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T Pohjasvaara

Publications and source records attributed to T Pohjasvaara.

At least 19 recordsLinked to original sources
PubMed2003

Fibrinogen gene promoter -455 A allele as a risk factor for lacunar stroke.

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.

Aged↗
PubMed2003

Alcohol misuse: a risk factor for putaminal damage by ischemic brain infarct?

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.

Aged↗
PubMed2002

Parasomnias decline during pregnancy.

OBJECTIVES: A survey of the effects of pregnancy on parasomnias. MATERIAL AND METHODS: In an area of a central hospital and the maternity care units in the nearby rural community, women were interviewed during and after their pregnancy with a series of five questionnaires to assess the frequency of their parasomnias. The first questionnaire covered the 3 months before becoming pregnant, the next three the trimesters of pregnancy and the last one the 3 months after delivery. Altogether 325 mothers filled all the five questionnaires and constitute the study group. RESULTS: The total number of parasomnias declined (P < 0.001) during pregnancy and even more among the primiparas than among the multiparas (difference until third trimester, P=0.02). Among various parasomnias reported, sleep talking and sleepwalking decreased from the prepregnant period to the second trimester (22.8 vs 12.6%, change P=0.003), and the reported sleep starts also diminished from the prepregnant time to the first trimester (78.5 vs 63.1%, P < 0.001), but these phenomena did not change further during the follow-up. Altogether 55.7% of the women reported having nightmares 3 months before the pregnancy, and 47.7, 49.5, 41.2 and 40.3% (change from the prepregnant period, P < 0.001), respectively, at first, second and third trimester and after the delivery. Reported hypnagogic hallucinations decreased from the prepregnant time to the first trimester (9.8 vs 6.5%, P=0.027), but returned thereafter to the previous level. During the prepregnant period, 25.8% of the women reported bruxism and only 19.9% during the first trimester (P=0.009). Though the prevalence of sleep paralysis decreased during the first trimester of pregnancy, it was the only parasomnia that increased during later pregnancy (from 5.7 to 13.3% in the second trimester, P < 0.013). CONCLUSIONS: The reported frequency of most parasomnias decreases during pregnancy and even more in primiparas than multiparas.

Adolescent↗
PubMed2002

Post-stroke depression, executive dysfunction and functional outcome.

The early diagnosis of vascular cognitive impairment has been challenged and executive control function has been suggested to be a rational basis for the diagnosis of vascular dementia. We sought to examine the correlates of executive dysfunction in a well-defined stroke cohort. A group of 256 patients from a consecutive cohort of 486 patients with ischaemic stroke, aged 55-85 years, was subjected to a comprehensive neuropsychological examination 3-4 months after ischaemic stroke and 188 of them in addition to detailed psychiatric examination. Basic and complex activities of daily living (ADLs) (bADLs and cADLs) post-stroke were assessed. The DSM-III-R criteria were used for the diagnosis of the depressive disorders. Altogether 40.6% (n=104) of the patients had executive dysfunction. The patients with executive dysfunction were older, had lower level of education, were more often dependent, did worse in bADLs and cADLs, had more often DSM-III dementia, had worse cognition as measured by Mini Mental State Examination (MMSE) and were more depressed as measured by the BECK depression scale, but not with the more detailed psychiatric evaluation. They had more often stroke in the anterior circulation and less often in the posterior circulation. The independent correlates of executive dysfunction were cADLs (OR 1.1, 95% CI 1.03-1.16), each point of worsening in cognition by MMSE (OR 1.7, 95% CI 1.42-1.97) and stroke in the posterior circulation area (OR 0.4, 95% CI 0.18-0.84). Clinically significant executive dysfunction is frequent after ischaemic stroke and is closely connected with cADLs and to overall cognitive status but could be distinguished from depression by detailed neuropsychological examination. Executive measures may detect patients at risk of dementia and disability post-stroke.

Activities of Daily Living↗
PubMed2002

Insomnia in ischemic stroke patients.

This is the first study that focuses on insomnia in stroke patients. A subgroup of 277 patients from a consecutive series of 486 stroke patients aged 55-85 years was subjected to a comprehensive psychiatric evaluation 3-4 months after ischemic stroke. Of 277 patients, 56.7% reported any insomnia complaint and 37.5% fulfilled the DSM-IV criteria of insomnia. In 38.6%, insomnia complaint/insomnia had already been present prior to the stroke and in 18.1%, it was a consequence of the stroke. Independent correlates of any insomnia complaint/insomnia were anxiety (Zung Anxiety Scale) and the use of psychotropic drug. Independent correlates of poststroke-onset insomnia complaint/insomnia were disability after stroke (Barthel Index), dementia, anxiety and use of psychotropic drug. Insomnia should be taken into consideration in treating and rehabilitating stroke patients.

Aged↗
PubMed2002

Cognitive functions and depression as predictors of poor outcome 15 months after stroke.

The prognostic predictors of poor outcome, as defined by death between 3 and 15 months and dependent living at 15 months, were examined in the Helsinki Stroke Aging Memory (SAM) study cohort. Death between 3 and 15 months was registered from the whole study group of 486 consecutive patients aged 55-85 years. Altogether 286 of the 486 patients went through a detailed follow-up examination both 3 and 15 months after stroke, including structured measures of emotion (Beck's Depression Inventory, BDI), cognition (Mini-Mental State Examination, MMSE), dementia assessment according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and handicap (Rankin scale, RS). The only independent correlate of death between 3 and 15 months was dependent living at 3 months (OR 2.6, 95% CI 1.2-5.8), which also had the most powerful association with dependent living at 15 months (OR 5.8, 95% CI 2.6-13.1). Also, both worsening in cognition (change in MMSE, OR for each point of worsening 1.2, 95% CI 1.1-1.3) and worsening of depression (change in BDI, OR for each point of worsening 1.1, 95% CI 1.02-1.12), between 3 and 15 months follow-up, had an independent effect on dependent living 15 months after ischemic stroke. This challenges the care and rehabilitation of these items even at the stable period after stroke.

Activities of Daily Living↗
PubMed2001

Magnetic resonance imaging correlates of depression after ischemic stroke.

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.

Aged↗
PubMed2001

Depression is an independent predictor of poor long-term functional outcome post-stroke.

The influence of depression on the long-term outcome of stroke patients was examined among 390 of 486 consecutive patients aged 55-85 years. They completed, at 3 months after ischaemic stroke, a detailed medical, neurological, and radiological stroke evaluation, structured measures of emotion (Beck's Depression Inventory, BDI), handicap (Rankin scale, RS), and assessment of activities of daily living (Barthel Index, BI). Further RS and BI was evaluated at 15-month follow-up from these 390 patients and BDI in 276 patients. A group of 256 patients completed, in addition to the 15-month follow-up, a comprehensive psychiatric evaluation, including the Present State Examination 3 months after stroke. The DSM-III-R criteria were used for diagnosis of the depressive disorders. BDI identified depression (cut-off point > or = 10 for depression) in 171 (43.9%) of 390 and in 123 (44.6%) of 276 patients at 3- and 15-month follow-up. DSM-III-R major depression was diagnosed in 66 (25.8%), and minor depression in 32 (12.5%), of 256 patients 3 months after stroke. Patients with BDI > or = 10, or major, but not minor, depression more often had poor functional outcome (RS > II and BI < 17) at 15 months. Poor functional outcome at 3 months also correlated with depression at 15 months. In logistic regression analysis, depression at 3 months (Beck > or = 10) correlated with poor functional outcome at 15 months (RS > II) (OR 2.5, 95% CI 1.6-3.8). More careful examination and treatment of depression in stroke patients is emphasized.

Aged↗
PubMed2001

Suicidal ideas in stroke patients 3 and 15 months after stroke.

Patients with stroke may have an increased risk of suicide. We sought to examine the frequency and clinical correlates of suicidal ideas 3 and 15 months after stroke. The study group comprised 286 of 486 consecutive patients aged 55-85 years who at 3 and 15 months after ischemic stroke completed a detailed medical, neurological and radiological stroke evaluation, structured measures of cognition (Mini Mental State Examination), emotion (Beck Depression Inventory, BDI), disability (Rankin scale), and assessment of dependent living. Suicidal ideas were present in 9.8% (n = 28) at 3 months' follow-up and in 14.0% (n = 40) at 15 months' follow-up. The patients with suicidal ideas were more depressed measured by BDI both at 3 (17.0 vs. 7.9, p < 0.001) and 15 months (20.5 vs. 8.5, p < 0.001) after stroke compared to the patients without suicidal ideas. Patients with suicidal ideas had more often a history of a stroke already before the index stroke (35 vs. 18.3%, p = 0.0154), right-sided stroke (60.0 vs. 41.9%, p = 0.0323), they were more disabled according to the Rankin scale (2.4 vs. 1.9; p = 0.0035) and more dependent in living (45.0 vs. 27.2%, p = 0.023) 15 months after stroke. An independent correlate of suicidal ideas 15 months after stroke was history of prior stroke (OR 2.4; 95% CI 1.14-4.97) in logistic regression analysis. The frequency of suicidal ideas increased with the time elapsed from stroke. Recurrent strokes, depressive symptoms, more disabling stroke and right-sided stroke correlated to suicidal ideas at 15 months after stroke. Early identification of these risk factors may lead to effective therapeutic intervention.

Aged↗
PubMed2000

MRI correlates of dementia after first clinical ischemic stroke.

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.

Aged↗
PubMed2000

How complex interactions of ischemic brain infarcts, white matter lesions, and atrophy relate to poststroke dementia.

BACKGROUND: Cerebrovascular disease is a major factor related to cognitive impairment. However, behavioral correlates of ischemic brain lesions are insufficiently characterized. OBJECTIVE: To examine magnetic resonance imaging correlates of dementia in a large, well-defined series of patients with ischemic stroke. METHODS: Detailed medical, neurological, and neuropsychological examinations were conducted 3 months after ischemic stroke for 337 of 486 consecutive patients aged 55 to 85 years. Infarcts (type, site, side, number, and volume), extent of white matter lesions (WMLs), and degree of atrophy were categorized according to magnetic resonance images of the head. The definition for dementia of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) was used. RESULTS: Dementia was diagnosed in 107 (31.8%) of the patients and stroke-related dementia in 87 (25.8%). Volumes, numbers, distinct sites of infarcts, extent of WMLs, and degree of atrophy were different for the demented and nondemented subjects. Particularly, volumes of infarcts in any (right- or left-sided) superior middle cerebral artery territory (27.3 vs 13.7 cm(3), P =. 002) and left thalamocortical connection (14.8 vs 4.0 cm(3), P =. 002) differentiated the 2 groups. Logistic regression analysis showed that the correlates of any dementia included the combination of infarct features (volume of infarcts in any superior middle cerebral artery: odds ratio [OR], 1.11; frequency of left-sided infarcts: OR, 1.21), extent of WMLs (OR, 1.3), medial temporal lobe atrophy (OR, 2.1), and host factors (education; OR, 0.91). In the patients with stroke-related dementia, the main correlate was volume of infarcts in the left anterior corona radiata (OR, 1.68). CONCLUSION: Correlates of poststroke dementia do not include merely 1 feature but a combination of infarct features, extent of WMLs, medial temporal lobe atrophy, and host features.

Aged↗
PubMed2000

Comparison of different clinical criteria (DSM-III, ADDTC, ICD-10, NINDS-AIREN, DSM-IV) for the diagnosis of vascular dementia. National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences.

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.

Aged↗
PubMed2000

MRI pontine hyperintensity after supratentorial ischemic stroke relates to poor clinical outcome.

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.

Activities of Daily Living↗
PubMed1999

Executive functions and speed of mental processing in elderly patients with frontal or nonfrontal ischemic stroke.

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.

Age Factors↗
PubMed1999

Clinical and radiological determinants of prestroke cognitive decline in a stroke cohort.

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.

Aged↗
PubMed1999

Magnetic resonance imaging white matter hyperintensities and mechanism of ischemic stroke.

BACKGROUND AND PURPOSE: We sought to determine the relations between infarct subtype and white matter hyperintensities (WMHIs) on MRI. MATERIALS AND METHODS: We studied 395 ischemic stroke patients with 1. 0-T MRI. The number of lacunar, border-zone, and cortical infarcts was registered. WMHIs were analyzed in 6 areas. Univariate and multivariate statistical analyses were used to find the risk factors for different infarct subtypes and to study the connections between WMHIs and brain infarcts. RESULTS: Lacunar infarcts were associated with hypertension (odds ratio [OR], 1.79; 95% CI, 1.17 to 2.73), alcohol consumption (OR, 1.96; 95% CI, 1.17 to 3.28), and age (OR, 1. 03; 95% CI, 1.00 to 1.06). Border-zone infarcts were associated with carotid atherosclerosis (OR, 2.20; 95% CI, 1.15 to 4.19). Atrial fibrillation (OR, 3.02; 95% CI, 1.66 to 5.50) and carotid atherosclerosis (OR, 1.94; 95% CI, 1.12 to 3.36) were independent positive predictors, and history of hyperlipidemia (OR, 0.44; 95% CI, 0.26 to 0.75) and migraine (OR, 0.48; 95% CI, 0.25 to 0.93) were negative predictors for cortical infarcts. Patients with lacunar infarcts had more severe WMHIs than patients with nonlacunar infarcts in all WM areas (P</=0.001). Patients with border-zone infarcts showed severe periventricular lesions (P=0.002), especially around posterior horns (P=0.003). The extent of WMHIs in patients with cortical infarcts did not differ from that in those without cortical infarcts. CONCLUSIONS: Various infarct subtypes have different risk profiles. The association between lacunar infarcts and WMHIs supports the concept of small-vessel disease underlying these 2 phenomena. The connection between border-zone infarcts and periventricular WMHIs again raises the question of the disputed periventricular vascular border zone.

Aged↗
PubMed1998

Clinical determinants of poststroke dementia.

BACKGROUND AND PURPOSE: Frequency of poststroke dementia is high, and stroke considerably increases the risk of dementia. The risk factors for dementia related to stroke are still incompletely understood. We sought to examine clinical determinants of poststroke dementia in a large well-defined stroke cohort. METHODS: The study group comprised 337 of 486 consecutive patients aged 55 to 85 years who 3 months after ischemic stroke completed a comprehensive neuropsychological test battery and MRI, including structured medical, neurological, and laboratory evaluations; clinical mental status examination; interview of a knowledgeable informant; detailed history of risk factors; and evaluation of stroke type, localization, and syndrome. The DSM-III definition for dementia was used. RESULTS: Frequency of any poststroke dementia was 31.8% (107/337), that of stroke-related dementia (mixed Alzheimer's disease plus vascular dementia excluded) was 28.4% (87/306), and that of dementia after first-ever stroke was 28.9% (79/273). The patients with poststroke dementia were older and more often had a low level of education, history of prior cerebrovascular disease and stroke, left hemispheric stroke (reflecting laterality), major dominant stroke syndrome (reflecting laterality and size), dysphasia, gait impairment, and urinary incontinence. The demented patients were also more frequently current smokers, had lower arterial blood pressure values, and more frequently had an orthostatic reaction compared with the nondemented stroke patients. The correlates of dementia in logistic regression analysis were dysphasia (odds ratio [OR], 5.6), major dominant stroke syndrome (OR, 5.0), history of prior cerebrovascular disease (OR, 2.0), and low educational level (OR, 1.1). When we excluded those with cerebrovascular disease plus Alzheimer's disease or those with recurrent stroke, the order of correlates remained the same. When the patients with dysphasia (n=30) were excluded, the correlates were major dominant syndrome (OR, 4.6) and low educational level (OR, 1.1). CONCLUSIONS: Our data suggest that a single explanation for poststroke dementia is not adequate; rather, multiple factors including stroke features (dysphasia, major dominant stroke syndrome), host characteristics (educational level), and prior cerebrovascular disease each independently contribute to the risk.

Age Factors↗