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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After stroke, the blood-brain barrier is transiently disrupted, allowing leukocytes to enter the brain and brain antigens to enter the peripheral circulation. This encounter of normally sequestered brain antigens by the systemic immune system could therefore present an opportunity for an autoimmune response to brain to occur after stroke. In this study, we assessed the immune response to myelin basic protein (MBP) in animals subjected to middle cerebral artery occlusion (MCAO). Some animals received an intraperitoneal injection of lipopolysaccharide (LPS; 1 mg/kg) at reperfusion to stimulate a systemic inflammatory response. At 1 month after MCAO, animals exposed to LPS were more likely to be sensitized to MBP (66.7% versus 22.2%; P=0.007) and had more profound and persistent neurologic deficits than non-LPS-treated animals. Exposure to LPS was associated with increased expression of the costimulatory molecule B7.1 early after stroke onset (P=0.009) and increased brain atrophy 1 month after MCAO (P=0.03). These data suggest that animals subjected to a systemic inflammatory insult at the time of stroke are predisposed to develop an autoimmune response to brain, and that this response is associated with worse outcome. These data may partially explain why patients who become infected after stroke experience increased morbidity.
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PMID:Sensitization to brain antigens after stroke is augmented by lipopolysaccharide. 1593 Nov 60

Cerebral small-vessel disease is common in older people and may contribute to the development of dementia. The objective of the present study was to evaluate the relationship between measures of cerebral small-vessel disease on MRI and the rate of decline in specific cognitive domains in participants from the prospective, population-based Rotterdam Scan Study. Participants were 60-90 years of age and free from dementia at baseline in 1995-1996. White matter lesions (WML), cerebral infarcts and generalized brain atrophy were assessed on the baseline MRI. We performed neuropsychological testing at baseline and repeatedly in 1999-2000 and in 2001-2003. We used random-effects models for repeated measures to examine the association between quantitative MRI measures and rate of decline in measures of global cognitive function, information processing speed, executive function and memory. There were a total of 2266 assessments for the 832 participants in the study, with an average time from the initial to last assessment of 5.2 years. Increasing severity of periventricular WML and generalized brain atrophy and the presence of brain infarcts on MRI were associated with a steeper decline in cognitive function. These structural brain changes were specifically associated with decline in information processing speed and executive function. The associations between MRI measures of cerebral small-vessel disease and cognitive decline did not change after additional adjustment for vascular risk factors or depressed mood. After exclusion of participants with an incident stroke, some of the associations of periventricular WML, brain infarcts and generalized brain atrophy with measures of information processing speed and executive function were no longer significant. This may indicate that stroke plays an intermediate role in the relationship between cerebral small-vessel disease and cognitive decline. Our results suggest that in older people cerebral small-vessel disease may contribute to cognitive decline by affecting information processing speed and executive function.
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PMID:Cerebral small-vessel disease and decline in information processing speed, executive function and memory. 1594 59

Risk of dementia increases after stroke, and poststroke dementia (PSD) is an important cause of disability in the elderly. The prevalence rates of PSD vary from 12.2% to 31.8% within 3 months to 1 year after stroke, depending on patient populations and the diagnostic criteria used in the numerous studies. Incidence rates of PSD increase with time after the stroke. Although vascular lesions and white matter changes can explain the cognitive disorders seen in stroke patients, an underlying neurodegenerative disorder may contribute to the development of PSD. Cognitive decline may pre-date the stroke and follow a progressive course after the stroke. The vascular and degenerative processes involved share common environmental and genetic risk factors. This review explains the mechanisms of dementia in stroke patients and identifies predictive factors for PSD. The following points are successively considered: (i) demographic characteristics of the patients, including age and level of education; (ii) prestroke cognitive decline; (iii) vascular risk factors, including diabetes mellitus and prior strokes; (iv) stroke characteristics, including severity and location of the vascular lesion; (v) co-morbid disorders; and (vi) abnormalities on brain imaging, including location, size and number of vascular lesions, white matter changes and cerebral atrophy. Older age, prestroke cognitive decline, stroke recurrence, hypoxic-ischaemic disorders, left-side infarcts, strategic infarcts and white matter lesions appear to be the main predictive factors of PSD. Prevention of stroke should reduce the morbidity and mortality associated with PSD. In addition, management of PSD with secondary prevention treatments could reduce occurrence of further strokes. Cholinesterase inhibitors may be beneficial not only in Alzheimer's disease associated with cerebrovascular lesions, but also for the treatment of cholinergic dysfunction arising from pure vascular dementia. Better knowledge of the risk factors for PSD, including environmental and genetic factors, should increase the effectiveness of preventive strategies in patients with this condition.
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PMID:Poststroke dementia in the elderly. 1597 39

Understanding the determinants of prestroke cognitive impairment (PCI) in stroke associated with small vessel disease (SVD) may shed light on how to prevent further cognitive deterioration after stroke. We administered the Informant Questionnaire on Cognitive Decline (IQCODE) to close informants of 78 consecutive stroke patients who had SVD. PCI, as defined by an average score of IQCODE > or =3.4 was found in 19 (24%) patients. Regression analyses were performed on the following risk factors for PCI: age, years of education, gender, previous stroke, volume of white matter changes, measures of silent lacunes, cerebral atrophy index, medial temporal lobe atrophy and frontal lobe atrophy. Multivariate regression analyses revealed that only cerebral atrophy index (OR 1.5, CI 1.2-1.9, p < 0.001) predicted PCI among patients with SVD.
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PMID:Determinants of prestroke cognitive impairment in stroke associated with small vessel disease. 1608 38

Abnormal gait in high-functioning older adults may indicate underlying subtle structural brain abnormalities. We tested the hypothesis that temporal and spatial parameters of gait, including speed, stride length and double support time, are cross-sectionally associated with white matter hyperintensity, subcortical infarcts or brain atrophy on brain MRI. We examined 321 men and women (mean age = 78.3) participating to the Cardiovascular Health Study who were free of dementia or stroke at the time of the gait assessment. Analyses were set with gait as independent variable and brain MRIs as dependent variables. Gait measures were determined from the footfalls recorded on a 4-meter-long instrumented walking surface, the GaitMat II. Brain MRIs were examined for the presence of white matter hyperintensity (WMG, graded from 0 to 9), brain infarcts (predominantly subcortical) and ventricular enlargement (graded from 0 to 9). Slower gait, shorter stride length and longer double support times were associated with greater prevalence of white matter grade > or =3 (p = 0.02), and at least 1 brain infarct (p = 0.04) independent of age. In multivariate logistic regression models adjusted for demographics and clinical cardiovascular diseases, those with gait speed <1.02 m/s were more likely to have WMG > or =3 and at least 1 brain infarct, compared with those with faster gait - odds ratio (OR): 2.85, 95% confidence interval (95% CI): 1.35, 6.02, and OR: 2.09, 95% CI: 1.04, 4.19. Shorter stride length was also associated with greater probability of having at least 1 brain infarct (gait stride <0.88 vs. >1.10 m: OR: 3.20, 95% CI: 1.49, 6.88), while longer double support times were associated with a greater probability of having WMG > or =3 (double support time >0.19 vs. <0.14 s: OR: 2.3, 95% CI: 1.1, 4.7) independent of demographics and clinical cardiovascular diseases. Gait parameters were not significantly associated with ventricular grade. In summary, in this group of high-functioning older adults, poorer gait speed, shorter stride and longer double support time are associated with high white matter disease and subclinical strokes.
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PMID:Quantitative measures of gait characteristics indicate prevalence of underlying subclinical structural brain abnormalities in high-functioning older adults. 1625 54

The association between stroke and dementia is frequent. The prevalence of poststroke dementia (PSD) ranges from 6 to 32%, depending on the population studied, the criteria used for the diagnosis of dementia, and the time interval between the stroke and the neuropsychological assessment. The risk of PSD is high immediately after stroke and remains higher than in controls in stroke patients nondemented 3 months after stroke. Not all cases of PSD are vascular in origin, with about one third of demented patients diagnosed as having Alzheimer's disease plus stroke. The pathophysiology of PSD is probably multifactorial, with an influence of vascular lesions, associated Alzheimer's lesions and white matter changes. The risk of dementia is higher in older patients and in patients with preexisting cognitive decline - no dementia, severe stroke, a history of stroke, white matter changes and cerebral atrophy. The influence of stroke location, vascular risk factors and silent infarcts remains to be determined. PSD adversely influences the outcome in stroke patients.
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PMID:Poststroke dementia. 1664 68

The objective of this study was to examine the prevalence and clinical correlates of poststroke cognitive impairment in Chinese stroke patients in Hong Kong. One hundred seventy-nine stroke patients were interviewed by a psychiatrist 3 months after their stroke. Cognitive impairment was determined according to the Mini-Mental State Examination score. Thirty-nine participants (21.8%) had cognitive impairment. Univariate analysis found that cognitive impairment was associated with age, female sex, level of education, previous stroke, prestroke Rankin score, National Institutes of Health Stroke Scale dysarthria and total scores, urinary incontinence, and cerebral atrophy index. Multivariate logistic regression suggested that female sex, education, National Institutes of Health Stroke Scale dysarthria score, urinary incontinence, and atrial fibrillation were independent risk factors of poststroke cognitive impairment. After removal of 54 patients with previous stroke from the sample, the frequency of cognitive impairment decreased to 18.4%. It was concluded that cognitive impairment is common among nondemented Chinese stroke patients in Hong Kong.
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PMID:Frequency and clinical determinants of poststroke cognitive impairment in nondemented stroke patients. 1669 Sep 90

A male residual schizophrenic out-patient of 65 years old had presented "heat stroke" and died in progressive course of 7 months. His mental condition had been stable and he had kept good drug compliance. In some summer day, he presented high fever and confusion, followed by convulsion. He showed over 40 degrees C high temperature (max 42 degrees C) for about 6 hours. After 10 day's high serum CPK, he gradually presented severe muscle atrophy (proximal dominant), flaccid quadriplegia and brain atrophy (especially in cerebellum). He died from pneumonia. His brain weight was 1,350g. Neuropathological study showed severe loss of Purkinje cell with gliosis. Neurons in dentate nucleus ware entirely lost and a great amount of fatty macrophages were present around the dentate nucleus. Fatty macrophages were observed from cerebellum to red nucleus through superior cerebellar peduncle. These findings have been known as findings of heat stroke. Addition to these findings, this case presented a neuronal loss in the substantita nigra and in the anterior horn of spinal cord and the degeneration of bilateral pyramidal tract. These findings have not been thus far reported, so this case is thought to be the valuable case on considering the variation of neuropathology of "heat stroke".
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PMID:[An autopsied case of schizophrenic patient who died from heat stroke]. 1678 54

Stroke is an important risk factor for dementia, but the exact mechanisms involved in cognitive decline remain unclear. In this study, we related baseline MRI brain measures with later cognitive decline. Seventy-nine stroke survivors aged 75+ years without dementia were recruited 3-month post-stroke. They underwent yearly neuropsychological assessments and had an MRI at baseline and 2 years. Medial temporal lobe atrophy (MTA) was scored and volume of white matter hyperintensities (WMH) was measured at baseline. The rate of ventricular enlargement was measured by comparing the baseline and repeat images. Linear regression indicated that memory loss was related to both baseline memory and MTA (p=0.001; standardized regression coefficient beta=-0.35) but not WMH volume. The only independent predictor of ventricular enlargement was MTA (p=0.003; beta=0.47). However, no baseline MRI variable differed between those who did (18%) and did not (82%) develop dementia. The association of MTA but not WMH with subsequent cognitive decline and increasing brain atrophy suggests a greater role for Alzheimer type than vascular pathology in delayed cognitive impairment after stroke.
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PMID:Medial temporal atrophy rather than white matter hyperintensities predict cognitive decline in stroke survivors. 1693 70

Patients with end-stage renal disease (ESRD) undergoing hemodialysis are known to suffer cognitive deficits and stroke of unknown etiology. It has been suspected that the treatment itself may contribute to the syndrome by unknown mechanisms, which we investigated in this study. End-stage renal disease patients on hemodialysis (n=19) or peritoneal dialysis (PD, n=5) were compared with 14 healthy controls. Subjects participated in magnetic resonance imaging (MRI) measurements of cerebral atrophy, cerebral blood flow (CBF) arterial spin labeled-MRI (ASL-MRI), quantitative Doppler blood flow through the internal carotid artery, and cerebral oxymetry. The Doppler and oxymetry procedures were also performed at the beginning and end of a single hemodialysis session. End-stage renal disease patients on hemodialysis showed significant cerebral atrophy, associated with longer hemodialysis duration and cognitive deficits, including focal bilateral lesions in the caudate nucleus and midbrain. Cerebral oxygenation was extremely low before dialysis (rSO(2) 41+/-13, compared with 70+/-2 in controls, P<0.02) and improved only slightly after dialysis. Carotid blood flow was also very low at the start of dialysis (115+/-28 mL/sec, versus 193+/-56 in controls, P<0.005) but normalized at the end of the session (181 mL/sec). The PD patients showed intermediate values, between the hemodialysis and controls. Notably, duration of hemodialysis treatment predicted global gray-matter volume (r=-0.74), change of blood flow during dialysis (r=-0.65), and baseline rSO(2) (r=-0.65). The findings suggest that ESRD patients on hemodialysis suffer low CBF during the interdialytic cycle. Coupled with low cerebral oxygenation levels and atherosclerosis, this may contribute significantly to the etiology of the observed cerebral atrophy, cognitive deficits, and high stroke prevalence.
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PMID:Cerebrovascular effects of hemodialysis in chronic kidney disease. 1740 58


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