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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

Vascular dementia (VaD) is the second most common form of dementia after Alzheimer's disease (AD), and one of the major causes of mental and physical disability in developed countries. As such, the identification and implementation of strategies which prevent the development of the condition or enable improvements in patients with VaD are healthcare objectives of the first order. VaD is now regarded as a combined group of clinical-pathological entities rather than one disease, that is, multiple pathogenic mechanisms and lesion types underlie a cognitive impairment of vascular origin. The clinical diagnosis of VaD is complex and difficult because of the heterogeneous nature of its clinical presentation and progression and the low sensitivity of existing clinical criteria. Moreover, there is growing evidence of the epidemiological significance of mixed forms of dementia, and that ischemic processes may precipitate and exacerbate cognitive impairment in AD. Numerous compounds have been proposed as potentially useful in the treatment of patients with VaD, comprising vasodilatative, antithrombotic, hemorrheological, nootropic, antiserotoninergic and, most recently, antiglutamatergic and cholinergic approaches. In spite of some initially favorable reports based on the use of memantine, donepezil and galantamine, there is as yet no conclusive evidence of a definitive treatment for VaD. Unsatisfactory results from VaD drug trials may be attributed in part to the diversity of the patients included (underlying pathogenic mechanisms, number, type, and location of vascular lesions), and to methodological limitations in the design of the trials (outcome measures, end-points, size, follow-up period). The treatment of modifiable vascular risk factors - hypertension, diabetes mellitus, hypercholesterolemia and heart disease - is an important strategy for the reduction of the risk of dementia, and is likely to slow the progress of cognitive decline.
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PMID:Neuroprotection in vascular dementia. 1665 21

Vascular dementia is a term used to describe a constellation of cognitive and functional impairment that can be viewed as a subset of the larger syndrome of vascular cognitive impairment associated with cerebrovascular brain injury. Vascular dementia is a common disorder among the elderly, although it can also occur in younger persons. Comprising 20% of all cases of dementia in the United States, vascular dementia is the second most common form of dementia after Alzheimer's disease. Patients with vascular dementia often exhibit mood and behavioral changes and may have focal neurological signs on neurological examination. Primary treatment is through primary or secondary modification of cerebrovascular risk factors such as hypertension, although symptomatic treatments with cholinesterase inhibitors have shown modest symptomatic benefit.
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PMID:Vascular dementia: emerging trends. 1722 43

Vascular dementia (VaD) is heterogeneous in its clinical, imaging, and etiological characteristics. Although VaD is common in India, its pattern is not completely known. In a hospital-based cohort, we aimed to characterize VaD by its subtypes and study patterns of risk factors and clinical, and neuropsychological profiles. Vascular mechanisms, known to have racial and genetic variations were identified. NINDS-AIREN criteria were used to diagnose VaD. Patients were subtyped into subcortical, cortical, cortical-subcortical, and strategic infarct dementia. Vascular mechanisms were detected by vascular imaging, cardiac evaluation, and laboratory tests. In the 42 consecutive patients with VaD, subcortical dementia was the most common type (52.4%), followed by cortical-subcortical (26.2%), strategic infarcts in (14.3%), and cortical dementia (7.1%). Stroke (81%), hypertension (71.4%), and diabetes (35.7%) were important risk factors. Small artery disease was the underlying vascular mechanism in 42.9%; intracranial large artery disease, in 16.7%; extracranial disease, in 2.3%; cardioembolism, in 2.3%; multiple mechanisms, in 19%; and unknown, in 16.7%. Subtypes were similar in risk factor profile and neuropsychological features but differed in clinical characteristics and vascular mechanisms. Gait disorder (59.1% vs. 0%) and urinary symptoms (77.3% vs. 16.7%) were more common in subcortical dementia than in strategic infarct dementia (P < .05). Small artery disease was most common in subcortical dementia (72.7%). Intracranial large artery disease was associated with all subtypes. The pattern of VaD demonstrated in our study is a reflection of mechanisms of cerebrovascular disease in India. Outcome depends on underlying mechanisms and thus is likely to differ from that in other ethnic populations.
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PMID:Pattern of vascular dementia in India: study of clinical features, imaging, and vascular mechanisms from a hospital dementia registry. 1790 48

Alzheimer's disease is the most prevalent and common form of cognitive impairment, ie, dementia, in the elderly followed in second place by vascular dementia due to the microangiopathy associated with poorly-controlled hypertension. Besides blood pressure elevation, advancing age is the strongest risk factor for dementia. Deterioration of intellectual function and cognitive skills that leads to the elderly patient becoming more and more dependent in his, her, activities of daily living, ie, bathing, dressing, feeding self, locomotion, and personal hygiene. It has been known and demonstrated for many years that lowering of blood pressure from a previous hypertensive point can result in stroke prevention yet lowering of blood pressure does not prevent the microangiopathy that leads to white matter demyelinization which when combined with the clinical cognitive deterioration is compatible with a diagnosis of vascular dementia. It is known from many large studies, ie, SHEP, SCOPE, and HOPE, that lowering of blood pressure gradually will not and should not worsen the cognitive impairment. However, if the pressure is uncontrolled a stroke which might consequently occur would further worsen their cognitive derangement. So an attempt at slow reduction of blood pressure since cerebral autoregulation is slower as age increases is in the patient's best interest. It is also important to stress that control of blood glucose can also be seen as an attempt to prevent vascular dementia from uncontrolled hyperglycemia. Vascular dementia is not considered one of the reversible causes of dementia. Reversible causes of cognitive impairment are over medication with centrally acting drugs such as sedatives, hypnotics, antidepressants, and antipsychotics, electrolyte imbalance such as hyponatremia, azotemia, chronic liver disease, and poor controlled chronic congestive heart failure. Criteria for the clinical diagnosis of vascular dementia include cognitive decline in regards to preceding functionally higher level characterized by alterations in memory and in two or more superior cortical functions that include orientation, attention, verbal linguistic capacities, visual spacial skills, calculation, executive functioning, motor control, abstraction and judgment. Patients with disturbances of consciousness, delirium (acute confusional states), psychosis, serious aphasia, or sensory-motor alterations that preclude proper execution of neuro-psychological testing are also considered to have probably vascular dementia. Furthermore, these are ten of the other essential cerebral or systematic pathologies present that would be able to produce a dementia syndrome.
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PMID:Hypertension and cognitive function in the elderly. 1809 Aug 79

Alzheimer's disease (AD) is a dementing neurological disorder that results in progressive memory loss and cognitive decline thought to be associated with buildup of amyloid plaques and neurofibrillary tangles in the brain. Vascular Dementia (VaD) is another common dementing disorder characterized by decreased brain perfusion. Together, AD and VaD constitute mixed dementia, an extremely common type of dementia associated with aging. Neuroimaging research suggests that brain vascular atrophy results in mild cognitive impairment (MCI), a possible precursor for AD. Additionally, literature suggests that attention to cardiovascular risk factors such as hypertension could reduce or delay the incidence of mixed dementia. Furthermore, foods and beverages rich in natural antioxidant flavanoids (i.e. epicatechin and catechin) are currently being advocated as possible preventative agents for a number of pathological conditions ranging from coronary heart disease to dementia. Experimental evidence is mounting that oxidative stress is involved in the pathophysiology of AD, and numerous studies are indicating that polyphenolic antioxidants found in fruits and vegetables can be useful in countering this and blocking neuronal death. More specifically, several cocoa studies suggest that daily intake of cocoa flavanols leads to cardiovascular benefits including vasodilatation via a nitric oxide mechanism and increased brain perfusion. The following text will consider an important question that thus arises regarding the potential of flavanols as effective agents for the prevention and delay of the onset of brain vascular atrophy and subsequently MCI and AD. It will also review the molecular mechanisms through which flavanols operate to accomplish their protective effects.
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PMID:Flavanols, mild cognitive impairment, and Alzheimer's dementia. 1907 72

Randomized controlled trials of primary and secondary prevention of vascular dementia demonstrate real effects on the cause or progression of disease (disease-modifying treatment). These strategies lead to a reduction in all cerebrovascular risk factors, in particular hypertension. Such treatment may prevent dementia by reducing stroke and possibly by other mechanisms that remain undetermined,such as those involved in neurodegeneration and cell death. Curative treatment of vascular dementia, particularly given recent studies on cholinesterase inhibitors (rivastigmine, donepezil and galantamine) and memantine, is still ineffective. There is insufficient evidence to support widespread use of these drugs in vascular dementia. Particular considerations should be taken into account in clinical trials. Vascular dementia is a heterogeneous disease with different subtypes and mechanisms.Therefore, well-designed, adequately powered trials accounting for this heterogeneity, with better clinical definitions and an assessment and detection of cognitive and global changes specific to vascular dementia, are needed.
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PMID:Is it possible to treat vascular dementia? 1918 67

Vascular cognitive impairment is an important cause of cognitive decline in the elderly. Ischemic lesions in the brain have an influence on the natural history of dementia. Vascular dementia can be caused by small-vessels disease (S-VaD) or by large-artery atherosclerosis with vascular lesions in strategic areas of the brain (M-VaD). In both cases changes in white matter are observed. In 60 patients with S-VaD and in 34 with M-VaD the presence of vascular and biochemical risk factors was evaluated and compared to age and sex matched 126 controls without dementia. Coronary artery disease, atrial fibrillation, hypertension and strokes were observed more frequently in both investigated groups. Of biochemical risk factors, hyperhomocysteinemia (associated with low levels of folic acid and vitamin B 12) and low HDL cholesterol levels were found in both forms of VaD.
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PMID:Vascular and biochemical risk factors of vascular dementia after lacunar strokes (S-VaD) and after multiinfarcts in strategic areas (M-VaD). 1933 23

Alzheimer's disease is the most prevalent and common form of cognitive impairment, ie, dementia, in the elderly followed in second place by vascular dementia due to the microangiopathy associated with poorly-controlled hypertension. Besides blood pressure elevation, advancing age is the strongest risk factor for dementia. Deterioration of intellectual function and cognitive skills that leads to the elderly patient becoming more and more dependent in his, her, activities of daily living, ie, bathing, dressing, feeding self, locomotion, and personal hygiene. It has been known and demonstrated for many years that lowering of blood pressure from a previous hypertensive point can result in stroke prevention yet lowering of blood pressure does not prevent the microangiopathy that leads to white matter demyelinization which when combined with the clinical cognitive deterioration is compatible with a diagnosis of vascular dementia. It is known from many large studies, ie, SHEP, SCOPE, and HOPE, that lowering of blood pressure gradually will not and should not worsen the cognitive impairment. However, if the pressure is uncontrolled a stroke which might consequently occur would further worsen their cognitive derangement. So an attempt at slow reduction of blood pressure since cerebral autoregulation is slower as age increases is in the patient's best interest. It is also important to stress that control of blood glucose can also be seen as an attempt to prevent vascular dementia from uncontrolled hyperglycemia. Vascular dementia is not considered one of the reversible causes of dementia. Reversible causes of cognitive impairment are over medication with centrally acting drugs such as sedatives, hypnotics, antidepressants, and antipsychotics, electrolyte imbalance such as hyponatremia, azotemia, chronic liver disease, and poor controlled chronic congestive heart failure. Criteria for the clinical diagnosis of vascular dementia include cognitive decline in regards to preceding functionally higher level characterized by alterations in memory and in two or more superior cortical functions that include orientation, attention, verbal linguistic capacities, visual spacial skills, calculation, executive functioning, motor control, abstraction and judgment. Patients with disturbances of consciousness, delirium (acute confusional states), psychosis, serious aphasia, or sensory-motor alterations that preclude proper execution of neuro-psychological testing are also considered to have probably vascular dementia. Furthermore, these are ten of the other essential cerebral or systematic pathologies present that would be able to produce a dementia syndrome.
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PMID:Hypertension and cognitive function in the elderly. 2018 99

Vascular dementia (VaD) has been suggested to be the most common form of dementia in old age, but clinico-pathologic studies showed big differences in its epidemiology. A retrospective hospital-based study of the frequency and pathology of "pure" VaD (due to cerebrovascular disease without other pathologies) was performed in 1110 consecutive autopsy cases of demented elderly in Vienna, Austria. It assessed clinical, general autopsy data and neuropathology including immunohistochemistry. Neuropathologic diagnosis followed current consensus criteria. Four age groups (7th to 10th decades) were evaluated. "Pure" VaD was observed in 10.8% of the total cohort, decreasing from age 60 to 90+. 85-95% had histories of diabetes, morphologic signs of hypertension, 65% myocardial infarction/cardiac decompensation, and 75% a history of stroke(s). Neuritic AD-pathology was low (mean Braak stages 1.2-1.6). Morphologic subtypes (multi-infarct (MID), subcortical arteriosclerotic (SAE)-the most frequent, and strategic infarct dementia (SID)) showed no age-related differences. By contrast, AD (without vascular or Lewy pathologies), mixed dementia (AD+cerebrovascular encephalopathy), and AD with minor cerebrovascular lesions increased with age. AD+Lewy pathology and other dementias decreased significantly over age 90. This retrograde study using strict morphologic diagnostic criteria confirmed the existence of "pure" VaD in old age, with a tendency to decline at age 90+, while AD and AD+cerebrovascular pathologies showed considerable age-related increase. Another autopsy study distinguishing two age groups of demented showed a significant increase of both AD and cerebral amyloid angiopathy (CAA), but decrease of VaD over age 85, while in a small subgroup of old subjects CAA without considerable AD-pathology may be an independent risk factor for cognitive decline.
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PMID:Is there pure vascular dementia in old age? 2086 29


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