidence of hypertension and diabetes mellitus, which also affect cognitive functions in stroke survivors.
Article
Background: Methyl isocynate (MIC) is a reactive, toxic, volatile and inflammable gas. Exposure to MIC causes neurotoxicity and somatic abnormalities in human beings. Aim: We compared neurocognitive function in MIC-exposed women and a control group, as well as cognitive function in the MIC group and examined them with reference to age. Methods: The study sample comprised 30 women and a control group of 30 women. Both the groups were subjected to a detailed neuropsychiatric examination along with assessment of neurocognitive function using the PGI-Battery of Brain Dysfunction (PGI-BBD). Results: Mean scores of immediate recall, visual retention, difference in performance quotient/verbal quotient, Nahar–Bensen and Bender–Gestalt test were significantly affected in MIC-exposed women. However, among MIC-exposed women, neurocognitive functions were similarly affected in women in various age groups. Conclusion: Women in the MIC-exposed group had significant neurocognitive dysfunction in some specific areas as compared to women in the control group. The mean score of dysfunction rating of the PGI-BBD showed significant differences in neurocognitive functions between MIC-exposed and non-exposed women.
Article
Vascular cognitive impairment, being the only treatable cause of dementia in the early stages, and having a diverse etiology, requires sensitive criteria for definition. This study aimed to study cognitive functions at 3 months post-stroke, utilising the Mini mental scale examination (MMSE) and the Frontal assessment battery (FAB), and to correlate the same with subgroups of ischemic stroke. 164 patients were studied, 108 of these having multiple infarcts. Pure cortical infarcts were seen in 41 patients. At 3 months, 112/164 patients had MMSE more than 24, with no frontal executive dysfunction. MMSE score less than 24 was seen in 24 patients, all of them having FAB score below 10. Normal MMSE with impaired FAB was seen in 28 patients. Impairment on either the MMSE or the FAB was thus seen in 31.7% patients (52/164), at 3 months after stroke. FAB impairment alone, with MMSE in normal range, was seen in 28/52 (53.8%) patients. Memory was significantly more commonly affected in muti-infarct strokes as compared to single infarcts. Frontal executive dysfunction was not significantly different when single and multiple infarcts, or cortical and subcortical infarcts, were compared.
Article
Computed tomography (CT) findings in 57 patients with senile dementia of Alzheimer type (SDAT), 19 patients with multi-infarct dementia and 85 controls of similar age and sex were studied. The SDAT patients differed from the controls of ventricular dilatation, frontal horn index, cella media index and the width of the third ventricle, and also in the index of cortical atrophy. Even the least severely demented SDAT patients differed from the controls. In the SDAT group with the increasing degree of intellectual impairment the ventricular dilatation increased, but cortical atrophy did not correlate with the psychological test score. The multi-infarct dementia patients differed from the controls in all CT variables including local changes. The SDAT patients had a more marked ventricular dilatation than the multi-infarct dementia patients. The multi-infarct dementia patients had more frequently local changes in SDAT patients. In the control group age correlated with ventricular dilatation, and the lower test scores correlated with cortical atrophy in the left temporal region.
Article
Possible specific risk factors for silent infarcts remain unknown. The aim of this study was to investigate whether risk factors for silent infarcts differ from those for symptomatic infarcts in stroke patients. Silent infarcts were defined as asymptomatic infarcts detected on computed tomographic scan in patients free of history of stroke and unrelated to the symptoms and signs of the index stroke. Of 595 consecutive patients with stroke or transient ischemic attacks, 116 (19%) had at least one silent infarct on the first computed tomographic scan performed within 24 hours after onset. They were compared with the 479 remaining patients for cerebrovascular risk factors and for presumed mechanism of stroke by means of the odds ratio method. A discriminant analysis was then performed in the subgroup of 216 patients with ischemic stroke who underwent an exhaustive cardiac and vascular workup. One hundred forty-one silent infarcts (99% confidence interval [CI], 29% to 41%) and 265 symptomatic infarcts (99% CI, 59% to 71%) were subcortical infarcts smaller than 15 mm. Univariate analysis showed that patients with silent infarcts were more likely to be older than 65 years (odds ratio [99% CI], 1.11 to 3.49) and to have left atrial enlargement on echocardiogram (odds ratio [99% CI], 1.02 to 26.70) and leukoaraiosis (odds ratio [99% CI], 1.39 to 4.21). Discriminant analysis found only two independent risk factors for silent infarcts: left atrial enlargement (P = .007) and age older than 65 years (P = .03); leukoaraiosis was not found to be an independent risk factor (P = .86). Age and left atrial enlargement are the main risk factors for silent infarcts in patients with ischemic stroke or transient ischemic attacks.
Article
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. 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. 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). 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.
Article
The aim was to study the frequently found white-matter changes on computerized tomography (CT) in patients with dementia and to relate these changes to clinical regional brain symptomatology, vascular factors, albumin ratio [indicator of blood-brain barrier (BBB) function] and other CT changes. The study included 85 patients, average age 71 +/- 8, with Alzheimer's disease (n = 56) and vascular dementia (n = 29), who underwent CT (Siemens Somatome DR 1) of the brain. They were inpatients in a psychiatric department specialized in dementia investigations. The degree of CT white-matter changes (absence, mild-moderate, severe) was the basis for the division of the patients into three groups. As the patients without white-matter changes were significantly younger than those with such changes, all statistical analyses were controlled for age. Subcortical symptomatology was significantly more frequent in the group with severe white-matter changes, whereas the reverse was true for parietal symptomatology. Diabetes mellitus, hypertension, ischemic cardiac disease and lacunas were significantly more common in patients with white-matter changes, whereas the frequency of transient ischemic attack/stroke episodes did not differ significantly between the groups. The albumin ratio was significantly higher in the groups with white-matter changes and highest in the group with severe white-matter changes. The findings indicate that white-matter changes in demented patients are at least partially an age- and stroke-independent disease manifestation of the vascular system and is associated with a specific symptom pattern. BBB dysfunction may be the link between the vasculature and the tissue damage.