Search

Background: White matter lesions (WMLs) are frequent in elderly people, and have been associated with impaired activities of daily living (ADL) and cognitive decline. We sought to examine the role of WMLs and their extent, in regard to basic ADL, instrumental ADL (IADL), and cognitive functions, in a large well-defined cohort examined 3 months after an ischemic stroke., Methods: The study group included 395 of 486 consecutive patients aged 55 to 85 years who, 3 months after an ischemic stroke, completed a neuropsychological test battery and magnetic resonance imaging, and structured medical, neurological, and laboratory evaluations; assessment included an interview with a knowledgeable informant., Results: The patients with the most severe WMLs (n = 213) were older, in comparison with those with moderate (n = 71) or mild/no (n = 111) WMLs. These patients also more often had Diagnostic and Statistical Manual of Mental Disorders, Third Edition dementia; had a lower Mini Mental Status score; were more often women; more often had impaired immediate and delayed memory performance, executive dysfunction, and impaired basic ADL and IADL functions; and had more infarcts and cortical or central atrophy in magnetic resonance imaging. However, there were no significant differences among the 3 groups in stroke severity measured on the Scandinavian Stroke Scale, in stroke-related depression as measured by the Beck Depression Inventory, or in stroke type. According to multiple logistic regression analysis, higher age (odds ratio 1.067, 95% confidence interval 1.036-1.01) and impaired IADL (odds ratio 0.852, 95% confidence interval 0.778-0.931) significantly correlated with severe WMLs., Conclusions: Although the degree of WMLs was not associated with stroke severity, it was associated with global cognitive function, impaired memory functions, executive dysfunction, sex, and impaired basic ADL. Age and IADL functions were independent correlates of severe WMLs.

Objectives: Cerebral white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) are a recognised risk factor for post-stroke dementia. Their specific relations to cognitive impairment are still not well known. The purpose of this study was to explore how the severity and location of WMHs predict neuropsychological test performance in the context of other brain lesions in elderly stroke patients., Methods: In the Helsinki Stroke Aging Memory Study, 323 patients, aged from 55 to 85 years, completed a detailed neuropsychological test battery and MRI 3 months after an ischaemic stroke. The demographic and MRI predictors of cognition were studied with sequential linear regression analyses., Results: After age, education and total infarct volume were controlled for, the overall degree of WMHs predicted poor performance in tests of mental speed, executive functions, memory, and visuospatial functions, but not in those of short term memory storage or verbal conceptualisation. However, the contribution of separate white matter regions was relatively low. Only the lesions along the bodies of lateral ventricles were independently associated with speed and executive measures. Additionally, general cortical atrophy clearly predicted a wide range of cognitive deficits while infarct volume had less relevance. Further analyses revealed that executive functions act as a strong mediator between the relationship of WMHs to memory and visuospatial functions., Conclusions: The degree of WMHs is independently related to post-stroke cognitive decline. The most affected cognitive domains seem to be executive functions and speed of mental processing, which may lead to secondary deficits of memory and visuospatial functions.

Objective: It has been suggested that executive dysfunction could be the core defect in patients with geriatric or vascular depression, and that this depression-dysexecutive syndrome (DES) might be related to frontal-subcortical circuit dysfunction. The authors tested this hypothesis in 158 poststroke patients, of whom 21 had both depression and executive dysfunction., Methods: In this cross-sectional cohort study, a neurological, psychiatric, and neuropsychological examination was carried out 3 months after ischemic stroke, and brain infarcts, white-matter changes, and brain atrophy were recorded by MRI., Results: The 21 patients with DES had significantly more brain infarcts affecting their frontal-subcortical circuit structures than the 137 patients without DES, or the 41 patients with depression but without executive dysfunction. Patients with DES also had more severe depressive symptoms and worse psychosocial functioning, and they coped less well in complex activities of daily living., Conclusions: DES is a valid concept and may define a subgroup of poststroke patients with frontal-subcortical pathology and with distinct prognosis and treatment options.

Medial temporal lobe atrophy (MTA) and its role in memory deficits have been studied extensively in patients with various dementias and non-degenerative neurologic diseases. In stroke patients MTA is a significant risk factor for dementia. However, its role in memory decline in non-demented stroke patients is not yet known. Our aim was to evaluate the relationship between MTA and cognitive functions in a large cohort of elderly patients, who underwent a comprehensive neuropsychologic examination and magnetic resonance imaging 3 months after an ischemic stroke. The study sample (n = 260) was divided into three groups according to the severity of MTA. After adjusting for age, volume of infarcts and cortical atrophy, we found that patients with moderate to severe MTA performed significantly worse in tests of learning, story recall, visual reproduction, block design and mental speed. In contrast, the groups did not differ in tests of digit span, flexibility, verbal fluency and conceptualization. Our conclusion is that in aged stroke patients, MTA is associated with poor performance in specific cognitive domains. The most vulnerable domains are memory and visuospatial functions, whereas verbal and executive functions seem to be unrelated to MTA.

Seventy patients with one brain infarct on magnetic resonance imaging (MRI) were studied 3 months after ischemic stroke by a standardized protocol to detail side, site, type, and extent of the brain infarct, as well as severity of white matter lesions and brain atrophy. Depression was diagnosed by DSM-III-R and DSM-IV criteria. The brain infarcts that affected structures of the frontal-subcortical circuits, (i.e., the pallidum and caudate, especially on the left side) predisposed stroke patients to depression. The size of the infarcts at these sites in the depressed patients was larger. Using a logistic regression analysis, the authors found that a brain infarct that affected pallidum was a strong independent MRI correlate for poststroke depression (odds ratio = 7.2).

Executive dysfunction (ED) may lead to problem behaviour and impaired activities of daily living in many neuropsychiatric disorders, but the neuroanatomical correlates of ED are still not well known. Different aspects of executive functions were studied by widely used neuropsychological tests in 214 elderly patients 3 months after ischaemic stroke, and a sum score of eight different measures was counted in each patient. The number and site of brain infarcts as well as severity and location of white matter lesions (WMLs) and brain atrophy on magnetic resonance imaging were recorded and compared between patients with and without ED. ED was present in 73 (34.1%) of the 214 patients. The mean frequency of brain infarcts in the brain and in the left hemisphere was higher in the patients with ED. Lesions affecting the frontal-subcortical circuits (e.g. pallidum, corona radiata or centrum semiovale) were more frequent in patients with ED than in those without. Also, patients with pontine brain infarcts frequently had ED, but this may have been due to more extensive ischaemic changes in these patients in general. Mean number of brain infarcts affecting the pons and posterior centrum semiovale on the left side, moderate to severe medial temporal atrophy, the Fazekas white matter score, the Mini-Mental State Examination score and low education were independent correlates of ED. Brain infarcts and WML affecting the frontal-subcortical circuits or the pons may increase risk for ED in stroke patients.

Background and Purpose: Elevated fibrinogen levels are suggested to increase the risk of myocardial infarction and stroke. Carriers of the A allele of the fibrinogen -455G/A polymorphism have increased plasma fibrinogen levels. We studied the association of this polymorphism with stroke subtype in the Stroke Aging Memory (SAM) cohort., Methods: The SAM cohort comprises 486 consecutive patients 55 to 85 years of age who, 3 months after ischemic stroke, completed a detailed stroke assessment. Stroke subtypes were examined with MRI. -455G/A genotype was determined by polymerase chain reaction. MRI and genotype data were available for the 299 patients who constitute the present study population., Results: Genotype distributions were 64.9% (GG), 31.8% (GA), and 3.3% (AA). In a logistic regression model with age, sex, hypertension, diabetes, hypercholesterolemia, hypertriglyceridemia, myocardial infarction, arrhythmia, atrial fibrillation, peripheral arterial disease, and smoking as possible confounders, there was a significant association between A+ genotype and >or=3 lacunar infarcts (odds ratio [OR], 2.57; 95% CI, 1.23 to 5.36; P=0.01). Hypertensive patients carrying the A allele had increased risk (OR, 4.24; 95% CI, 1.29 to 13.99; P=0.02) for >or=3 lacunar infarcts. A similar increase in risk was observed among smokers with the A+ genotype (OR, 2.67; 95% CI, 0.92 to 7.77; P=0.07)., Conclusions: Stroke patients carrying the A allele of the Bbeta-fibrinogen -455G/A polymorphism frequently presented with multiple lacunar infarcts. This association was stronger among hypertensives and smokers. These associations suggest that the A allele may predispose to atherothrombotic events in cerebrovascular circulation.

The relationship between alcohol consumption and the risk of ischemic stroke has been widely studied, whereas the effect of alcohol use on stroke features is not well established. This study compared the clinical and stroke features of ischemic stroke in two groups of patients with ischemic stroke: those with a history of alcohol misuse and those with a history of more social drinking. DSM-IV criteria were used to diagnose alcohol use disorder (dependency or abuse) in 275 of 486 consecutive patients aged 55-85 years, 3-4 months after ischemic stroke. Magnetic resonance imaging of the head was performed 3 months after stroke. Alcohol use disorder was diagnosed in 37/275 (13.5%) of ischemic stroke patients. These patients had more frequently (70.3 vs. 34.5%; OR 4.5; 95% CI 2.2-9.1; p < 0.000) an infarct affecting the putamen compared with patients who indulged in more social drinking. Another predisposed area was the superior anterior cerebral artery area. The stroke due to large- artery atherosclerosis was more common in patients with alcohol use disorder. The misuse of alcohol seemed to be associated with cerebral infarct localization in the putamen and superior anterior cerebral artery area. Prospective studies are needed to verify our preliminary finding., (Copyright 2003 S. Karger AG, Basel)

Background: Depression affects up to 40% of patients with ischemic stroke. The relationship between site and size of brain infarcts and poststroke depression is still not well characterized. Further possible contribution and interaction of white matter lesions and brain atrophy has not been studied previously. We conducted a magnetic resonance image-based study of the radiologic correlates of depression in a large, well-defined series of patients with ischemic stroke., Methods: Modified DSM-III-R and DSM-IV criteria were used to diagnose depressive disorders during a comprehensive psychiatric evaluation in 275 of 486 consecutive patients aged 55 to 85 years 3 to 4 months after ischemic stroke. A standardized magnetic resonance imaging protocol detailed side, site, type, and extent of brain infarcts and extent of white matter lesions and brain atrophy., Results: Depressive disorders were diagnosed in 109 patients (40%). Patients with depression had a higher number and larger volume of infarcts affecting the prefrontosubcortical circuits, especially the caudate, pallidum, and genu of internal capsule, with left-sided predominance. Extent of white matter lesions and atrophy did not differ in patients with and without depression. Independent correlates of poststroke depression in a logistic regression model were mean frequency of infarcts in the genu of internal capsule on the left side (odds ratio [OR], 3.2; 95% confidence interval [CI], 1.0-10.1), mean frequency of infarcts in the pallidum of any side (OR, 1.6; 95% CI, 1.1-2.3), and mean volume of infarcts in the right occipital lobe (OR, 0.98; 95% CI, 0.96-0.99)., Conclusion: Lesions affecting the prefrontosubcortical circuits, especially on the left side, are correlates of depression after ischemic stroke.

Background and Purpose: The criteria for vascular dementia (VaD) include definition of the cognitive syndrome and the vascular cause. Different criteria for dementia identify different frequencies and clusters of patients. In addition, variation in defining the cause and etiology may have an effect. We compared different clinical criteria for VaD in series of patients with poststroke dementia., Methods: The study group comprised 107 patients fulfilling the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) definition for dementia from a cohort of consecutive patients with ischemic stroke who completed a comprehensive neuropsychological test battery and MRI. The mean age (SD) of the patients was 71.4 (7.6) years. The definitions of vascular cause of VaD were those of the DSM-III (1980), Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC; 1992), International Statistical Classification of Diseases, 10th Revision (ICD-10; 1992), National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN; 1993), and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV; 1994)., Results: The number of cases that could be classified as VaD according to the different criteria varied considerably: 36.4% (n=39) by DSM-III, 86.9% (n=93) by ADDTC, 32.7% (n=35) by NINDS-AIREN, 36.4% (n=39) by ICD-10, and 91.6% (n=98) by DSM-IV criteria. The concordance between DSM-III/ICD-10 was perfect (100%; kappa=1.0), between ICD-10/NINDS-AIREN and ADDTC/DSM-IV good to moderate (85.0% and 87. 3%; kappa=0.87 and 0.37, respectively), but otherwise poor between the other criteria. Only 31 patients fulfilled all the criteria for VaD applied. Major discriminating factors between the criteria were requirement of (1) focal neurological signs, (2) unequal distribution of deficits in higher cortical functions, and (3) evidence of relevant CVD based on brain imaging findings., Conclusions: Current criteria of VaD identify different frequencies and clusters of patients and are not interchangeable. Optimally, prospective studies with clinicopathological correlation could identify new criteria. Meanwhile, focus on more homogeneous subtypes (eg, small-vessel subcortical VaD) and detailed neuroimaging criteria could improve the diagnostics.

Background and Purpose: Dementia after first clinical stroke frequently has been found, but the clinical and radiological correlates have not been fully detailed. We examined magnetic resonance imaging (MRI) correlates of dementia in a large well-defined series of patients with first clinical ischemic stroke., Methods: Detailed medical, neurological and neuropsychological examination was conducted 3 months after ischemic stroke for 273 patients with first clinical stroke from a consecutive series of 486 patients aged 55-85 years. MRI of the head categorised infarcts (type, site, side, number, volume), extent of white matter lesions (WMLs) and degree of atrophy. The DSM-III definition for dementia was used., Results: Dementia was diagnosed in 79 (28.9%) of the patients with first clinical stroke. Volumes, numbers, distinct sites of infarcts, extent of WMLs and degree of atrophy were different for the demented and nondemented subjects. Logistic regression analysis showed that the correlates of dementia included the combination of infarct features (volume of infarcts in left-sided anterior corona radiata; OR 1.86), extent of WMLs (OR 1. 37), medial temporal lobe atrophy (OR 3.4) and host factors (low education; OR 1.11). The additive effect of having more than one correlate was detected (OR 2.53)., Conclusions: Dementia occurring after first clinical stroke is frequent and not solely due to a single stroke, but contain a combination of infarcts features, extent of WMLs, medial temporal lobe atrophy and host factors reflecting more than one underlying pathology.

Background and Purpose: MRI studies in patients with atherosclerosis often reveal ill-defined hyperintensity in the pons on T2-weighted images. This pontine hyperintensity (PHI) does not fulfill the criteria of a brain infarct, and its clinical relevance is not established. We examined the frequency, as well as the radiological and clinical correlates, of PHI in poststroke patients., Methods: Three hundred nineteen patients were studied 3 months after supratentorial ischemic stroke with the use of 1.0-T MRI. Brain infarcts, atrophy, white matter hyperintensities, and PHI were registered. The clinical outcome was assessed 3 and 15 months after the stroke., Results: Of the patients, 152 (47.6%) had PHI. The risk factors for stroke did not differ in patients without or with PHI. PHI was related to a higher frequency (P=0.002) and larger volume (P<0.001) of supratentorial brain infarcts, to parietal (P=0.020) and temporal (P=0.002) atrophy, to central atrophy (P< or =0.040), and to white matter hyperintensity grade (P<0.001). Brain infarcts that affected the corpus striatum (putamen, caudate, and pallidum) (P< or =0. 011) or pyramidal tract (P<0.001) were more frequent in patients with PHI. The 3- and 15-month outcomes were worse in patients with PHI (P< or =0.004). The total volume of brain infarcts (OR 1.22), mean atrophy (OR 3.59), and PHI (OR 3.76) were independent correlates of a poor 15-month outcome., Conclusions: PHI after supratentorial ischemic stroke deserves attention because it relates to poor clinical outcome.

Objectives: Stroke seems to be related to dementia more often than previously assumed and vascular factors are also related to Alzheimer's disease. The pathophysiology of poststroke dementia includes ischaemic changes in the brain, a combination of degenerative and vascular changes, and changes only related to Alzheimer's disease. Some cognitive decline recognised after a stroke may be due to pre-existing cognitive decline. The aim of this study was to determine the clinical and radiological determinants of prestroke cognitive decline., Methods: The study group comprised 337 of 486 consecutive patients aged 55 to 85 years who 3 months after ischaemic stroke completed a comprehensive neuropsychological test battery; structured medical, neurological, and mental status examination; interview of a knowledgeable informant containing structured questions on abnormality in the cognitive functions; assessment of social functions before the index stroke; and MRI., Results: Frequency of prestroke cognitive decline including that of dementia was 9.2% (31/337). The patients with prestroke cognitive decline were older, more often had less than 6 years of education, and had history of previous stroke. Vascular risk factors did not differ significantly between these two groups. White matter changes (p=0.004), cortical entorhinal, hippocampal, and medial temporal atrophy (p<0.001), cortical frontal atrophy (p=0.008); and any central atrophy (p<0.01), but not the frequencies or volumes of old, silent, or all infarcts on MRI differentiated those with and without prestroke cognitive decline. The correlates of prestroke cognitive decline in logistic regression analysis were medial temporal cortical atrophy (odds ratio (OR) 7.5, 95% confidence interval (95%CI) 3.2-18.2), history of previous ischaemic stroke (OR 4.4, 95% CI 1.8-10.6), and education (OR 0.9, 95% CI 0.8-0.9)., Conclusions: History of previous stroke, but not volumes or frequencies was found to correlate with prestroke cognitive decline. Other associating factors were rather those usually associated with degenerative dementia: white matter changes and cerebral atrophy; and in multiple models medial temporal cortical atrophy and education. The possible overlap between two or more underlying diseases must be remembered in diagnosis and treatment of patients with vascular cognitive impairment.

Impairments in executive functions have been related to aging and frontal lobe lesions. Aging also causes slowing of mental processing. We examined whether ischemic stroke in the frontal brain area results in dysexecutive syndrome, or whether the frontal stroke causes increased slowing of mental processing. Neurological, radiological and neuropsychological examinations were carried out 3 months post-stroke on 250 ischemic stroke patients (55-85 years) and on 39 healthy control subjects. Of the patients, 62 had frontal and 188 had nonfrontal lesions. The neuropsychological examination comprised several cognitive domains, including tests considered to measure executive functions. The frontal group was slower than the nonfrontal group in tasks measuring speed of mental processing which were time-limited (Trail Making A, Stroop dots and fluency). They were also inferior in the Digit Span backwards task. There were no differences between the groups in other cognitive domains, nor in some tests which are considered to be measures of executive functions (e.g. WCST). Impairments in executive functions were evident in both the frontal and the nonfrontal groups compared with the controls, but no dysexecutive syndrome specifically related to frontal lesions was found. Frontal stroke related mainly to the slowing of mental processing., (Copyright 1999 Lippincott Williams & Wilkins)

No uniform criteria currently exist for rating white-matter (WM) high-signal foci on MRI. Ratings are based on descriptive terms, different pulse sequences and different WM areas. Reports on the prevalence and clinical correlates of high-signal foci have been contradictory. We wanted to examine the contribution of the pulse sequence and WM area on rating WM changes. We analysed WM changes separately on T2-, protondensity (PD)- and T1-weighted images in periventricular, subcortical, watershed area and deep WM. The difference between T2- and PD-weighted images was significant for frontal caps, counting small foci or analysing subcortical changes. T1-weighted images showed significantly less change, but the number of foci detected was greater than previously thought. The prevalence of WM high-signal foci was greatest in the watershed zone and smallest in the subcortical area. There was a significant correlation between foci in different areas.