Examination and Test Findings

Mental status assessment may reveal dysfunction in multiple cognitive domains. Executive dysfunction may be more prominent than dysfunction in other domains. The neurological examination will reveal cranial nerve dysfunction and focal pyramidal and extrapyramidal abnormalities. Gait and balance abnormalities are frequently seen. Urinary incontinence is also seen in many VaD patients.

No laboratory study can diagnose VaD. However, these patients often have laboratory abnormalities that reflect risk factors for VaD, such as elevated cholesterol or blood glucose levels.

The electroencephalogram is often more normal than it is in patients with AD. Focal infarcts can produce corresponding focal abnormalities on the EEG, and EEG abnormalities in VaD are usually more asymmetric than in AD. Subcortical infarcts are often electrically silent.

Structural neuroimaging (CT or MRI) reveals focal infarcts and/or extensive white matter ischemic changes in patients with VaD. Infarctions in the brain watershed areas (frontal/parietal) can be found after acute episodes of hypoperfusion. Functional neuroimaging usually reveals patchy areas of decreased blood flow or metabolism consistent with ischemia and/or infarcts. Abnormalities in the primary sensorimotor or visual cortices are usually due to cerebrovascular disease as these areas are relatively spared in AD.

Neuropsychological assessment may produce a patchy pattern of cognitive deficits with executive dysfunction and psychomotor slowing that can complicate the assessment of other functions. In patients with VaD there is usually a relative preservation of language abilities unless the language areas have been damaged by an infarct. However, as noted above, the neuropsychological presentation of VaD is quite variable.

Neuropathology. Pathological examination of the brains of VaD patients can reveal different types of cerebral infarcts. Emboli, arterial thrombosis, or other causes of arterial occlusion can cause infarcts in the territory distal to the obstruction. Small lacunar infarcts can be seen, and these are most often found in the basal ganglia and thalamus. Widespread lacunes can produce the vascular dementia syndrome known as the lacunar state. Infarctions of the white matter can also be seen; widespread white matter microinfarcts are sometimes referred to as Binswanger's disease. Lacunes and white matter infarcts are usually associated with fibrinoid necrosis of small arteries and arterioles. Episodes of decreased cerebral perfusion due to cardiac arrhythmia or other causes can cause watershed infarctions in the distal, overlapping areas between the major arterial distributions. Pathological examination can also reveal areas of incomplete ischemic injury as well as ischemia-induced atrophy (Olsson et al., 1996).

Areas of functionally abnormal tissue are frequently present and may not be detectable on routine pathological examination. Focal infarcts are often surrounded by a penumbra of dysfunctional tissue, and areas of the brain far-removed from an infarct can develop secondary functional impairment (diaschisis).

In rare cases, the syndrome of dementia can be caused by a single stroke located in a "strategic" area. For example, infarction of the angular gyrus can manifest as dementia (Benson et al., 1982).

Neurochemical Changes. Cerebrospinal fluid (CSF) levels of acetylcholine are reduced in patients with vascular dementia. CSF acetylcholine levels are higher in VaD than in AD, although the frequent comorbidity of these two diseases complicates the interpretation of these findings. The activity of choline acetyltransferase, acetylcholine's synthetic enzyme, is also reduced in VaD (Tohgi et al., 1996).

Abnormalities in the dopaminergic system have also been described in VaD. CSF dopamine levels are increased in VaD and correlate with disease progression. CSF levels of homovanillic acid (HVA), a dopamine metabolite, are decreased in VaD (Tohgi et al., 1992). Dopamine D2 receptors in the caudate nuclei of VaD patients have a decreased binding affinity for dopamine when compared to receptors from control subjects. This difference in binding affinity does not seem to correlate with prior use of neuroleptic medication (Allard et al., 2002).

Different findings have been reported in studies of the serotonergic system in VaD. Measures of presynaptic and postsynaptic serotonergic cell density have been found to be equal in cases of VaD and controls (Hansson et al., 1996). Serotonin metabolism seems to be decreased, though, and CSF levels of 5-HIAA, a metabolite of serotonin, have been found to be decreased in VaD (Tohgi et al., 1992). Increased activity of the hypothalamic/pituitary/adrenal axis can be seen in VaD and may be a consequence of decreased serotonergic inhibition of this system (Gottfries et al., 1994).

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