Objective -To determine the validity of the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE) as screening tools for cognitive impairment after stroke. Materials and methods -Cognitive assessments were administered over 2 sessions (1 week apart) at 3 months post-stroke. Scores on the MoCA and MMSE were evaluated against a diagnosis of cognitive impairment derived from a comprehensive neuropsychological battery (the criterion standard). Results -Sixty patients participated in the study [mean age 72.1 years (SD = 13.9), mean education 10.5 years (SD = 3.9), median acute NIHSS score 5 (IQR 3-7)]. The MoCA yielded lower scores (median = 21, IQR = 17-24; mean = 20.0, SD = 5.4) than the MMSE (median = 26, IQR = 22-27; mean = 24.2, SD = 4.5). MMSE data were more skewed towards ceiling than MoCA data (skewness = À1.09 vs À0.73). Area under the receiver operator curve was higher for MoCA than for MMSE (0.87 vs 0.84), although this difference was not significant (v 2 = 0.48, P = 0.49). At their optimal cut-offs, the MoCA had better sensitivity than the MMSE (0.92 vs 0.82) but poorer specificity (0.67 vs 0.76). Conclusions -The MoCA is a valid screening tool for post-stroke cognitive impairment; it is more sensitive but less specific than the MMSE. Contrary to the prevailing view, the MMSE also exhibited acceptable validity in this setting.

The ultrastructural changes in the pyramidal neurons of the CA1 region of the hippocampus were studied 6 h, 24 h, 48 h, and 72 h following a transient 10 min period of cerebral ischemia induced by common carotid occlusion combined with hypotension. The pyramidal neurons showed delayed neuronal death (DND), i.e. at 24 h and 48 h postischemia few structural alterations were noted in the light microscope, while at 72 h extensive neuronal degeneration was apparent. The most prominent early ultrastructural changes were polysome disaggregation, and the appearance of electron-dense fluffy dark material associated with tubular saccules. Mitochondria and nuclear elements appeared intact until frank neuronal degeneration. The dark material accumulated with extended periods of recirculation in soma and in the main trunks of proximal dendrites, often beneath the plasma membrane, less frequently in the distal dendrites and seldom in spines. Protein synthesis inhibitors (anisomycin, cycloheximide) and an RNA synthesis inhibitor (actinomycin D), administered by intrahippocampal injections or subcutaneously, did not mitigate neuronal damage. Therefore, DND is probably not apoptosis or a form of programmed cell death. We propose that the dark material accumulating in the postischemic period represents protein complexes, possibly aggregates of proteins or internalized plasma membrane fragments, which may disrupt vital cellular structure and functions, leading to cell death.

Background and Purpose: The economic burden of stroke is substantial and is likely to increase with an increasing number of elderly individuals in the population. There is thus a need for information on the use of health care resources and costs among these elderly stroke patients. We examined the impact of the cognitive impairments on the ability to perform activities of daily living (ADL) and utilization and costs of health care in a cohort of elderly stroke patients. Methods: One hundred and forty-nine patients aged ≧70 years with acute stroke were included. The patients were assessed regarding their ability to carry out ADL and health resource utilization and cost during the first year after stroke. Cognitive impairments were assessed 18 months after the index stroke. Results: Stroke severity in acute stroke andcognitive impairment at 18 months after stroke onset was associated with impairment in ADL and increased costs for utilisation of care during the first year. Patients with cognitive impairment were more dependent on personal assistance in ADL. Costs per patient during the study were three times higher for patients with cognitive impairment. Hospital care, institutional living and different kinds of support from society accounted forthe highest costs. Conclusions: Costs of care utilisation during the first year after stroke were associated with cognitive impairments, stroke severity and dependence in ADL. The results should be interpreted cautiously as the assessment of cognitive function was made 18 months after stroke onset and costs were estimated for the first year after stroke.

Promoting physical activity in school by means of a curriculum-based intervention program may improve children's educational outcome.

Curriculum-based physical activity in school may improve the academic achievement and psychological health of children, particularly for girls.

Background and Purpose-Depression is common after stroke. Reported frequencies vary widely between studies because of differences in patient selection, time from stroke to assessment, evaluation methods and diagnostic criteria. Poststroke depression is related to increased mortality and poorer rehabilitation outcome. Few studies have been done in the elderly, and there is a lack of studies with population-based controls. We aimed to examine the risk of depression in elderly patients one and a half years after stroke and to compare the risk with a population-based control sample. Methods-We examined 149 elderly stroke survivors and 745 age-and sex-matched controls from the general population with semistructured psychiatric examinations and cognitive assessments. Diagnoses were made according to DSM-III-R. Independent samples t test and 2 test were used to test for significance, Mantel-Haenszel odds ratios with 95% CI for relative risk and Tarone statistics for risk differences between groups. Results-The frequency of depression was 34% in stroke patients and 13% in population controls (odds ratio, 3.4; 95% CI, 2.3 to 5.0). The risk of depression was increased in both men and women and in all age groups but not related to the predominant side of stroke symptoms. Conclusion-Depression is common after stroke. It is therefore important to identify depression in stroke patients because it is a treatable condition that may have implications for poorer outcome in relation to rehabilitation and mortality.

Background and Purpose: Dementia is common after stroke, but the dementia syndrome does not cover the whole spectrum of cognitive impairment. Our aim was to quantify and compare dementia and cognitive impairments in elderly patients 1.5 years after stroke and a matched normal population. Subjects and Methods: We examined dementia and cognitive impairments in 149 out of an initial total of 243 acute stroke patients after a mean 20 months. Inclusion criteria were age ≧70 years, not living in an institution and no previous cerebral lesion. The patients’ mean age was 81 years. Five controls matched by age and gender and fulfilling the same exclusion criteria were selected for each patient (n = 745) from a population-based survey in the same area. Dementia was diagnosed according to the DSM-III-R criteria, and impairments in different dimensions of cognitive function were assessed. Results: The prevalence of dementia was 28% in the stroke patients and 7.4% in the controls (OR 4.7; 95% CI 3.0–7.5). Seventy-two percent of the patients had cognitive impairments compared to 36% in the controls. Cognitive impairments were more common in nondemented stroke patients than in nondemented controls: 61 vs. 31% (OR 3.5; 95% CI 2.3–5.3). The risk increase attributable to stroke was highest for patients below 80 years of age. Conclusions: Stroke confers an increased risk of dementia and cognitive impairments in the elderly, especially in the younger ones. Apraxia is the most frequent neuropsychiatric impairment after stroke. The concept of dementia does not describe cognitive impairments well, since it underestimates their extent not only after stroke but also in normal ageing.

Erythropoietin (EPO) has shown promise as a neuroprotectant in animal models of ischemic stroke. EPO is thought not only to protect neurons from cell death, but also to promote regeneration after stroke. Here, we report a systematic review and meta-analysis of the efficacy of EPO in animal models of focal cerebral ischemia. Primary outcomes were infarct size and neurobehavioral outcome. Nineteen studies involving 346 animals for infarct size and 425 animals for neurobehavioral outcome met our inclusion criteria. Erythropoietin improved infarct size by 30.0% (95% CI: 21.3 to 38.8) and neurobehavioral outcome by 39.8% (33.7 to 45.9). Studies that randomized to treatment group or that blinded assessment of outcome showed lower efficacy. Erythropoietin was tested in animals with hypertension in no studies reporting infarct size and in 7.5% of the animals reporting neurobehavioral outcome. These findings show efficacy for EPO in experimental stroke, but when the impact of common sources of bias are considered, this efficacy falls, suggesting we may be overestimating its potential benefit. As common human co-morbidities may reduce therapeutic efficacy, broader testing to delineate the range of circumstances in which EPO works best would be beneficial.