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Cognitive Impairment After Stroke

DOI:10.7759/cureus.335
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Pushpendra Nath Renjen at Indraprastha Apollo Hospitals
Pushpendra Nath Renjen
Charu Gauba at Indraprastha Apollo Hospitals
Charu Gauba
Dinesh Mohan Chaudhari at Indraprastha Apollo Hospitals
Dinesh Mohan Chaudhari
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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.
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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.
References
1. del Ser T, Barba R, Morin MM, Domingo J, Cemillan C, Pondal M, Vivancos J: Evolution of
cognitive impairment after stroke and risk factors for delayed progression. Stroke. 2005 ,
36:2670-75. 10.1161/01.STR.0000189626.71033.35
2. Khedr EM, Hamed SA, El-Shereef HK, Shawky OA, Mohamed KA, Awad EM, Ahmed MA, Shehata
GA, Eltahtawy MA: Cognitive impairment after cerebrovascular stroke: Relationship to vascular
risk factors. Neuropsychiatr Dis Treat. 2009, 5:103–116.
3. Ingles JL, Boulton DC, Fisk JD, Rockwood K: Preclinical vascular cognitive impairment and
alzheimer disease: neuropsychological test performance 5 years before diagnosis. Stroke. 2007,
38:1148–53. 10.1161/01.STR.0000259716.04739.60
4. Snaphaan L, De Leeuw FE : Poststroke memory function in nondemented patients: a systematic
review on frequency and neuroimaging correlates. Stroke. 2007, 38:198–203.
10.1161/01.STR.0000251842.34322.8f
5. Mounier-Vehier F, Leys D, Rondepierre P, Godefroy O, Pruvo JP: Silent infarcts in patients with
ischemic stroke are related to age and size of the left atrium. Stroke. 1993, 24:1347–51.
10.1161/01.STR.24.9.1347
6. Murray AD, Staff RT, Shenkin SD, Deary IJ, Starr JM, Whalley LJ: Brain white matter
hyperintensities: relative importance of vascular risk factors in nondemented elderly people.
Radiology. 2005, 237:251–57. 10.1148/radiol.2371041496
7. Soininen H, Puranen M, Riekkinen PJ: Computed tomography findings in senile dementia and
2015 Renjen et al. Cureus 7(9): e335. DOI 10.7759/cureus.335 8 of 9
normal aging. J Neurol Neurosurg Psychiatry. 1982, 45:50–4. 10.1136/jnnp.45.1.50
8. Serrano S, Domingo J, Rodríguez-Garcia E, Castro MD, del Ser T: Frequency of cognitive
impairment without dementia in patients with stroke: a two-year follow-up study. Stroke.
2007, 38:105–10. 10.1161/01.STR.0000251804.13102.c0
9. Sahu RN, Naik GP, Dusad A, Agrawal VK: Neurocognitive function in women affected by the
Bhopal gas disaster. Indian J Psychiatry. 2005, 47:51–3. 10.4103/0019-5545.46076
10. Sachdev PS, Brodaty H, Valenzuela MJ, Lorentz L, Looi JCL, Berman K, Ross A, Wen W, Zagami
AS: Clinical determinants of dementia and mild cognitive impairment following ischaemic
stroke: the sydney stroke study. Dement Geriatr Cogn Disord. 2006, 21:275-83.
10.1159/000091434
11. Pohjasvaara T, Erkinjuntti T, Ylikoski R, Hietanen M, Vataja R, Kaste M: Clinical determinants
of post stroke dementia. Stroke. 1998, 29:75–81. 10.1161/01.STR.29.1.75
12. Tatemichi TK, Desmond DW, Stern Y, Paik M, Sano M, Bagiella E: Cognitive impairments after
stroke: frequency, patterns, and relationship to functional abilities. J Neurol Neurosurg
Psychiatry. 1994, 57:202–7. 10.1136/jnnp.57.2.202
13. Stroke in India factsheet. (2012). Accessed: Jan 11, 2013:
https://www.researchgate.net/publication/264116605_Stroke_in_India_-_Fact-
sheet_%28Updated_2012%29.
14. Sundar U, Adwani S: Post-stroke cognitive impairment at 3 months . Ann Indian Acad Neurol.
2010, 13:42–6. 10.4103/0972-2327.61276
15. Das SK, Bose P, Biswas A, Dutt A, Banerjee TK, Hazra AM, Raut DK, Chaudhuri A, Roy T: An
epidemiologic study of mild cognitive impairment. Neurology. 2007, 68:2019–26.
10.1212/01.wnl.0000264424.76759.e6
16. Mukhopadhyay A, Sundar U, Adwani S, Pandit D: Prevalence of stroke and post-stroke cognitive
Impairment in the elderly in Dharavi, Mumbai. J Assoc Physicians India. 2012, 60:29–32.
17. Lodder J: Poststroke cognition and the fight against the hard problem: vascular neurologists,
enter the arena!. Stroke. 2007, 38:7–8. 10.1161/01.STR.0000252663.85193.a2
18. Selnes OA, Vinters HV: Vascular cognitive impairment. Nat Clin Pract Neurol. 2006, 2:538-47.
10.1038/ncpneuro0294
19. Wallin A, Sjögren M, Edman A, Blennow K, Regland B: Symptoms, vascular risk factors and
blood-brain barrier function in relation to CT white-matter changes in dementia. Eur Neurol.
2000, 44:229–35. 10.1159/000008242
20. Swartz RH, Stuss DT, Gao F, Black SE: Independent cognitive effects of atrophy and diffuse
subcortical and thalamico-cortical cerebrovascular disease in dementia. Stroke. 2008, 39:822–
30. 10.1161/STROKEAHA.107.491936
2015 Renjen et al. Cureus 7(9): e335. DOI 10.7759/cureus.335 9 of 9
... 14 Previous studies have also tended to use brief cognitive screening tools (e.g., t-MMSE) 15 that classify patients as "impaired" or "not impaired" at a broad level of cognitive functioning, without delineating between different domain-specific cognitive impairments (e.g., visuospatial neglect and apraxia). 12, [16][17][18] In clinical practice, cognitive screening tools designed specifically for stroke populations (e.g., Oxford Cognitive Screen: OCS 19 ) are increasingly recommended, 20,21 as they offer advantages over brief screening. Domainspecific screening is more sensitive to different types of domain-specific PSCI 22 and facilitates more nuanced understanding of cognitive status in different domains, which offers advantages for tailoring care packages and supporting return to work/education. ...
... This is a novel finding that stems from our ability to analyse CT neuroimaging data alongside domain-specific cognitive data from multiple timepoints after stroke, in contrast to previous studies that have conducted brief cognitive screening at a single timepoint. 12, 16,17 Whilst the pathophysiological mechanisms linking cortical atrophy to increased risk of persistent cognitive impairment are unclear from the present study, stroke infarcts may interact with cortical atrophy to exacerbate post-stroke cognitive decline or impede neural recovery mechanisms. Interactions between neurodegenerative and vascular imaging markers have similarly been proposed to explain poor cognitive outcomes in non-stroke populations, including patients with Alzheimer's disease, 37 symptomatic atherosclerotic disease, 38 cerebral small vessel disease, 39 and older adults. ...
Association of Neuroimaging Markers on Clinical CT Scans With Domain-Specific Cognitive Impairment in the Early and Later Post-Stroke Stages
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  • Sep 2023
Background Post-stroke cognitive impairment (PSCI) is associated with neuroimaging markers, including cortical atrophy and white matter lesions (WMLs), on clinically acquired CT neuroimaging. Objectives To investigate the association between cortical atrophy/WMLs and PSCI in specific cognitive domains in the acute/subacute and chronic stages after stroke, in order to provide clarity on the relationship between these neuroimaging markers and the temporal evolution of PSCI. Methods We visually assessed cortical atrophy using the Global Cortical Atrophy (GCA) scale and WMLs using the Fazekas scale. Oxford Cognitive Screen (OCS) or Birmingham Cognitive Screen (BCoS) assessed PSCI at two timepoints (acute/subacute and chronic) in six domains (language, memory, number processing, executive function, attention, praxis). We binarised domain-specific performance as impaired/unimpaired using normative cut-offs. Multivariable linear and logistic regression analyses evaluated associations between GCA/Fazekas scores with acute/subacute/chronic global and domain-specific PSCI, and ANCOVAs examined whether these scores were significantly different in patients with recovered versus persistent PSCI. Age, sex, education, NIHSS, lesion volume, and recurrent stroke were covariates in these analyses. Results Among 411 stroke patients ( Mdn/IQR age= 76.16/16.64; 193 female; 346 ischaemic stroke; 107 recurrent stroke), GCA and Fazekas scores were not associated with global cognitive impairment in the acute/subacute stage after stroke, but GCA score was associated with chronic global PSCI ( B = 0.01, p < .001, 95% CI [0.00 0.01]). In domain-specific analyses, GCA score was associated with chronic impairment in the memory ( B = 0.06, p < .001, 95% CI [0.03 0.10]) and attention ( B = 0.05, p = .003, 95% CI [0.02 0.09]) domains, and patients with persistent PSCI these domains showed significantly higher GCA scores than patients who had recovered (Memory: F (1,157) = 6.63, p = .01, η 2 G = .04; Attention: F (1,268) = 10.66, p = .001, η 2 G = .04). Conclusions The present study highlights the potential impact of cortical atrophy on the cognitive recovery process after stroke and demonstrates the prognostic utility of CT neuroimaging for post-stroke cognitive outcomes. Clinical neuroimaging could help identify patients at long-term risk of PSCI during acute hospitalisation.
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... Memory loss and cognitive impairment are common after stroke; more than 70% of stroke survivors develop cognitive impairment in the first year (Lee et al., 2021). A study by Renjen et al. (2015) revealed that 72% of patients have cognitive impairment after stroke, with risk factors are including old age, male sex, low education, hemorrhages, and recurrence or severe stroke. Blood flow is impaired by stroke, which also causes excitotoxicity, calcium overloading, oxidative stress, dysfunction of the blood-brain barrier (BBB), microvascular injury, hemostatic activation, injury-related inflammation, immune responses, and cell death involving neurons, glia, and endothelial cells. ...
... Educational, occupational, lifestyle, medical comorbid, and other factors unique to each person may have an impact on the behavioral and clinical symptoms of neuropathological loads (Shin et al., 2019;Suda et al., 2020). Moreover, cognitive impairment does not follow a linear time course after stroke; short-term studies may over-diagnose cognitive post-stroke dysfunction (Renjen et al., 2015). Therefore, perhaps further follow-up or longitudinal study can reveal in more detail the impact of stroke recurrence on cognitive decline. ...
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... It was found that cognitive functions are affected by higher degrees following haemorrhagic stroke in comparison with ischemic stroke and this appeared at MOCA scale scores as MOCA scores of ischemic stroke was 21.640 while hemorrhagic stroke was 20.000. This coincides with the results of Renjen., 2015 who reported that many patients with haemorrhagic strokes about 84.6% had cognitive impairment compared to those with ischemic strokes with percentage of about 67.5%, P = 0.077 [28] . Concerning to figural memory, it was found that it was affected at haemorrhagic stroke patients more than ischemic stroke patients and this appeared at levels as mean values of figural memory levels at GA (Healthy subjects) was 6.600, at GB (ischemic stroke) was 4.480 and at GC (haemorrhagic stroke) was 3.920 so the levels reached by ischemic stroke patients were higher than those reached by hemorrhagic stroke patients. ...
Journal of Population Therapeutics & Clinical Pharmacology Cognitive Dysfunction in Ischemic versus Hemorrhagic stroke
Article
Full-text available
  • Mar 2023
Background: Stroke is one of the major causes of physical and mental disability among people. Vascular cognitive impairment (VCI) represents a wide spectrum from mild cognitive impairment to dementia following cerebrovascular disorder that is resulting in either ischemic or hemorrhagic stroke. Purpose of study: This study was conducted to investigate the difference in cognitive functions' affection following ischemic versus hemorrhagic stroke. Subjects: 75 subjects were enrolled in this study, 25 healthy subjects and 50 stroke patient (25 ischemic and 25 hemorrhagic stroke patients) of both sexes with age range between 45 and 55 years old, duration of illness was between 6 to 12 months and years of education of patients and subjects participated in this study was at least nine years. The patients were selected from outpatient clinic, Faculty of Physical Therapy, Cairo University, Egypt. Subjects were classified into three groups: GA (25 healthy subjects), GB (25 ischemic stroke patients) and GC (25 hemorrhagic stroke patients). Methods: Both of healthy subjects and stroke (ischemic and hemorrhagic) patients received cognitive assessment via Montreal cognitive assessment scale (MOCA) and Rehacom system as four categories were assessed which are figural memory, attention concentration, reaction behavior and logical thinking; each category was assessed for 30min. Results: This study results showed that there was a significant difference between the results of MOCA scale and Rehacom system among the three groups , with (P ≤ 0.05). Also, there was a significant difference between GB (ischemic stroke) and GC (hemorrhagic stroke). Conclusion: on the basis of the present data , it can be concluded that healthy subjects have better preserved cognitive functions in comparison with stroke patients (either ischemic or hemorrhagic stroke) , based on MOCA scale results , deterioration in cognitive functions in hemorrhagic stroke was greater than in ischemic stroke , based on Rehacom System results , figural memory and logical thinking were more affected in patients with hemorrhagic stroke in comparison with ischemic stroke patients and reaction behavior and attention concentration were more affected in patients with ischemic stroke in comparison with haemorrhagic stroke patients. INTRODUCTION The world health organization defined stroke as rapidly developing clinical signs of localized or generalized cerebral functions with symptoms lasting about 24 hours or more or leading to death without any other cause of vascular origin [1]. Stroke is considered the second-leading cause of death and the third-leading cause of death, disability and impairment in activities of daily living (ADL) in the world [2] .
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... Motor deficit after stroke, including falls, general pain, neuropathic pain at 3 and 12 month, fatigue, shoulder subluxation, joint contractures, muscle spasticity, DVT, and pressure ulcers were contributing to the reduction in MMSE scores, similarly to numerous international studies (Graber et al., 2019;Harrison & Field, 2015;Lui & Nguyen, 2018;Renjen et al., 2015;Segev-Jacubovski et al., 2011). Survivors usually experience sleep disturbances, low motivation, low self-esteem, mood changes, chronic stress, and worries about their future due to disabilities. ...
Factors associated with cognitive impairment at 3, 6, and 12 months after the first stroke among Lebanese survivors
Article
Full-text available
  • Dec 2022
Introduction This study aimed to calculate the rate of post‐stroke cognitive impairment (PSCI) by evaluating the cognitive domains among Lebanese stroke survivors at 3, 6, and 12 months post‐stroke, and to identify the contributing factors including pre‐ and post‐stroke related factors. Methods A multicenter longitudinal prospective study was conducted in 10 hospitals from Beirut and Mount Lebanon for a 15‐month period. Mini‐Mental State Examination (MMSE), modified Rankin Scale, Short Form Health Survey, National Institutes of Health Stroke Scale (NIHSS), and Hospital Anxiety and Depression Scale (HADS) were used to assess cognitive function, disability degree, quality of life, stroke severity, and levels of anxiety and depression, respectively. Then, univariate and multivariable analyses were performed to identify the predictors of PSCI. Results Low MMSE scores were found among survivors during the first 3 months post‐stroke (74.8%) of whom 53.7% presented with an MMSE ≤ 17, followed by 46.7% in the 6 months, and 37.6% at 12 months post‐stroke. Follow‐up comparisons showed a significant increase of MMSE scores over time (p < .001), indicating a 37% improvement of the cognitive function over time. The most affected cognitive domain was the attention and concentration at the three time points. Independent factors that were positively associated with low MMSE scores were as follows: sedentary behavior ≥ 12 h/day (AOR = 3.062, p = .033), involvement of the left hemisphere (AOR = 2.710, p = .006), HADS ≥ 11 (AOR = 2.536, p = .049), and high NIHSS scores (AOR = 3, p = .009). Age was the main predictor in the three time periods (AOR ≈ 3, p < .05). Inversely, female gender (AOR = 0.09, p = .027), high educational level (AOR = 0.2, p < .02), employment post‐stroke (AOR = 0.3, p = .023), high PCS of QoL (AOR = 0.8, p < .001), and the use of anti‐diabetic treatment post‐stroke (AOR = 0.17, p = .016) improved MMSE scores to > 23. Conclusion The risk of PSCI among Lebanese stroke survivors was high especially in the acute phase, depending on various determinants. Health care providers are invited to implement an emergency rehabilitation program for an appropriate successful management of the risk factors in order to reduce stroke burden and to improve overall cognitive performance.
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... 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. ...
Factors Influencing Post-Stroke Cognitive Impairment in Patients with Type 2 Diabetes Mellitus
Article
Full-text available
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.
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Constituent isoflavones of Puerariae radix as a potential neuroprotector in cognitive impairment: Evidence from preclinical studies
Article
  • Aug 2023
With the increasing aging population worldwide, the incidence of senile cognitive impairment (CI) is increasing, posing a serious threat to the health of elderly persons. Despite developing new drugs aimed at improving CI, progress in this regard has been insufficient. Natural preparations derived from plants have become an unparalleled resource for developing new drugs. Puerariae radix (PR) has a long history as Chinese herbal medicine. PR is rich in various chemical components such as isoflavones, triterpenes, and saponins. The isoflavones (puerarin, daidzein, formononetin, and genistein) exhibit potential therapeutic effects on CI through multiple mechanisms. Relevant literature was organized from major scientific databases such as PubMed, Elsevier, SpringerLink, ScienceDirect, and Web of Science. Using "Puerariae radix," "Pueraria lobata," "isoflavones," "puerarin," "antioxidant," "daidzein," "formononetin," "genistein," "Alzheimer"s disease," and "vascular cognitive impairment" as keywords, the relevant literature was extracted from the databases mentioned above. We found that isoflavones from PR have neuroprotective effects on multiple models of CI via multiple targets and mechanisms. These isoflavones prevent Aβ aggregation, inhibit tau hyperphosphorylation, increase cholinergic neurotransmitter levels, reduce neuroinflammation and oxidative stress, improve synaptic plasticity, promote nerve regeneration, and prevent apoptosis. PR has been used as traditional Chinese herbal medicine for a long time, and its constituent isoflavones exert significant therapeutic effects on CI through various neuroprotective mechanisms. This review will contribute to the future development of isoflavones present in PR as novel drug candidates for the clinical treatment of CI.
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Predictors of post-stroke cognitive impairment at three-month following first episode of stroke among patients attended at tertiary hospitals in Dodoma, central Tanzania: A protocol of a prospective longitudinal observational study metadata
Article
Full-text available
Introduction: Neurocognitive deficits after stroke are a common manifestation and pose a significant impact on the quality of life for patients and families; however, little attention is given to the burden and associated impact of cognitive impairment following stroke. The study aims to determine the prevalence and predictors of post-stroke cognitive impairment (PSCI) among adult stroke patients admitted to tertiary hospitals in Dodoma, Tanzania. Methodology: A prospective longitudinal study is conducted at tertiary hospitals in the Dodoma region, central Tanzania. Participants with the first stroke confirmed by CT/MRI brain aged ≥ 18 years who meet the inclusion criteria are enrolled and followed up. Baseline socio-demographic and clinical factors are identified during admission, while other clinical variables are determined during the three-month follow-up period. Descriptive statistics are used to summarize data; continuous data will be reported as Mean (SD) or Median (IQR), and categorical data will be summarized using proportions and frequencies. Univariate and multivariate logistic regression analysis will be used to determine predictors of PSCI.
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Aspek Imunologi Peran Homosistein Dalam Patogenesis Gangguan Kognitif Pasca Stroke Iskemik
Article
Full-text available
  • Oct 2020
Sekitar 70% pasien stroke iskemik akut mengalami gangguan kognitif dapat terjadi akibat langsung dari stroke iskemik itu sendiri atau merupakan interaksi dari stroke iskemik dan faktor-faktor risiko yang menyertainya. Kondisi hiperhomosisteinemia merupakan salah satu faktor risiko vaskuler yang secara patofisiologik dapat menyebabkan terjadinya gangguan kognitif pasca stroke iskemik. Kondisi tersebut dapat terjadi karena peningkatan rasio SAM/SAH akibat diet tinggi kadar methionin, predisposisi genetik berupa mutasi gen pengkode enzim, dan defisiensi vitamin B6 dan asam folat. Peran homosistein dalam patogenesis terjadinya gangguan kognitif pasca stroke saat ini belum banyak diteliti. Homosistein bersifat toksik dan dapat menginduksi terjadinya respon inflamasi sistemik, disrupsi sawar darah otak, neuroinflamasi, dan kematian sel-sel neuronal yang mengarah pada proses neurodegeneratif. Proses neurodegeneratif pada struktur otak yang mengemban fungsi domain kognitif tertentu akan menyebabkan terganggunya fungsi dari domain kognitif tersebut. Pemahaman aspek imunologi peran homosistein dalam terjadinya gangguan fungsi kognitif pada pasien stroke iskemik tersebut dapat memberikan celah kemungkinan intervensi terhadap homosistein dan respon imunologis yang ditimbulkannya sebagai bagian dari tatalaksana optimal terhadap gangguan kognitif pasca stroke iskemik.
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Predictors of post-stroke cognitive impairment at three-month following first episode of stroke among patients attended at tertiary hospitals in Dodoma, central Tanzania: a protocol of a prospective longitudinal observational study
Preprint
Full-text available
  • Aug 2022
Introduction Neurocognitive deficits after stroke are a common manifestation and pose a significant impact on the quality of life for patients and families; however, little attention is given to the burden and associated impact of cognitive impairment following stroke. The study aims to determine the prevalence and predictors of post-stroke cognitive impairment (PSCI) among adult stroke patients admitted to tertiary hospitals in Dodoma, Tanzania Methodology A prospective longitudinal study is conducted at tertiary hospitals in the Dodoma region, central Tanzania. So far, participants with the first stroke confirmed by CT/MRI brain aged ≥ 18 years who meet the inclusion criteria are enrolled and followed up. Baseline socio-demographic and clinical factors are identified during admission, while other clinical variables are determined during the three-month follow-up period. Descriptive statistics are used to summarize data; continuous data will be reported as Mean (SD) or Median (IQR), and categorical data will be summarized using proportions and frequencies. Univariate and multivariate logistic regression analysis will be used to determine predictors of PSCI
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The Impact of Visual Impairment on Completion of Cognitive Screening Assessments: A Post-Hoc Analysis from the IVIS Study
Article
Full-text available
  • Jun 2022
Aim: The aim of this study was to evaluate completed cognitive screens in stroke survivors with and without visual impairment to explore whether the presence of visual impairment impacts on completion of cognitive screening. Materials and methods: Cognitive screening assessment was undertaken using the Oxford Cognitive Screen (OCS). Data from visual function assessments (inclusive of visual acuity, visual fields, eye movements and visual perception evaluation) were analysed to determine whether presence and/or type of visual impairment impacted on cognitive screening scores achieved. Covariates, including glasses use, gender, age at stroke onset and stroke type, were used to assess confounding impacts on scores attained during cognitive screening. Results: 1500 stroke admissions were recruited. One hundred ninety-seven who completed the OCS, were identified from the IVIS study database. Those who reported visual symptoms performed worse statistically on all cognitive tasks except the recall recognition (p = 0.232) and executive tasks (p = 0.967). Visual symptoms did not prevent participants from completing every section of the OCS (p = 0.095). In certain tasks, those not wearing their required glasses performed worse, including the executive function (p = 0.012), broken hearts and sentence reading tasks. Conclusions: Many tasks within cognitive screening assessment are impacted by presence of visual deficits, and adjustments, where possible (e.g. good lighting, large print) should be used to facilitate completion of cognitive screening. It is important to ensure required reading correction is worn during screening.
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Post-stroke cognitive impairment at 3 months
Article
Full-text available
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.
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Cognitive impairment after cerebrovascular stroke: Relationship to vascular risk factors
Article
Full-text available
  • Apr 2009
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 impairment after stroke: Frequency, patterns, and relationship to functional abilities
Article
Full-text available
  • Feb 1994
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.
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Prevalence of stroke and post-stroke cognitive Impairment in the elderly in Dharavi, Mumbai
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.
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Neurocognitive function in women affected by the Bhopal gas disaster
Article
  • Jan 2005
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.
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Computed tomography findings in senile dementia and normal aging
Article
  • Feb 1982
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.
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Silent infarcts in patients with ischemic stroke are related to age and size of the left atrium
Article
  • Oct 1993
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.
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Clinical Determinants of Poststroke Dementia
Article
  • Feb 1998
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.
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Symptoms, Vascular Risk Factors and Blood-Brain Barrier Function in Relation to CT White-Matter Changes in Dementia
Article
  • Feb 2000
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.
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