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Epidemiology of post-stroke dementia
Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320
stroke survivors are likely to acquire features of Alzheimer type of dementia with greater survival. Supported by grant awards from the Medical Research Council (UK), Alzheimer's Research Trust (UK) and the NINDS, National Institutes of Health (USA). Keywords: Alzheimer's disease; Apolipoprotien E; Cognitive impairment; Dementia; Infarcts; Medial temporal atrophy; Stroke.
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the whole population—and would additionally improve the quality of life for everybody affected. Here we provide an overview on the role of major vascular risk factors for cerebral endorgan damage including hypertension, diabetes, atrial fibrillation, and other potential risk factors. doi:10.1016/j.jns.2009.02.138
doi:10.1016/j.jns.2009.02.135 Cerebral hemodynamics, cognition and mood before and after antihypertensive therapy Epidemiology of post-stroke dementia D. Leys University Lille II (EA 2691), Department of Neurology, Stroke Department, Lille, France Dementia is one of the major causes of dependency after stroke. The prevalence of post-stroke dementia (PSD), defined as any dementia occurring after stroke, is likely to increase in the future. In community-based studies, the prevalence of PSD in stroke survivors is approximately 30% and the incidence of new onset dementia after stroke increases from 7% after 1 year, up to 48% after 25 years. Stroke doubles the risk of dementia. Patient-related variables associated with an increased risk of PSD are increasing age, low education level, dependency before stroke, pre-stroke cognitive decline without dementia, diabetes mellitus, arterial fibrillation, myocardial infarction, epileptic seizures, sepsis, cardiac arrhythmias, congestive heart failure, silent cerebral infarcts, global and medial temporal lobe atrophy, and white matter changes. Stroke-related variables associated with an increased risk of PSD are stroke severity, cause, and location, and recurrence. doi:10.1016/j.jns.2009.02.136
Diabetic encephalopathy G.J. Biessels Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands It is increasingly recognized that diabetes is associated with long-term complications in the brain. These complications are reflected in cognitive dysfunction and abnormalities on brain imaging and may be referred to as “diabetic encephalopathy”. The nature and severity of cognitive decrements associated with diabetes appear to be dependent on age and diabetes type. In my presentation I will primarily address the impact of diabetes on cognition in adults. I will report on recent longitudinal data on cognition in patients with type 1 diabetes (DM1), provide an update on imaging studies in patients with DM1 and discuss possible determinants of accelerated cognitive decline in this patient group. Next I will address the associations between type diabetes (DM2) cognitive impairment, dementia, and abnormalities on brain imaging and discuss possible metabolic and vascular risk factors. doi:10.1016/j.jns.2009.02.137
Role of vascular risk factors for cerebral endorgan damage S. Knecht Dept. of Neurology, University of Münster, Münster, Germany Age is associated with cognitive decline. Neurodegenerative processes, genetic disposition, vascular risk and lifestyle factors like social and physical activity contribute to variations in cognition in age. We do not know how much each of these factors contributes to cognitive health, what other factors play a role and how they interact. This situation is deplorable, since there are millions of people affected by cognitive impairment and frank dementia. Effective control of critical risk factors for cognitive decline could delay onset and retard progression of cognitive impairment. In view of the large number of people affected, even small effects would translate into massive improvements across
K. Csapóa, Cs. Szekeresb, Z. Bajkób, E. Nyitrayc, P. Soltészd, L. Csibaa Neurology, Debrecen University, Debrecen, Hungary b Neurology, University Targu Mures, Targu Mures, Romania c Institute of Psychology, Debrecen University, Debrecen, Hungary d 3rd Department of Internal Medicine, Debrecen University, Debrecen, Hungary a
Background: There is a high prevalence of both hypertension and cognitive impairment in the aging population. Vascular dementia has been proven to be linked to a number of cardiovascular factors and impaired cerebral hemodynamics. Population-based studies showed hypertension is a well documented vascular risk factor for cognitive impairment. Our purpose was to assess the efficacy of antihypertensive treatment by noninvasive techniques in untreated, recently diagnosed middle-aged hypertensive patients before and after a 6 month and 1 year-long antihypertensive therapy, respectively. Methods: Hemodynamic parameters were recorded by transcranial Doppler and beat-to-beat blood pressure monitoring during head up tilttable testing. Cognitive performance was evaluated by neuropsychological tests including depression, anxiety, memory disturbances and reaction-time. Forty hypertensive patients were enrolled at baseline and 2/3 of them were examined after 6 month-long therapy. We hypothesized that antihypertensive drugs would improve cerebral hemodynamics, but no significant differences in cerebral reactivity was found between the hypertensive and control group. However, both depression scale and cognitive performance indicate a tendency of improvement after antihypertensive treatment. doi:10.1016/j.jns.2009.02.139
The spectrum of vascular dementia: Diagnostic limitations F. Fazekas Department of Neurology, Medical University Graz, Austria Vascular dementia (VD) is thought to result from various types of ischaemic and haemorrhagic brain tissue damage which leads to both variable patterns of neuropsychologic dysfunction and associated morphologic changes of the brain. For the latter, both the location and the severity of tissue damage are thought to be critical. While lesion topography, especially in the context of the occurrence of acute neurologic and/or cognitive deficits, can be defined by morphologic imaging and especially MRI to a satisfactory extent, estimation of the grade of severity of tissue destruction causing VD is much more demanding. To date, most definitions of lesion severity have also relied on rather arbitrary thresholds. This is especially true when considering the extent of leukoencephalopathy required as defined in some of the imaging criteria of VD. Not infrequently, VD or vascular cognitive impairment (VCI) appears to develop also in a rather chronic progressive manner which complicates establishing the timely relation with tissue damage. This is especially true for VD and VCI in association with small vessel disease. Therefore, for a long time, this etiologic link was viewed rather critically but has now been confirmed by a number of prospective studies which allowed pinpointing the temporal relationship of the evolution of both morphologic and cognitive changes. However, our understanding is still complicated by the observation of concurrent atrophic changes of the brain which may imply coexistent degenerative processes. Until clear in vivo markers for degenerative types of dementia such as amyloid imaging are readily available, it is difficult to discern if vascular and degenerative pathophysiologies just add up to the development of neuropsychologic dysfunction or may add to brain tissue destruction in a multiplicative manner. In conclusion, the concepts of vascular cognitive impairment and VD have been refined over the past years by more detailed cross-sectional and
stroke survivors are likely to acquire features of Alzheimer type of dementia with greater survival. Supported by grant awards from the Medical Research Council (UK), Alzheimer's Research Trust (UK) and the NINDS, National Institutes of Health (USA). Keywords: Alzheimer's disease; Apolipoprotien E; Cognitive impairment; Dementia; Infarcts; Medial temporal atrophy; Stroke.
275
the whole population—and would additionally improve the quality of life for everybody affected. Here we provide an overview on the role of major vascular risk factors for cerebral endorgan damage including hypertension, diabetes, atrial fibrillation, and other potential risk factors. doi:10.1016/j.jns.2009.02.138
doi:10.1016/j.jns.2009.02.135 Cerebral hemodynamics, cognition and mood before and after antihypertensive therapy Epidemiology of post-stroke dementia D. Leys University Lille II (EA 2691), Department of Neurology, Stroke Department, Lille, France Dementia is one of the major causes of dependency after stroke. The prevalence of post-stroke dementia (PSD), defined as any dementia occurring after stroke, is likely to increase in the future. In community-based studies, the prevalence of PSD in stroke survivors is approximately 30% and the incidence of new onset dementia after stroke increases from 7% after 1 year, up to 48% after 25 years. Stroke doubles the risk of dementia. Patient-related variables associated with an increased risk of PSD are increasing age, low education level, dependency before stroke, pre-stroke cognitive decline without dementia, diabetes mellitus, arterial fibrillation, myocardial infarction, epileptic seizures, sepsis, cardiac arrhythmias, congestive heart failure, silent cerebral infarcts, global and medial temporal lobe atrophy, and white matter changes. Stroke-related variables associated with an increased risk of PSD are stroke severity, cause, and location, and recurrence. doi:10.1016/j.jns.2009.02.136
Diabetic encephalopathy G.J. Biessels Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands It is increasingly recognized that diabetes is associated with long-term complications in the brain. These complications are reflected in cognitive dysfunction and abnormalities on brain imaging and may be referred to as “diabetic encephalopathy”. The nature and severity of cognitive decrements associated with diabetes appear to be dependent on age and diabetes type. In my presentation I will primarily address the impact of diabetes on cognition in adults. I will report on recent longitudinal data on cognition in patients with type 1 diabetes (DM1), provide an update on imaging studies in patients with DM1 and discuss possible determinants of accelerated cognitive decline in this patient group. Next I will address the associations between type diabetes (DM2) cognitive impairment, dementia, and abnormalities on brain imaging and discuss possible metabolic and vascular risk factors. doi:10.1016/j.jns.2009.02.137
Role of vascular risk factors for cerebral endorgan damage S. Knecht Dept. of Neurology, University of Münster, Münster, Germany Age is associated with cognitive decline. Neurodegenerative processes, genetic disposition, vascular risk and lifestyle factors like social and physical activity contribute to variations in cognition in age. We do not know how much each of these factors contributes to cognitive health, what other factors play a role and how they interact. This situation is deplorable, since there are millions of people affected by cognitive impairment and frank dementia. Effective control of critical risk factors for cognitive decline could delay onset and retard progression of cognitive impairment. In view of the large number of people affected, even small effects would translate into massive improvements across
K. Csapóa, Cs. Szekeresb, Z. Bajkób, E. Nyitrayc, P. Soltészd, L. Csibaa Neurology, Debrecen University, Debrecen, Hungary b Neurology, University Targu Mures, Targu Mures, Romania c Institute of Psychology, Debrecen University, Debrecen, Hungary d 3rd Department of Internal Medicine, Debrecen University, Debrecen, Hungary a
Background: There is a high prevalence of both hypertension and cognitive impairment in the aging population. Vascular dementia has been proven to be linked to a number of cardiovascular factors and impaired cerebral hemodynamics. Population-based studies showed hypertension is a well documented vascular risk factor for cognitive impairment. Our purpose was to assess the efficacy of antihypertensive treatment by noninvasive techniques in untreated, recently diagnosed middle-aged hypertensive patients before and after a 6 month and 1 year-long antihypertensive therapy, respectively. Methods: Hemodynamic parameters were recorded by transcranial Doppler and beat-to-beat blood pressure monitoring during head up tilttable testing. Cognitive performance was evaluated by neuropsychological tests including depression, anxiety, memory disturbances and reaction-time. Forty hypertensive patients were enrolled at baseline and 2/3 of them were examined after 6 month-long therapy. We hypothesized that antihypertensive drugs would improve cerebral hemodynamics, but no significant differences in cerebral reactivity was found between the hypertensive and control group. However, both depression scale and cognitive performance indicate a tendency of improvement after antihypertensive treatment. doi:10.1016/j.jns.2009.02.139
The spectrum of vascular dementia: Diagnostic limitations F. Fazekas Department of Neurology, Medical University Graz, Austria Vascular dementia (VD) is thought to result from various types of ischaemic and haemorrhagic brain tissue damage which leads to both variable patterns of neuropsychologic dysfunction and associated morphologic changes of the brain. For the latter, both the location and the severity of tissue damage are thought to be critical. While lesion topography, especially in the context of the occurrence of acute neurologic and/or cognitive deficits, can be defined by morphologic imaging and especially MRI to a satisfactory extent, estimation of the grade of severity of tissue destruction causing VD is much more demanding. To date, most definitions of lesion severity have also relied on rather arbitrary thresholds. This is especially true when considering the extent of leukoencephalopathy required as defined in some of the imaging criteria of VD. Not infrequently, VD or vascular cognitive impairment (VCI) appears to develop also in a rather chronic progressive manner which complicates establishing the timely relation with tissue damage. This is especially true for VD and VCI in association with small vessel disease. Therefore, for a long time, this etiologic link was viewed rather critically but has now been confirmed by a number of prospective studies which allowed pinpointing the temporal relationship of the evolution of both morphologic and cognitive changes. However, our understanding is still complicated by the observation of concurrent atrophic changes of the brain which may imply coexistent degenerative processes. Until clear in vivo markers for degenerative types of dementia such as amyloid imaging are readily available, it is difficult to discern if vascular and degenerative pathophysiologies just add up to the development of neuropsychologic dysfunction or may add to brain tissue destruction in a multiplicative manner. In conclusion, the concepts of vascular cognitive impairment and VD have been refined over the past years by more detailed cross-sectional and