Thomas K. Tatemichi

Cognitive impairment after stroke: frequency, patterns, and relationship to functional abilities.

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.

Dementia after stroke Baseline frequency, risks, and clinical features in a hospitalized cohort

We determined the frequency of dementia in a cohort of 251 patients aged ⩾60 years hospitalized with acute ischemie stroke, based on examinations performed 3 months after stroke onset. Using modified DSM-III-R criteria, we found dementia in 66 patients (26.3%). Diagnostic agreement among raters was excellent (kappa = 0.96). In a control sample of 249 stroke-free subjects recruited from the community and matched by age, we found dementia in eight subjects (3.2%). Using a logistic regression model to estimate the risk of dementia associated with stroke in the combined samples, the odds ratio (OR) for stroke patients compared with control subjects was 9.4 (p <0.001). Advancing age and fewer years of education were significant, independent correlates of dementia, with a trend evident for race (non-white versus white). Confining the analysis to subjects residing in the Washington Heights-Inwood community of northern Manhattan, the OR was 10.3 (p <0.001) with significant age and race effects. We conclude that ischemie stroke significantly increases the risk of dementia, with independent contributions by age, education, and race.

Risk of dementia after stroke in a hospitalized cohort: Results of a longitudinal study

Stroke is considered the second most common cause of dementia, but the magnitude of the risk posed by stroke has not been fully clarified. The aim of this study was to determine the long-term risk of developing dementia after stroke onset in a hospitalized cohort. We prospectively examined 185 nondemented patients aged ≥60 years hospitalized with ischemic stroke and 241 age-matched nondemented controls without stroke from the same community using neurologic, neuropsychological, and functional assessments given annually. Using criteria modified from the DSM-III-R, we diagnosed incident dementia based on the annual examination findings. We used life-table methods to estimate incidence in the two groups, Kaplan-Meier analysis to determine the proportion surviving without dementia, and Cox proportional-hazards analysis to compute the relative risk (RR) of dementia after 1 to 4 years of follow-up. The incidence of dementia was 8.4 per 100 person-years in the stroke group and 1.3 per 100 person-years in the control group. After 52 months of follow-up, the cumulative proportion (±SE) surviving without dementia was 66.3 ± 5.5% for stroke and 90.3 ± 4.3% for control subjects. The RR of dementia associated with stroke compared with controls was 5.5 (95% CI, 2.5 to 11.1) after adjusting for demographic factors. Older age at stroke onset and fewer years of education were significant covariates, but sex and race were not. A low score on the Mini-Mental State Examination at baseline was a significant predictor when added to this model. We conclude that ischemic stroke in elderly persons increases the long-term risk of developing dementia by approximately five-fold compared with those without stroke. Age, education, and baseline intellectual function contribute independently to that risk.

Dementia in stroke survivors in the Stroke Data Bank cohort. Prevalence, incidence, risk factors, and computed tomographic findings.

We determined the prevalence of dementia in 927 patients with acute ischemic stroke aged greater than or equal to 60 years in the Stroke Data Bank cohort based on the examining neurologists best judgment. Diagnostic agreement among examiners was 68% (kappa = 0.34). Of 726 testable patients, 116 (16%) were demented. Prevalence of dementia was related to age but not to sex, race, handedness, educational level, or employment status before the stroke. Previous stroke and previous myocardial infarction were related to prevalence of dementia although hypertension, diabetes mellitus, atrial fibrillation, and previous use of antithrombotic drugs were not. Prevalence of dementia was most frequent in patients with infarcts due to large-artery atherosclerosis and in those with infarcts of unknown cause. Computed tomographic findings related to prevalence of dementia included infarct number, infarct site, and cortical atrophy. Among 610 patients who were not demented at stroke onset, we used methods of survival analysis to determine the incidence of dementia occurring during the 2-year follow-up. Incidence of dementia was related to age but not sex. Based on logistic regression analysis, the probability of new-onset dementia at 1 year was 5.4% for a patient aged 60 years and 10.4% for a patient aged 90 years. With a multivariate proportional hazards model, the most important predictors of incidence of dementia were a previous stroke and the presence of cortical atrophy at stroke onset.

Early clinical differentiation of cerebral infarction from severe atherosclerotic stenosis and cardioembolism.

Hyperacute cerebral infarction trials require early differentiation of infarction subtype. Our aim was to determine clinical factors predictive of infarction subtype from data collected in the early hours of admission. Methods Using the 1,273 patients enrolled in the Stroke Data Bank, stroke risk factors and demographic, clinical, and radiological features were compared between the 246 cardioembolic and 113 large-vessel atherosclerotic cerebral infarcts. Results Stroke Data Bank definitions ensured more transient ischemic attacks in atherosclerotic infarcts and more cardiac disease in cardioembolic infarcts, but the diagnosis was distinguished further using a logistic regression model. Fractional arm weakness (shoulder different from hand) (odds ratio 3.1, 95% confidence interval [CI] 1.6-5.8), hypertension (odds ratio 2.8, CI 1.4-5.3), diabetes (odds ratio 2.5, CI 1.2-5.1) and male gender (odds ratio=2.2, CI 1.2-4.1) occurred more frequently in patients with atherosclerotic than cardioembolic infarcts. Reduced consciousness (odds ratio=3.2, CI 1.4-7.3) was more frequent in cardioembolism. For a male patient with hypertension, diabetes, and fractional arm weakness, the estimated odds of an atherosclerotic infarction were 47-fold that of a cardioembolic infarction. Patients with atherosclerotic infarcts were more likely to have a fractional arm weakness regardless of infarct size, whereas, for those with cardioembolic infarctions, fractional weakness was more frequent in infarcts less than 20 cc in volume. Conclusions Clinical features that are observed at stroke onset can help distinguish cerebral infarction subtypes and may allow for early stratification in therapeutic trials.

The role of transcranial Doppler in confirming brain death: Sensitivity, specificity, and suggestions for performance and interpretation

We performed transcranial Doppler (TCD) examinations on 54 comatose patients over a 1-year period. Of 49 patients with technically adequate TCD examinations, 23 met criteria for determination of brain death by clinical and EEG criteria (21) or clinical criteria alone (2; EEG not performed). A TCD waveform abnormality, consisting of absent or reversed diastolic flow, or small early systolic spikes, in at least 2 intracranial arteries, occurred in 21 brain-dead patients, but in none of the other patients in coma. With appropriate guidelines for performance and interpretation, TCD could be incorporated into institutional protocols as a rapid and convenient alternative to EEG for confirmation of brain death.

Dementia after stroke is a predictor of long-term survival.

The aim of this study was to determine whether dementia after stroke adversely influences long-term survival. Methods Subjects were 251 patients ≥60 years of age with ischemic stroke who were given neurological, neuropsychological, and functional examinations 3 months after hospitalization and were followed up prospectively. Using criteria modified from the Diagnostic and Statistical Manual of Mental Disorders-III-R, dementia was found in 66 (26.3%) patients at the 3-month baseline examination. Life-table methods were used to estimate mortality rates in the groups with and without dementia after 1 to 5 years of follow-up, Kaplan-Meier curves to estimate the cumulative proportion surviving with and without dementia, and Cox proportional-hazards analysis to compute the relative risk of mortality associated with dementia at baseline, after adjusting for other potential predictors of stroke mortality. Results The mortality rate was 19.8 deaths per 100 personyears with dementia compared with 6.9 deaths per 100 personyears without dementia. The cumulative proportion surviving after a median follow-up of 58.6 months was 38.9±0.08% for those with dementia and 74.5 ±0.04% for those without dementia. The relative risk associated with dementia was 3.11 (95% confidence interval, 1.79 to 5.41) after adjusting for the effects of demographic factors, cardiac disease, severity of stroke (Barthel Index), stroke type (lacunar versus nonlacunar), and recurrent stroke (examined as a time-dependent variable). When the Mini-Mental State Examination score at baseline was examined instead of the diagnosis of dementia, the results of the model were similar. Conclusions Our study is the first to demonstrate that dementia or cognitive impairment adversely influences longterm survival after stroke, even after adjusting for other commonly accepted predictors of stroke mortality. Impairment in intellectual function after stroke, independent of physical disability, has a significant impact on prognosis. Both cognitive and physical functions should be assessed in clinical studies of stroke outcome.

How acute brain failure becomes chronic: A view of the mechanisms of dementia related to stroke

My aim in this review is to review some current ideas about the independent and interacting contributions of vascular disease and brain degeneration to dementia syndromes related to stroke, and to formulate these ideas into the potential vascular mechanisms involved in the pathogenesis of dementia from cerebrovascular disease

Risk Factors for Incident Dementia After Stroke Role of Hypoxic and Ischemic Disorders

BACKGROUND AND PURPOSE Stroke significantly increases the risk of dementia in the elderly, yet the risk factors for incident dementia after ischemic stroke are not well understood. We attempted to determine whether hypoxic-ischemic (HI) disorders, which may result from comorbid medical conditions (eg. seizures, cardiac arrhythmias, pneumonia), would be an independent risk factor for the development of new dementia after stroke. METHODS We prospectively followed 185 initially nondemented patients with ischemic stroke (age, 70.3 +/- 7.7 years) for a maximum of 52.8 months. We diagnosed the presence of dementia at annual examinations based on neuropsychological testing and modified DSM-III-R criteria. HI disorders were identified by record review or examination during hospitalization. We used Kaplan-Meier analysis to determine the cumulative proportion of patients with and without HI disorders who survived free of dementia and used Cox models to estimate the relative risk of dementia associated with HI disorders. RESULTS The cumulative proportion (+/- SE) surviving without dementia was 51.7 +/- 10.9% in the HI group versus 78.2 +/- 4.3% in the non-HI group after 52.8 months of observation. The relative risk of incident dementia associated with HI events was 4.3 (95% confidence interval = 1.9 to 9.6) after we adjusted for demographic factors, recurrent stroke, and baseline cognitive function. CONCLUSIONS We conclude that HI disorders may be a significant independent risk factor for incident dementia after stroke, even after adjustment for other recognized predictors of cognitive decline. Recognition of HI cerebral damage as a possible pathogenic mechanism for dementia after stroke may allow targeted therapeutic interventions to prevent subsequent cognitive deterioration.

Perfusion insufficiency in limb-shaking transient ischemic attacks.

We describe a 63-year-old man with severe bilateral internal carotid artery disease who presented with repeated, brief attacks of left limb shaking precipitated by his standing up. Cerebral blood flow measured by xenon-133 inhalation showed reduced resting flows and a focal perfusion deficit in the right dorsofrontal and upper rolandic regions. Blood flow velocity and pulsatility index of the right middle cerebral artery measured by transcranial Doppler ultrasonography were also reduced. With hypercapnic challenge, both hemispheric tissue perfusion and blood flow velocity showed impaired reactivity. With induced hypotension, the focal perfusion deficit in the right dorsofrontal region was accentuated. Following right internal carotid endartectomy, resting cerebral blood flow and blood flow velocity improved, as did hypercapnic vasoreactivity. These reversible deficits in cerebral blood flow and vasoregulation, which were maximal in the dorsofrontal region, are consistent with low perfusion in the border zone territory or the distal fields and demonstrate that hemodynamic failure is the likely mechanism for limb-shaking transient ischemic attacks from severe carotid artery disease.