Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000024432.34557.10
J. Meyer, Gelin Xu, J. Thornby, M. Chowdhury, Minh Quach
Background and Purpose Individuals with mild cognitive impairment (MCI) are at increased risk of Alzheimer’s disease (AD) and probably other forms of dementia. Some subtypes of vascular dementia (VaD) may possess minor neuropathological changes of AD that may contribute to cognitive impairments. It was posited that MCI, identified by criteria described here, might present as a prodrome for VaD and AD. Methods— Serial Mini-Mental State Examination was administered at 3- to 6-month intervals, and neuroimaging was performed annually. Subtle cognitive dysfunctions were weighted and measured according to MCI criteria defined here. Subjects identified with MCI were then followed up for an additional 3.88±3.01 years. Diagnoses of VaD and AD were made according to established criteria. Results— During 3.72±2.94 years of follow-up of the original normative subjects, 73 of 291 (25.1%) developed MCI. Of the 27 subjects who developed VaD, 15 (55.6%) had prodromal MCI. Of these, two thirds were subclassified as having small-vessel dementia. The remaining 12 patients with VaD (44.4%) were diagnosed directly from a cognitively normal status without preceding MCI. These were predominantly multi-infarct or strategic-infarct dementia (66.7%). An additional 35 MCI subjects (47.9%) developed AD. Both VaD and AD diagnosed after MCI prodromes manifested similar spectral domains of cognitive impairments, which included memory, during their MCI stages. Conclusions— In some VaD subtypes, particularly those caused by subcortical microvascular disease, dementia may be preceded by MCI, which has similar domains of cognitive impairment and a similar progressive course that may mimic AD.
{"title":"Is Mild Cognitive Impairment Prodromal for Vascular Dementia Like Alzheimer’s Disease?","authors":"J. Meyer, Gelin Xu, J. Thornby, M. Chowdhury, Minh Quach","doi":"10.1161/01.STR.0000024432.34557.10","DOIUrl":"https://doi.org/10.1161/01.STR.0000024432.34557.10","url":null,"abstract":"Background and Purpose Individuals with mild cognitive impairment (MCI) are at increased risk of Alzheimer’s disease (AD) and probably other forms of dementia. Some subtypes of vascular dementia (VaD) may possess minor neuropathological changes of AD that may contribute to cognitive impairments. It was posited that MCI, identified by criteria described here, might present as a prodrome for VaD and AD. Methods— Serial Mini-Mental State Examination was administered at 3- to 6-month intervals, and neuroimaging was performed annually. Subtle cognitive dysfunctions were weighted and measured according to MCI criteria defined here. Subjects identified with MCI were then followed up for an additional 3.88±3.01 years. Diagnoses of VaD and AD were made according to established criteria. Results— During 3.72±2.94 years of follow-up of the original normative subjects, 73 of 291 (25.1%) developed MCI. Of the 27 subjects who developed VaD, 15 (55.6%) had prodromal MCI. Of these, two thirds were subclassified as having small-vessel dementia. The remaining 12 patients with VaD (44.4%) were diagnosed directly from a cognitively normal status without preceding MCI. These were predominantly multi-infarct or strategic-infarct dementia (66.7%). An additional 35 MCI subjects (47.9%) developed AD. Both VaD and AD diagnosed after MCI prodromes manifested similar spectral domains of cognitive impairments, which included memory, during their MCI stages. Conclusions— In some VaD subtypes, particularly those caused by subcortical microvascular disease, dementia may be preceded by MCI, which has similar domains of cognitive impairment and a similar progressive course that may mimic AD.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"10 1","pages":"1981-1985"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82624621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000023579.61630.AC
M. Wintermark, M. Reichhart, O. Cuisenaire, P. Maeder, J. Thiran, P. Schnyder, J. Bogousslavsky, R. Meuli
Background and Purpose— Besides classic criteria, cerebral perfusion imaging could improve patient selection for thrombolytic therapy. The purpose of this study was to compare quantitative perfusion CT imaging and qualitative diffusion- and perfusion-weighted MRI (DWI and PWI) in acute stroke patients at the time of their emergency evaluation. Methods— Thirteen acute stroke patients underwent perfusion CT and DWI or PWI on admission. The size of infarct and ischemic lesion (infarct plus penumbra) on the admission perfusion CT was compared with that of the MR abnormalities as shown on the DWI trace and on the relative cerebral blood volume, cerebral blood flow, time to peak, and mean transit time maps calculated from PWI studies. Results— The most significant correlation was found between infarct size on the admission perfusion CT and abnormality size on the admission DWI map (r =0.968, P <0.001). A significant correlation was also observed between the size of the ischemic lesion (infarct plus penumbra) on the admission perfusion CT and the abnormality size on the mean transit time map calculated from admission PWI (r =0.946, P <0.001). Information about cerebral infarct and total ischemia (infarct plus penumbra) carried by both imaging techniques was similar, with slopes of 0.913 and 0.905, respectively. Conclusions— An imaging technique may be helpful in the identification of cerebral penumbra in acute stroke patients and thus in the selection of patients for thrombolytic therapy. Perfusion CT and DWI/PWI are equivalent in this task.
背景与目的-除了经典标准外，脑灌注成像还可以改善患者对溶栓治疗的选择。本研究的目的是比较急性脑卒中患者在紧急评估时的定量灌注CT成像和定性扩散和灌注加权MRI (DWI和PWI)。方法:13例急性脑卒中患者入院时行灌注CT及DWI或PWI检查。将入院灌注CT上梗死灶和缺血性病变(梗死灶加半暗带)的大小与DWI示迹的MR异常以及PWI研究计算的相对脑血容量、脑血流量、峰值时间和平均传递时间图进行比较。结果:入院灌注CT上的梗死面积与入院DWI图上的异常面积相关性最显著(r =0.968, P <0.001)。入院灌注CT上的缺血性病变(梗死+半暗带)大小与入院PWI计算的平均过境时间图上的异常大小也有显著相关性(r =0.946, P <0.001)。两种成像技术所显示的脑梗死和全缺血(梗死加半暗区)信息相似，斜率分别为0.913和0.905。结论:一种成像技术可能有助于识别急性脑卒中患者的大脑半暗区，从而选择患者进行溶栓治疗。灌注CT与DWI/PWI在此任务中是等效的。
{"title":"Comparison of Admission Perfusion Computed Tomography and Qualitative Diffusion- and Perfusion-Weighted Magnetic Resonance Imaging in Acute Stroke Patients","authors":"M. Wintermark, M. Reichhart, O. Cuisenaire, P. Maeder, J. Thiran, P. Schnyder, J. Bogousslavsky, R. Meuli","doi":"10.1161/01.STR.0000023579.61630.AC","DOIUrl":"https://doi.org/10.1161/01.STR.0000023579.61630.AC","url":null,"abstract":"Background and Purpose— Besides classic criteria, cerebral perfusion imaging could improve patient selection for thrombolytic therapy. The purpose of this study was to compare quantitative perfusion CT imaging and qualitative diffusion- and perfusion-weighted MRI (DWI and PWI) in acute stroke patients at the time of their emergency evaluation. Methods— Thirteen acute stroke patients underwent perfusion CT and DWI or PWI on admission. The size of infarct and ischemic lesion (infarct plus penumbra) on the admission perfusion CT was compared with that of the MR abnormalities as shown on the DWI trace and on the relative cerebral blood volume, cerebral blood flow, time to peak, and mean transit time maps calculated from PWI studies. Results— The most significant correlation was found between infarct size on the admission perfusion CT and abnormality size on the admission DWI map (r =0.968, P <0.001). A significant correlation was also observed between the size of the ischemic lesion (infarct plus penumbra) on the admission perfusion CT and the abnormality size on the mean transit time map calculated from admission PWI (r =0.946, P <0.001). Information about cerebral infarct and total ischemia (infarct plus penumbra) carried by both imaging techniques was similar, with slopes of 0.913 and 0.905, respectively. Conclusions— An imaging technique may be helpful in the identification of cerebral penumbra in acute stroke patients and thus in the selection of patients for thrombolytic therapy. Perfusion CT and DWI/PWI are equivalent in this task.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"373 1","pages":"2025-2031"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74224823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000024433.36590.1B
J. Ingles, C. Wentzel, J. Fisk, K. Rockwood
Background— Vascular cognitive impairment that does not fulfill dementia criteria (ie, vascular cognitive impairment, no dementia [CIND]) is common. Although progression to dementia is frequent, little is known about factors that predict progression. We examined whether performance on neuropsychological tests administered at baseline could predict incident cases of dementia in patients with vascular CIND after 5 years. Summary of Report— The Canadian Study of Health and Aging is a prospective, cohort study of 10 263 randomly selected persons aged ≥65 years. Of 149 people diagnosed with vascular CIND, 125 completed a battery of neuropsychological tests at baseline. Follow-up cognitive diagnoses were available for 102 individuals. After 5 years, 45 patients (44%) developed dementia. Low baseline scores on tests of memory and category fluency were associated with incident dementia. Conclusions— Neuropsychological measures can indicate risk of dementia in patients with vascular CIND. This study did not suggest a prediction-to-progression profile distinct from that seen in Alzheimer disease.
{"title":"Neuropsychological Predictors of Incident Dementia in Patients With Vascular Cognitive Impairment, Without Dementia","authors":"J. Ingles, C. Wentzel, J. Fisk, K. Rockwood","doi":"10.1161/01.STR.0000024433.36590.1B","DOIUrl":"https://doi.org/10.1161/01.STR.0000024433.36590.1B","url":null,"abstract":"Background— Vascular cognitive impairment that does not fulfill dementia criteria (ie, vascular cognitive impairment, no dementia [CIND]) is common. Although progression to dementia is frequent, little is known about factors that predict progression. We examined whether performance on neuropsychological tests administered at baseline could predict incident cases of dementia in patients with vascular CIND after 5 years. Summary of Report— The Canadian Study of Health and Aging is a prospective, cohort study of 10 263 randomly selected persons aged ≥65 years. Of 149 people diagnosed with vascular CIND, 125 completed a battery of neuropsychological tests at baseline. Follow-up cognitive diagnoses were available for 102 individuals. After 5 years, 45 patients (44%) developed dementia. Low baseline scores on tests of memory and category fluency were associated with incident dementia. Conclusions— Neuropsychological measures can indicate risk of dementia in patients with vascular CIND. This study did not suggest a prediction-to-progression profile distinct from that seen in Alzheimer disease.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"3 1","pages":"1999-2002"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90046770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000024523.82311.77
O. Suter, Thanomphone Sunthorn, R. Kraftsik, J. Straubel, P. Darekar, K. Khalili, J. Miklossy
Background and Purpose— The watershed cortical areas are the first to be deprived of sufficient blood flow in the event of cerebral hypoperfusion and will be the sites of watershed microinfarcts. Cerebral hypoperfusion is associated with Alzheimer disease (AD), but information regarding the occurrence of watershed cortical infarcts in AD is lacking. Methods— Brains of 184 autopsy cases (105 definite AD cases and 79 age-matched controls) were selected and analyzed by histochemical and immunohistochemical techniques. The 3-dimensional reconstruction of the whole cerebrum, with 3-mm spaced serial sections, was performed in 6 AD cases to study the intrahemispheric and interhemispheric distribution of the cortical microinfarcts. Results— A significant association (P =0.001) was found between the occurrence of watershed cortical infarcts and AD (32.4% versus 2.5% in controls). The microinfarcts were restricted to the watershed cortical zones. Congophilic angiopathy was revealed to be an important risk factor. Perturbed hemodynamic factors (eg, decreased blood pressure) may play a role in the genesis of cortical watershed microinfarcts. Conclusions— In AD, cerebral hypoperfusion induces not only white matter changes but cortical watershed microinfarcts as well, further aggravating the degenerative process and worsening dementia. To prevent the formation of watershed cortical microinfarcts in AD, monitoring blood pressure and treating arterial hypotension are essential.
{"title":"Cerebral Hypoperfusion Generates Cortical Watershed Microinfarcts in Alzheimer Disease","authors":"O. Suter, Thanomphone Sunthorn, R. Kraftsik, J. Straubel, P. Darekar, K. Khalili, J. Miklossy","doi":"10.1161/01.STR.0000024523.82311.77","DOIUrl":"https://doi.org/10.1161/01.STR.0000024523.82311.77","url":null,"abstract":"Background and Purpose— The watershed cortical areas are the first to be deprived of sufficient blood flow in the event of cerebral hypoperfusion and will be the sites of watershed microinfarcts. Cerebral hypoperfusion is associated with Alzheimer disease (AD), but information regarding the occurrence of watershed cortical infarcts in AD is lacking. Methods— Brains of 184 autopsy cases (105 definite AD cases and 79 age-matched controls) were selected and analyzed by histochemical and immunohistochemical techniques. The 3-dimensional reconstruction of the whole cerebrum, with 3-mm spaced serial sections, was performed in 6 AD cases to study the intrahemispheric and interhemispheric distribution of the cortical microinfarcts. Results— A significant association (P =0.001) was found between the occurrence of watershed cortical infarcts and AD (32.4% versus 2.5% in controls). The microinfarcts were restricted to the watershed cortical zones. Congophilic angiopathy was revealed to be an important risk factor. Perturbed hemodynamic factors (eg, decreased blood pressure) may play a role in the genesis of cortical watershed microinfarcts. Conclusions— In AD, cerebral hypoperfusion induces not only white matter changes but cortical watershed microinfarcts as well, further aggravating the degenerative process and worsening dementia. To prevent the formation of watershed cortical microinfarcts in AD, monitoring blood pressure and treating arterial hypotension are essential.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"9 4","pages":"1986-1992"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91491943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000017285.73172.91
R. Barba, M. Morin, C. Cemillán, C. Delgado, J. Domingo, T. del Ser
Background and Purpose— We sought to determine whether previous or incident dementia increases the risk of mortality after stroke. Methods— We assessed clinical, functional, and cognitive status in 324 consecutive stroke patients who were followed up for 24 months. Prestroke dementia was diagnosed at admission (Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria) and poststroke dementia 3 months after stroke (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria). The proportion of patients surviving in the groups with and without dementia and the relative risk of mortality were calculated with Kaplan-Meier and with Cox proportional hazards analyses, respectively, for prestroke, stroke-related, and poststroke dementia. Results— Forty-nine patients (15.1% of the total sample) were found to have prestroke dementia. Three months after stroke, 75 cases had poststroke dementia: 50 incident cases (20% of 251 reexamined cases) with stroke-related dementia and 25 already demented before the stroke. After a mean follow-up of 16.1±9.9 months, the proportion of survivors was 20.4% in patients with and 72.6% in those without prestroke dementia. After a mean follow-up of 22.1±6.7 months, the proportion of survivors was 58.3% in patients with and 95.4% in those without stroke-related dementia. Using multivariate analysis and adjusting for age, sex, hypertension, diabetes, previous stroke, heart disease, and severity and recurrence of stroke, we found the relative risk of mortality associated with prestroke dementia to be 2.1 (95% CI, 1.2 to 3.6), with stroke-related dementia 6.3 (95% CI, 2.3 to 17.3), and with poststroke d ementia 8.5 (95% CI, 3.4 to 20.9). Conclusions— Both previous dementia and incident dementia adversely influence long-term survival after stroke, even after adjustment for other predictors of stroke mortality.
{"title":"Previous and Incident Dementia as Risk Factors for Mortality in Stroke Patients","authors":"R. Barba, M. Morin, C. Cemillán, C. Delgado, J. Domingo, T. del Ser","doi":"10.1161/01.STR.0000017285.73172.91","DOIUrl":"https://doi.org/10.1161/01.STR.0000017285.73172.91","url":null,"abstract":"Background and Purpose— We sought to determine whether previous or incident dementia increases the risk of mortality after stroke. Methods— We assessed clinical, functional, and cognitive status in 324 consecutive stroke patients who were followed up for 24 months. Prestroke dementia was diagnosed at admission (Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria) and poststroke dementia 3 months after stroke (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria). The proportion of patients surviving in the groups with and without dementia and the relative risk of mortality were calculated with Kaplan-Meier and with Cox proportional hazards analyses, respectively, for prestroke, stroke-related, and poststroke dementia. Results— Forty-nine patients (15.1% of the total sample) were found to have prestroke dementia. Three months after stroke, 75 cases had poststroke dementia: 50 incident cases (20% of 251 reexamined cases) with stroke-related dementia and 25 already demented before the stroke. After a mean follow-up of 16.1±9.9 months, the proportion of survivors was 20.4% in patients with and 72.6% in those without prestroke dementia. After a mean follow-up of 22.1±6.7 months, the proportion of survivors was 58.3% in patients with and 95.4% in those without stroke-related dementia. Using multivariate analysis and adjusting for age, sex, hypertension, diabetes, previous stroke, heart disease, and severity and recurrence of stroke, we found the relative risk of mortality associated with prestroke dementia to be 2.1 (95% CI, 1.2 to 3.6), with stroke-related dementia 6.3 (95% CI, 2.3 to 17.3), and with poststroke d ementia 8.5 (95% CI, 3.4 to 20.9). Conclusions— Both previous dementia and incident dementia adversely influence long-term survival after stroke, even after adjustment for other predictors of stroke mortality.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"12 1","pages":"1993-1998"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89129773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000021902.33129.69
C. Frijns, L. Kappelle
Background— In this review we discuss the role of inflammatory cell adhesion molecules (CAMs) in ischemic stroke and in delayed cerebral ischemia after subarachnoid hemorrhage. Vascular endothelial cells and leukocytes express several inflammatory adhesion receptors, the most important of which are the selectins, immunoglobulin gene superfamily CAMs, and &bgr;2 integrins. They mediate the transmigration process of leukocytes to the abluminal side of the endothelium. Summary of Review— There is ample evidence from animal models of middle cerebral artery occlusion that expression of CAMs is associated with cerebral infarct size. Absence of CAMs in knockout animals resulted in reduced infarct size. When middle cerebral artery occlusion in experimental stroke was followed by reperfusion, administration of anti-CAM antibodies decreased infarct size. Thus far, anti-CAM treatment has not been successful in patients with ischemic stroke. Inflammatory CAM may also play a role in the pathogenesis of delayed cerebral ischemia after subarachnoid hemorrhage. In animal models, increased expression of CAMs has been observed in vasospastic arteries. Increased concentrations of CAMs have also been found in cerebrospinal fluid of patients with subarachnoid hemorrhage. Conclusions— Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies.
{"title":"Inflammatory Cell Adhesion Molecules in Ischemic Cerebrovascular Disease","authors":"C. Frijns, L. Kappelle","doi":"10.1161/01.STR.0000021902.33129.69","DOIUrl":"https://doi.org/10.1161/01.STR.0000021902.33129.69","url":null,"abstract":"Background— In this review we discuss the role of inflammatory cell adhesion molecules (CAMs) in ischemic stroke and in delayed cerebral ischemia after subarachnoid hemorrhage. Vascular endothelial cells and leukocytes express several inflammatory adhesion receptors, the most important of which are the selectins, immunoglobulin gene superfamily CAMs, and &bgr;2 integrins. They mediate the transmigration process of leukocytes to the abluminal side of the endothelium. Summary of Review— There is ample evidence from animal models of middle cerebral artery occlusion that expression of CAMs is associated with cerebral infarct size. Absence of CAMs in knockout animals resulted in reduced infarct size. When middle cerebral artery occlusion in experimental stroke was followed by reperfusion, administration of anti-CAM antibodies decreased infarct size. Thus far, anti-CAM treatment has not been successful in patients with ischemic stroke. Inflammatory CAM may also play a role in the pathogenesis of delayed cerebral ischemia after subarachnoid hemorrhage. In animal models, increased expression of CAMs has been observed in vasospastic arteries. Increased concentrations of CAMs have also been found in cerebrospinal fluid of patients with subarachnoid hemorrhage. Conclusions— Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"33 1","pages":"2115-2122"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81375607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000023445.20454.A8
D. Anderson, L. Kappelle, M. Eliasziw, V. Babikian, L. Pearce, H. Barnett
Background and Purpose— The goal of this study was to examine the hypotheses that retinal ischemia is caused more often by carotid atherosclerosis than by atrial fibrillation and that the odds of retinal events compared with hemispheric events increase with worsening carotid stenosis. Methods— We used data from the Stroke Prevention in Atrial Fibrillation (SPAF) I through III trials and North American Symptomatic Carotid Endarterectomy Trial (NASCET), calculating hemispheric:retinal (H:R) odds for the territory of ischemic events during follow-up in patients with atrial fibrillation and medically treated 50% to 99% carotid stenosis or occlusion in the respective trials. Results— The H:R odds were 25:1 in the SPAF aspirin-assigned patients and 2:1 for NASCET vessels. In NASCET patients, the H:R odds of recurrent ischemic events were 1:4 for vessels randomized initially for retinal symptoms compared with 6:1 for those randomized for hemispheric events (significant difference;P <0.001). Moreover, the H:R odds of first events in the territory of the contralateral asymptomatic artery were 1:1 if the randomized vessel had retinal symptoms compared with 4:1 if the randomized vessel had hemispheric symptoms (significant difference;P <0.01). Increasing carotid stenosis in the 50% to 99% range had no effect on H:R odds (P =0.8). Conclusions— These findings confirm that retinal symptoms are more typical of carotid stenosis. Hemodynamic effects do not appear to be more important in the pathogenesis of retinal events than hemispheric ones in carotid stenosis. The retinal versus hemispheric location of initial symptoms is strongly predictive of the location of subsequent events in patients with carotid stenosis, even when new symptoms are contralateral to the original ones.
{"title":"Occurrence of Hemispheric and Retinal Ischemia in Atrial Fibrillation Compared With Carotid Stenosis","authors":"D. Anderson, L. Kappelle, M. Eliasziw, V. Babikian, L. Pearce, H. Barnett","doi":"10.1161/01.STR.0000023445.20454.A8","DOIUrl":"https://doi.org/10.1161/01.STR.0000023445.20454.A8","url":null,"abstract":"Background and Purpose— The goal of this study was to examine the hypotheses that retinal ischemia is caused more often by carotid atherosclerosis than by atrial fibrillation and that the odds of retinal events compared with hemispheric events increase with worsening carotid stenosis. Methods— We used data from the Stroke Prevention in Atrial Fibrillation (SPAF) I through III trials and North American Symptomatic Carotid Endarterectomy Trial (NASCET), calculating hemispheric:retinal (H:R) odds for the territory of ischemic events during follow-up in patients with atrial fibrillation and medically treated 50% to 99% carotid stenosis or occlusion in the respective trials. Results— The H:R odds were 25:1 in the SPAF aspirin-assigned patients and 2:1 for NASCET vessels. In NASCET patients, the H:R odds of recurrent ischemic events were 1:4 for vessels randomized initially for retinal symptoms compared with 6:1 for those randomized for hemispheric events (significant difference;P <0.001). Moreover, the H:R odds of first events in the territory of the contralateral asymptomatic artery were 1:1 if the randomized vessel had retinal symptoms compared with 4:1 if the randomized vessel had hemispheric symptoms (significant difference;P <0.01). Increasing carotid stenosis in the 50% to 99% range had no effect on H:R odds (P =0.8). Conclusions— These findings confirm that retinal symptoms are more typical of carotid stenosis. Hemodynamic effects do not appear to be more important in the pathogenesis of retinal events than hemispheric ones in carotid stenosis. The retinal versus hemispheric location of initial symptoms is strongly predictive of the location of subsequent events in patients with carotid stenosis, even when new symptoms are contralateral to the original ones.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"21 1","pages":"1963-1968"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85294108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000021903.52901.97
H. Kato, M. Izumiyama, H. Koizumi, A. Takahashi, Y. Itoyama
Background and Purpose— Motor functional recovery from stroke can occur, but the mechanisms underlying this restorative process remain to be elucidated. We used near-infrared spectroscopic (NIRS) topography in comparison with functional MRI (fMRI) to evaluate the compensatory motor activation of cortical regions in patients who recovered from hemiparesis after cortical cerebral infarction. Methods— We examined 6 right-handed patients who suffered cerebral infarction of the middle cerebral artery territory with minimal or mild residual contralateral hemiparesis (4 men and 2 women, 59 to 79 years old, all had left hemiparesis). Both fMRI and NIRS were studied during a hand movement task at chronic stages. Five right-handed, normal subjects (3 men and 2 women, 44 to 81 years old) served as controls. Results— fMRI and NIRS detected very similar cerebral cortical activation, although NIRS detected only superficial activation. The spatial resolution of NIRS was less than that of fMRI, but NIRS provided a dynamic profile of activation. Normal subjects activated predominantly the contralateral primary sensorimotor cortex and supplementary motor areas during each hand movement. All the stroke patients exhibited the normal activation pattern during normal hand movement. On affected hand movement, the stroke patients showed extended activation not only in the contralateral motor cortex but also in the ipsilateral motor cortex (primary motor cortex and supplementary motor areas). Conclusions— Both fMRI and NIRS studies provided evidence for the contribution of ipsilateral motor cortical compensation or reorganization to the recovery from poststroke hemiparesis. The result demonstrated that NIRS was a unique tool to monitor poststroke alterations in cortical motor functions.
{"title":"Near-Infrared Spectroscopic Topography as a Tool to Monitor Motor Reorganization After Hemiparetic Stroke: A Comparison With Functional MRI","authors":"H. Kato, M. Izumiyama, H. Koizumi, A. Takahashi, Y. Itoyama","doi":"10.1161/01.STR.0000021903.52901.97","DOIUrl":"https://doi.org/10.1161/01.STR.0000021903.52901.97","url":null,"abstract":"Background and Purpose— Motor functional recovery from stroke can occur, but the mechanisms underlying this restorative process remain to be elucidated. We used near-infrared spectroscopic (NIRS) topography in comparison with functional MRI (fMRI) to evaluate the compensatory motor activation of cortical regions in patients who recovered from hemiparesis after cortical cerebral infarction. Methods— We examined 6 right-handed patients who suffered cerebral infarction of the middle cerebral artery territory with minimal or mild residual contralateral hemiparesis (4 men and 2 women, 59 to 79 years old, all had left hemiparesis). Both fMRI and NIRS were studied during a hand movement task at chronic stages. Five right-handed, normal subjects (3 men and 2 women, 44 to 81 years old) served as controls. Results— fMRI and NIRS detected very similar cerebral cortical activation, although NIRS detected only superficial activation. The spatial resolution of NIRS was less than that of fMRI, but NIRS provided a dynamic profile of activation. Normal subjects activated predominantly the contralateral primary sensorimotor cortex and supplementary motor areas during each hand movement. All the stroke patients exhibited the normal activation pattern during normal hand movement. On affected hand movement, the stroke patients showed extended activation not only in the contralateral motor cortex but also in the ipsilateral motor cortex (primary motor cortex and supplementary motor areas). Conclusions— Both fMRI and NIRS studies provided evidence for the contribution of ipsilateral motor cortical compensation or reorganization to the recovery from poststroke hemiparesis. The result demonstrated that NIRS was a unique tool to monitor poststroke alterations in cortical motor functions.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"177 1","pages":"2032-2036"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76975662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000024110.82735.5A
I. van der Schaaf, Y. Ruigrok, G. Rinkel, A. Algra, J. van Gijn
Background and Purpose— Methods of performing and reporting randomized clinical trials (RCTs) are available, but weaknesses still occur. For observational studies, methodology is less well described, and weaknesses are even more likely. In recent guidelines for patients with subarachnoid hemorrhage (SAH), 25% of treatment recommendations are based on clinical trials. To interpret the results of research on the therapeutic effect of treatment modalities, definition of outcome measures is essential. We assessed quality of study design and outcome measures and presence and precision of definitions concerning major complications of SAH in studies evaluating treatment strategies in patients with aneurysmal SAH. Methods— We retrieved and reviewed all articles on treatment strategies in patients with SAH that fulfilled a prespecified set of criteria and were published during 1990–1999 in 10 general, neurosurgical, or neurological journals. We categorized articles into RCTs, observational studies with a control group, and observational studies without a control group. We assessed study design by means of a prespecified set of methodological criteria. For outcome measures we assessed whether a prespecified outcome measurement was defined and whether any handicap scale was used. For complications after SAH we assessed whether the definition included a description of the clinical features and a technical investigation with criteria for abnormal results. Results— We identified 18 RCTs, 24 observational studies with a control group, and 41 uncontrolled observational studies. Two RCTs, no observational studies with a control group, and 15 observational studies without a control group met all criteria for study design. A primary outcome measure was specified in 67 of the 83 studies and was defined in 59. Any measure of handicap or information on degree of dependence was given in 65 of 83 studies. A complete definition of delayed cerebral ischemia was given in 13 of 66 studies, of rebleeding in 2 of 26 studies, and of hydrocephalus in 2 of 14 studies. Conclusions— Most studies on treatment strategies in SAH suffer from methodological weaknesses. This implies that current management of patients with SAH is based on weak evidence.
{"title":"Study Design and Outcome Measures in Studies on Aneurysmal Subarachnoid Hemorrhage","authors":"I. van der Schaaf, Y. Ruigrok, G. Rinkel, A. Algra, J. van Gijn","doi":"10.1161/01.STR.0000024110.82735.5A","DOIUrl":"https://doi.org/10.1161/01.STR.0000024110.82735.5A","url":null,"abstract":"Background and Purpose— Methods of performing and reporting randomized clinical trials (RCTs) are available, but weaknesses still occur. For observational studies, methodology is less well described, and weaknesses are even more likely. In recent guidelines for patients with subarachnoid hemorrhage (SAH), 25% of treatment recommendations are based on clinical trials. To interpret the results of research on the therapeutic effect of treatment modalities, definition of outcome measures is essential. We assessed quality of study design and outcome measures and presence and precision of definitions concerning major complications of SAH in studies evaluating treatment strategies in patients with aneurysmal SAH. Methods— We retrieved and reviewed all articles on treatment strategies in patients with SAH that fulfilled a prespecified set of criteria and were published during 1990–1999 in 10 general, neurosurgical, or neurological journals. We categorized articles into RCTs, observational studies with a control group, and observational studies without a control group. We assessed study design by means of a prespecified set of methodological criteria. For outcome measures we assessed whether a prespecified outcome measurement was defined and whether any handicap scale was used. For complications after SAH we assessed whether the definition included a description of the clinical features and a technical investigation with criteria for abnormal results. Results— We identified 18 RCTs, 24 observational studies with a control group, and 41 uncontrolled observational studies. Two RCTs, no observational studies with a control group, and 15 observational studies without a control group met all criteria for study design. A primary outcome measure was specified in 67 of the 83 studies and was defined in 59. Any measure of handicap or information on degree of dependence was given in 65 of 83 studies. A complete definition of delayed cerebral ischemia was given in 13 of 66 studies, of rebleeding in 2 of 26 studies, and of hydrocephalus in 2 of 14 studies. Conclusions— Most studies on treatment strategies in SAH suffer from methodological weaknesses. This implies that current management of patients with SAH is based on weak evidence.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"42 1","pages":"2043-2046"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91525423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000023577.65990.4E
M. Selim, J. Fink, Sandeep Kumar, L. Caplan, C. Horkan, Yi Chen, I. Linfante, G. Schlaug
Background and Purpose— Hemorrhagic transformation (HT) is a potentially dangerous complication of thrombolytic therapy. Recent studies suggest that diffusion-weighted MRI (DWI) can help to predict the risk of intracerebral hemorrhage (ICH) after thrombolysis. We sought to examine which pretreatment DWI parameters and clinical data are predictive of ICH after intravenous thrombolysis. Methods— We retrospectively reviewed our prospective stroke database for patients with ischemic stroke treated with intravenous recombinant tissue plasminogen activator (rtPA) within 3 hours from symptom onset who had DWI before treatment and MRI with T2* sequence or CT 24 to 48 hours later to assess for ICH over the past 4 years. We measured the volumes and voxel-by-voxel apparent diffusion coefficient (ADC) values of the initial DWI lesions and retrieved demographic data, risk factors, National Institutes of Health Stroke Scale (NIHSS) scores on admission, and blood tests results. We examined several variables using univariate and multivariate regression analyses to determine predictors of ICH. Results— Twenty-nine patients fulfilled our inclusion criteria; 17 patients (58%) had ICH, and of these 4 (13%) had symptomatic ICH and fatal outcome. On univariate analysis, higher systolic blood pressure, NIHSS score, serum glucose level, volume of initial DWI lesion, and absolute number of voxels with ADC value ≤550×10−6 mm2/s were statistically associated with ICH, and all were subjected to multivariate analysis. However, only the absolute number of voxels, ie, volume of ischemic tissue on DWI, with ADC ≤550×10−6 mm2/s emerged as an independent predictor of ICH. Conclusions— Our findings suggest that volumetric ADC analysis can be used to assess ICH risk after thrombolysis. This may be particularly helpful if rtPA is to be given outside the 3-hour window.
{"title":"Predictors of Hemorrhagic Transformation After Intravenous Recombinant Tissue Plasminogen Activator: Prognostic Value of the Initial Apparent Diffusion Coefficient and Diffusion-Weighted Lesion Volume","authors":"M. Selim, J. Fink, Sandeep Kumar, L. Caplan, C. Horkan, Yi Chen, I. Linfante, G. Schlaug","doi":"10.1161/01.STR.0000023577.65990.4E","DOIUrl":"https://doi.org/10.1161/01.STR.0000023577.65990.4E","url":null,"abstract":"Background and Purpose— Hemorrhagic transformation (HT) is a potentially dangerous complication of thrombolytic therapy. Recent studies suggest that diffusion-weighted MRI (DWI) can help to predict the risk of intracerebral hemorrhage (ICH) after thrombolysis. We sought to examine which pretreatment DWI parameters and clinical data are predictive of ICH after intravenous thrombolysis. Methods— We retrospectively reviewed our prospective stroke database for patients with ischemic stroke treated with intravenous recombinant tissue plasminogen activator (rtPA) within 3 hours from symptom onset who had DWI before treatment and MRI with T2* sequence or CT 24 to 48 hours later to assess for ICH over the past 4 years. We measured the volumes and voxel-by-voxel apparent diffusion coefficient (ADC) values of the initial DWI lesions and retrieved demographic data, risk factors, National Institutes of Health Stroke Scale (NIHSS) scores on admission, and blood tests results. We examined several variables using univariate and multivariate regression analyses to determine predictors of ICH. Results— Twenty-nine patients fulfilled our inclusion criteria; 17 patients (58%) had ICH, and of these 4 (13%) had symptomatic ICH and fatal outcome. On univariate analysis, higher systolic blood pressure, NIHSS score, serum glucose level, volume of initial DWI lesion, and absolute number of voxels with ADC value ≤550×10−6 mm2/s were statistically associated with ICH, and all were subjected to multivariate analysis. However, only the absolute number of voxels, ie, volume of ischemic tissue on DWI, with ADC ≤550×10−6 mm2/s emerged as an independent predictor of ICH. Conclusions— Our findings suggest that volumetric ADC analysis can be used to assess ICH risk after thrombolysis. This may be particularly helpful if rtPA is to be given outside the 3-hour window.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"6 1","pages":"2047-2052"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83433580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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