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Vascular dementia (VaD) is the second commonest dementia after Alzheimer's disease (AD). Epidemiological studies of this condition suffer from many shortcomings related to definition of the disease, diagnostic criteria and assessment of subjects. The prevalence of VaD increases linearly with age and varies greatly from country to country, ranging from 1.2 to 4.2% of people over 65 years old, even after adjustment for age and sex. The incidence of VaD is more homogeneous than prevalence and is estimated at 6-12 cases per 1,000 persons over 70 years per year. The mean duration of the disease is around 5 years and survival is less than for the general population and for AD. The major risk factors for VaD appear to be hypertension, diabetes, heart disease and stroke. Although some of these risk factors are modifiable, there is no study on efficacy of prevention of VaD.
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PMID:Epidemiology of vascular dementia. 747 66

Vascular dementia is a clinical syndrome of acquired intellectual impairment resulting from brain injury due to a cerebrovascular disorder. It is a complex diagnosis, and diagnostic criteria vary. In community practice, the physician can probably make the diagnosis based on the history and medical examination. CT demonstration of one or more infarcts increases the likelihood of this diagnosis. Hypertension is a major risk factor for vascular dementia. Others include smoking, hyperlipidemia, atrial fibrillation, diabetes, and a sedentary lifestyle. Cerebrovascular disease is an important cause of cognitive decline in older patients. Therefore, it is important to recognize risk factors for stroke and institute measures for prevention.
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PMID:Vascular dementia: stroke prevention takes on new urgency. 822 23

Cerebrovascular disease is a major public health problem in Eastern European countries. A Hungarian post-stroke population was examined to estimate the rate of dementia, the risk factors for cognitive impairment, and the applicability of a recently established Canadian diagnostic checklist in this cohort. Chronic cerebrovascular outpatients were screened for cognitive impairment with a combined checklist: the Diagnostic Checklist for Vascular Dementia established by the Consortium of Canadian Centres for Clinical Cognitive Research using the Mini Mental State Examination instead of the detailed neuropsychological part of the Checklist. Of the 247 consecutive patients at a cerebrovascular outpatient unit, 176 had cerebrovascular disorder diagnosed either by computed tomography (CT; n=126) or by the clinical signs. Of these, 15% were cognitively impaired and 5% fulfilled the criteria of dementia. The mean age of the patients with cognitive impairment was significantly higher than that of patients with normal cognition (68.2+/-10.2 and 60.5+/-10.5 years, P<0.001). The Barthel index was significantly lower in the cognitively affected group than in non-affected patients (92.4+/-16.0 and 97.1+/-8.7, P=0.027). Diabetes and more than two subcortical infarcts on CT or magnetic resonance imaging were more frequent in patients with cognitive loss (P=0.043 and P=0.013, respectively). Cognitive performance was also influenced by the level of education. Higher age, diabetes, motor deficits, and multiple subcortical infarcts are risk factors for cognitive impairment after stroke. The combined checklist appears to be a practical screening test for cognitive impairment in patients with chronic cerebrovascular diseases.
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PMID:Screening of vascular cognitive impairment on a Hungarian cohort. 1020 Dec 82

Vascular dementia (VD) is more prevalent than Alzheimer's disease (AD) in Japan, while AD is more common in Western countries. In the Hisayama study, a community-based cohort study of Japan, the prevalence of VD decreased in men during the 7-years (1985-1992) follow-up period, while the prevalence of AD remained unchanged both in men and women. The incidence of dementia increases with age, particularly AD aged 85 or older. Hypertension is a major risk factor for VD. Other risk factors include age, prior stroke, diabetes, alcohol intake, heart disease, and smoking. In contrast, age, a family history of dementia, a low educational level, and low physical activity are risk factors for AD. The role of hypertension in AD remains controversial; there has been positive, negative, or no association existed between blood pressure levels and AD. A recent clinical trial has disclosed the potential preventive effect of antihypertensive treatment on the incidence of dementia, especially of AD. Although the role of vascular factors for the pathogenesis of AD is becoming recognized, the effectiveness of antihypertensive treatment on the prevention of AD should be further clarified in the future studies.
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PMID:Hypertension and dementia. 1042 14

Vascular dementia (VaD) is the second-most-common cause of dementia in the elderly, after Alzheimer's disease (AD). VaD is defined as loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions due to cerebrovascular disease or cardiovascular pathology. Diagnosis requires the following criteria: cognitive loss, often predominantly subcortical; vascular brain lesions demonstrated by imaging; a temporal link between stroke and dementia; and exclusion of other causes of dementia. Poststroke VaD may be caused by large-vessel disease with multiple strokes (multiinfarct dementia) or by a single stroke (strategic stroke VaD). A common form is subcortical ischemic VaD caused by small-vessel occlusions with multiple lacunas and by hypoperfusive lesions resulting from stenosis of medullary arterioles, as in Binswanger's disease. Unlike with AD, in VaD, executive dysfunction is commonly seen, but memory impairment is mild or may not even be present. The cholinesterase inhibitors used for AD are also useful in VaD. Prevention strategies should focus on reduction of stroke and cardiovascular disease, with attention to control of risk factors such as hypertension, diabetes mellitus, hypercholesterolemia, and hyperhomocysteinemia.
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PMID:Vascular dementia: distinguishing characteristics, treatment, and prevention. 1280 86

Vascular dementia is the second most common type of dementia. The subcortical ischaemic form (SIVD) frequently causes cognitive impairment and dementia in elderly people. SIVD results from small-vessel disease, which produces either arteriolar occlusion and lacunes or widespread incomplete infarction of white matter due to critical stenosis of medullary arterioles and hypoperfusion (Binswanger's disease). Symptoms include motor and cognitive dysexecutive slowing, forgetfulness, dysarthria, mood changes, urinary symptoms, and short-stepped gait. These manifestations probably result from ischaemic interruption of parallel circuits from the prefrontal cortex to the basal ganglia and corresponding thalamocortical connections. Brain imaging (computed tomography and magnetic resonance imaging) is essential for correct diagnosis. The main risk factors are advanced age, hypertension, diabetes, smoking, hyperhomocysteinaemia, hyperfibrinogenaemia, and other conditions that can cause brain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, and orthostatic hypotension. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL)and some forms of cerebral amyloid angiopathy have a genetic basis. Treatment is symptomatic and prevention requires control of treatable risk factors.
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PMID:Subcortical ischaemic vascular dementia. 1284 65

Significant progress in the field of VaD resulted from publication of the NINIDS-AIREN Diagnostic Criteria for VaD (G.C. Roman, T.K. Tatemichi, T. Erkinjuntti, et al., Vascular dementia (VaD): diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology 43 (1993) 250-260). Epidemiological studies confirmed the importance of VaD as the second most common cause of dementia in the elderly, representing 15-20% of all cases of dementia. In Europe and North America, Alzheimer's disease (AD) predominates over VaD in a 2:1 ratio; in contrast, in Japan and China VaD accounts for almost 50% of all dementias. Case-control studies have identified risk factors for VaD including ageing, hypertension, diabetes mellitus, hyperlipidemia, recurrent stroke, cardiac disease, smoking, sleep apnea, and more recently, hyperhomocysteinemia, among others. Hypertension treatment may prevent VaD and AD. This finding has enormous importance from the Public Health viewpoint to decrease the future number of patients with dementia in the elderly. Along with advances in the field of VaD came a number of controversies and damaging misconceptions and myths. Myth no. 1--Vascular dementia is a non-entity: The false idea that VaD does not exist is particularly destructive because it creates the perspective that VaD is unworthy of study or research. A condition that either does not exist or represents only a minute proportion of all cases of dementia in the elderly, lacks public health relevance and becomes a low priority for research by funding agencies and industry. In fact, vascular brain lesions are the commonest and most important component of dementia in the elderly. Myth no. 2--Vascular dementia is so difficult to diagnose that only experts can recognize and identify it accurately: VaD does exist and the diagnosis of post-stroke VaD, in particular is straightforward. Most cases fulfill NINDS-AIREN criteria for probable VaD; i.e., (1) there is acute onset of dementia demonstrated by impairment of memory and two other cognitive domains, such as orientation, praxis or executive dysfunction; (2) relevant cerebrovascular lesions are demonstrated by neuroimaging; and (3) a temporal relation between stroke and cognitive loss is evident. In the donepezil trials on VaD, post-stroke dementia represented about 75% of the >1,200 patients enrolled. Myth no. 3--Improvement in clinical trials of cholinergics in VaD is due to underlying AD, not to the vascular lesions. Experimental, clinical and pathological evidence has demonstrated cholinesterase deficits in VaD (independently of any concomitant AD pathology), including low acetylcholine in cerebrospinal fluid, and reduced choline acetyltransferase (ChAT) in the brain.
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PMID:Facts, myths, and controversies in vascular dementia. 1553 19

Vascular dementia is an overarching superordinate category of which multiinfarct vascular dementia is only one subtype. To contribute to the definition of vascular dementia, method involved investigation of mental status, oral language and comprehension in 81 consecutive vascular patients comprising two vascular samples: cerebral infarct sample (n=43) and cerebral noninfarct sample (n=38). To determine baseline, method also involved investigation of 36 demographically equivalent normal elderly. Results indicate both vascular samples performed significantly worse than normal elderly. Results further indicate there were no robust, reliable, significant differences between cerebral infarct and cerebral noninfarct patients. The lack of significant differences between cerebral infarct and cerebral noninfarct vascular samples brings into focus the ambiguous transition between diffuse, generalized disease and the multifocality underlying the vascular dementia-Alzheimer dementia spectrum. Cross-cutting infarct and noninfarct vascular populations were vascular factors of arteriosclerosis, abnormal blood pressure, diabetes mellitus, abnormal electrocardiogram, peripheral vascular disease, and other variables implicated in the distal causality of both infarct and noninfarct vascular dementias. Results indicate cerebral infarction is not the only path to the final common phenotype of vascular dementia. Vascular dementia is reconceptualized so as to include noninfarct vascular dementia: vascular dementia caused by underlying vascular factors other than cerebral infarction. It is suggested that one form of the subtype of noninfarct vascular dementia is Alzheimer-type vascular dementia.
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PMID:Noninfarct vascular dementia and Alzheimer dementia spectrum. 1576 Jun 16

Vascular dementia is the second most prevalent type of dementia in the United States today. This article includes a review of its pathophysiology, which involves the damage of small vessels in the brain, an abundance of which are in the subcortical region, thus creating a subcategory called subcortical vascular dementia (SVD). Various diseases, such as diabetes and high blood pressure, predispose the individual to damage to these small vessels. The symptoms of SVD are included as a review and helpful outline to differentiate SVD from Alzheimer's dementia and depression. Additionally, evidence-based interventions are reviewed. Nurses play a unique role in preventing and minimizing this dementia, which afflicts such a large percentage of our elderly population.
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PMID:Subcortical vascular dementia. 1582 27

Alzheimer's disease [AD] is the most common cause of dementia among people age 65 and older. One of the biggest stumbling blocks in developing effective drug therapy for Alzheimer's disease has been the lack of a comprehensive hypothesis that explains the mechanism behind all of the histopathological changes seen in patients suffering from Alzheimer's disease. An overview of the currently popular 'amyloid' and 'vascular' hypotheses for AD demonstrates that neither hypothesis by itself can explain all the known histopathological and biochemical lesions seen in Alzheimer's disease. The paper presents a hypothesis that tries to explain the mechanism behind almost all the histopathological changes, and varying clinical manifestations seen in both diagnosed AD and Vascular Dementia [VaD]. The new hypothesis is based on the known dual toxicity of beta amyloid to both vascular and neuronal tissues, their synergy and the resultant net effect on the onset and progression of AD. The new hypothesis therefore will be known as the Amyloid Beta Synergistic Endothelial and Neuronal Toxicity [ABSENT] hypothesis. The ABSENT hypothesis will try to show the common chemical mechanism behind almost all of the pathological changes seen in AD. According to the ABSENT hypothesis, beta amyloid itself generates all the free radicals that cause both vascular dysfunction and the neuronal damage seen in AD. The chemical mechanism proposed is based on evidence from physical chemistry experiments, calculations as well as in vitro/in vivo experiments. The ABSENT hypothesis does not favor one mode of beta amyloid-induced brain damage over the other, rather it considers the net effects of the neuronal stress/damage caused by both the cerebrovascular dysfunction and direct neurotoxicity caused by beta amyloid. The hypothesis states that each patient has a different balance of predisposing factors that modulate the extent of neurotoxicity and cerebrovascular dysfunction caused by beta amyloid and thereby explains the wide range and mixed nature of damage and dysfunction seen in the studies done on patients diagnosed with AD, VaD or 'mixed dementias'. According to the hypothesis, beta amyloid peptides are necessary if not sufficient to cause AD, VaD and mixed senile dementias. The hypothesis, therefore, proposes the term Beta Amyloid Dementias [BAD] to describe the conditions currently covered by the diagnoses of 'AD', 'VaD' and 'Mixed [senile] Dementias'. Finally, the ABSENT hypothesis tries to put forth a direct chemical mechanism behind the apparent synergy and increased association between old age, pre- and coexisting vascular disease, diabetes and AD.
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PMID:Alzheimer's disease and the 'ABSENT' hypothesis: mechanism for amyloid beta endothelial and neuronal toxicity. 1589 29


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