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   Vascular Dementia   
      
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   By DeepDiveAdmin, Wed, March 30, 2011   
   Vascular Dementia   
      
   Vascular dementia is the second most common form of dementia after Alzheimer   
   disease (AD). The condition is not a single disease; it is a group of   
   syndromes relating to different vascular mechanisms. Vascular dementia is   
   preventable; therefore, early    
   detection and an accurate diagnosis are important.   
   Patients who have had a stroke are at increased risk for vascular dementia.   
   Recently, vascular lesions have been thought to play a role in AD.   
   As early as 1899, arteriosclerosis and senile dementia were described as   
   different syndromes. In 1969, Mayer-Gross et al described this syndrome and   
   reported that hypertension is the cause in approximately 50% of patients. In   
   1974, Hachinski et al coined    
   the term multi-infarct dementia. In 1985, Loeb used the broader term vascular   
   dementia. Recently, Bowler and Hachinski introduced a new term, vascular   
   cognitive impairment.   
      
   Many subtypes of vascular dementia have been described to date. The spectrum   
   includes:   
   mild vascular cognitive impairment   
   multi-infarct dementia   
   vascular dementia due to a strategic single infarct   
   vascular dementia due to lacunar lesions   
   vascular dementia due to hemorrhagic lesions   
   Binswanger disease, and mixed dementia ( combination of AD and vascular   
   dementia ).   
   Vascular dementia is sometimes further classified as cortical or subcortical   
   dementia.   
   Vascular disease produces either focal or diffuse effects on the brain and   
   causes cognitive decline. Focal cerebrovascular disease occurs secondary to   
   thrombotic or embolic vascular occlusions. Common areas of the brain   
   associated with cognitive decline    
   are the white matter of the cerebral hemispheres and the deep gray nuclei,   
   especially the striatum and the thalamus. Hypertension is the major cause of   
   diffuse disease, and in many patients, both focal and diffuse disease are   
   observed together. The 3    
   most common mechanisms of vascular dementia are multiple cortical infarcts, a   
   strategic single infarct, and small vessel disease.   
   Mild vascular cognitive impairment can occur in elderly persons. It is   
   associated with cognitive decline that is worse than expected for age and   
   educational level, but the effects do not meet the criteria for dementia and   
   are not associated with vascular    
   risk factors or evidence of silent strokes or extensive white matter infarcts   
   on CT scanning. These people have subjective and objective evidence of memory   
   problems, but their daily functional living skills are within normal limits.   
   In multi-infarct dementia, the combined effects of different infarcts produce   
   cognitive decline by affecting the neural nets.   
   In single-infarct dementia, different areas in the brain can be affected,   
   which may result in significant impairment in cognition. This may be observed   
   in cases of anterior cerebral artery infarct, parietal lobe infarcts, thalamic   
   infarction, and    
   singular gyrus infarction.   
   Small vessel disease affects all the small vessels of the brain and produces 2   
   major syndromes, Binswanger disease and lacunar state. Small vessel disease   
   results in arterial wall changes, expansion of the Virchow-Robin spaces, and   
   perivascular    
   parenchymal rarefaction and gliosis.   
   Lacunar disease is due to small vessel occlusions and produces small cavitary   
   lesions within the brain parenchyma secondary to occlusion of small   
   penetrating arterial branches. These lacunae are found more typically in the   
   internal capsule, deep gray    
   nuclei, and white matter. Lacunar state is a condition in which numerous   
   lacunae, which indicate widespread severe small vessel disease, are present.   
   Binswanger disease (also known as subcortical leukoencephalopathy) is due to   
   diffuse white matter disease. In Binswanger disease, vascular changes observed   
   are fibrohyalinosis of the small arteries and fibrinoid necrosis of the larger   
   vessels inside the    
   brain.   
   In cerebral amyloid angiopathy-associated vasculopathy, aneurysm formation and   
   stenosis in the leptomeningeal and cortical vessels cause damage to the   
   subcortical white matter. In hereditary cystatin-C amyloid angiopathy,   
   patients have recurrent cerebral    
   hemorrhages before age 40 years that can lead to dementia.   
   Cerebral autosomal dominant arteriopathy with subcortical infarcts and   
   leukoencephalopathy is a rare autosomal dominant condition localized to   
   chromosome arm 19q12 that affects small vessels supplying the deep white   
   matter. Pathologically, multiple small    
   infarcts are observed in the white matter, thalamus, basal ganglia, and pons.   
   Other less common syndromes may lead to vascular dementia. Rare arteriopathies   
   such as inflammatory arteriopathy (eg, polyarteritis nodosa, temporal   
   arteritis) and noninflammatory arteriopathy (eg, moyamoya disease,   
   fibromuscular dysplasia) can cause    
   multiple infarcts and can lead to vascular dementia. Hypoperfusion due to   
   large vessel or cardiac disease can affect the watershed areas of the brain   
   and lead to vascular dementia.   
   Mixed dementia is diagnosed when patients have evidence of Alzheimer dementia   
   and cerebrovascular disease, either clinically or based on neuroimaging   
   evidence of ischemic lesions. Growing evidence indicates that vascular   
   dementia and Alzheimer dementia    
   often coexist, especially in older patients with dementia.   
   Autopsy studies have shown the association between AD and vascular lesions.   
   Several recent studies also suggest that the risk of developing AD is   
   increased when a patient is exposed to vascular risk factors such as   
   hypertension, diabetes mellitus,    
   peripheral arterial disease, and smoking, which usually are associated with   
   cerebrovascular disease and vascular dementia. Recent evidence suggests that   
   the vascular processes in both disorders may mutually induce each other.   
   Apolipoprotein E may play a    
   role in AD and vascular dementia. Apolipoprotein E-IV also increases the risk   
   of dementia in stroke survivors and is a strong risk factor for the   
   development of cerebral amyloid angiopathy in patients with AD. In elderly   
   individuals, many cases of    
   dementia may be caused by the cumulative effect of cerebrovascular and   
   Alzheimer pathology.   
   Frequency:   
      
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