engleski

Update in vascular dementia: Ultrasonographic diagnostics

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. Many subtypes of vascular dementia have been described including: (1 ) mild vascular cognitive impairment, (2) multi-infarct dementia, (3) vascular dementia due to a strategic single infarct, (4) vascular dementia due to lacunar lesions, (5) vascular dementia due to hemorrhagic lesions, (6) Binswanger disease, and (7) mixed dementia (combination of AD and vascular 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. Hypertension is the major cause of diffuse disease, and in many patients, both focal and diffuse diseases are observed together. Lacunar state is a condition in which numerous lacunae indicating widespread severe small vessel disease. In Binswanger disease (subcortical leukoencephalopathy), vascular changes like fibrohyalinosis of the small arteries and fibrinoid necrosis of the larger vessels inside the brain cause diffuse white matter disease. 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 the age 40 of years that can lead to dementia. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare autosomal dominant condition affecting small vessels leading to multiple small infarcts in the white matter, thalamus, basal ganglia, and pons. Other less common syndromes may lead to vascular dementia, like inflammatory or noninflammatory arteriopathy, causing multiple infarcts. 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.Risk factors for vascular dementia include hypertension, smoking, hypercholesterolemia, diabetes mellitus, and cardiovascular and cerebrovascular disease. Different criteria may be used in diagnosing vascular dementia: NINDS-AIREN criteria are the most specific, and Hachinski ischemic score is the most simple for differentiation from AD. Neuroimaging studies are important, and neurosonology will show evidence for vascular involvement. By means of carotid color coded Doppler flow imaging (CCDFI) the evidence for impaired cerebral blood flow can be obtained: advanced carotid stenosis or occlusion, but also subclinical markers of atherosclerosis as increased carotid intima-media thickness (IMT), presence of carotid plaques or hemodynamic changes with increased carotid peripheral resistance. Transcranial Doppler sonography (TCD) will show impaired perfusion, and may be used in differentiation from AD. Carotid artery imaging White matter hyperintensities (WMH) are often observed on cerebral magnetic resonance imaging (MRI) of elderly individuals. Epidemiological studies have shown that age and hypertension are associated with WMH, suggesting vascular mechanism in its pathogenesis. The EVA study (1 ) confirmed an association between carotid atherosclerosis, evaluated by carotid IMT and plaques, with WHM independently of age and hypertension in 4-year follow up. Carotid plaques at baseline were significantly associated with the presence of severe WMH (OR=1.70 ; 95% CI: 1.05-2.74), stronger in males than in females. A 0.1 mm increase of baseline IMT was associated with an increased risk of severe WMH in both gender (adjusted OR=1.17 ; 95% CI: 0.96-1.41 ), but the association was not significant (p=0.12). Cross sectional relationships showed that the group of subjects who had already plaques at the study entry had more severe WMH. The group of Watanabe and Yamamotto (2, 3, 4) showed that carotid IMT and plaques, LDL-C, lipoprotein (a), lipid peroxides, hs-CRP, IgG and IgA C. pneumoniae seropositivity, lower serum insulin-like growth factor-1 may be a risk factor for vascular dementia. Results of our group (5) showed that increased IMT and stiffness with endothelial dysfunction are a part of normal aging process as well as an increase in systolic blood pressure and pulse pressure values and are referred to as vascular remodeling. Ultrasound can be used to determine proper vascular age of individuals offering proposition of different strategies for reduction or retardation of clinical manifestation of cerebrovascular disease. Since some of the changes attributed to normal aging have been identified in hypertensive individuals at an earlier age it is believed that they can be recognized as "unsuccessful" aging and subclinical vascular disease. Recent findings in a cohort of subjects with ultrasound-assessed carotid stenosis, recruited from a healthy population - Tromso Study, showed reduced neuropsychological test performance compared to controls (6). MRI lesions (WMH, lacunar and cortical infarcts) were recorded, and cortical infarcts and WMH were equally distributed among persons with and without carotid stenosis.Lacunar infarcts were more frequent in stenosis group. Interpretation of cognitive impairment in persons with asymptomatic carotid stenosis was less likely the result of silent emboli. Transcranial Doppler (TCD) investigations According to the etiology and pathophysiology of vascular dementia and its definition at the beginning as multi-infarct dementia (MID), the first investigations were focused on the intracranial hemodynamics. The first obtained results by TCD showed lower mean blood flow velocities (MBFV) in the basal cerebral arteries compared to healthy age-matched controls, while patients with AD had lower MBFV than the controls, but higher than patients with MID (7). Vasoreactivity testing in patients with MID was impaired, although less than in patients with other types of dementia (8, 9). Further vasoreactivity testing was conducted during stimuli tasks (10). Cerebral reactivity to apnea was significantly lower in MID compared to AD and the controls, during the motor task a nearly selective increase of MBFV contralateral to the hand movement was recorded in AD patients and the controls, and bilateral increase in MID patients. With respect to baseline values, the cognitive tasks produced significant and distinct effects on the left and right side in the controls but not in the patients. While the controls expressed a design discrimination task side-toside increase in MBFV, a bilateral and comparable increase of BFV was observed in all patients during performance of the same cognitive tasks. TCD assessment during cognitive and motor tasks thus provide useful complementary information for comprehension changes in cerebral activity in patients with dementia. As other types of vascular dementia were recognized, further TCD vasoreactivity testing was conducted. In CADASIL a reduction of both C02 reactivity and basal MBFV were obtained, suggesting functional impairment related to vascular smooth muscle cell dysfunction (11). The reduction of C02 reactivity in nondisabled CADASIL individuals suggested an early role of impaired cerebral vasoreactivity in the evolution of the disease. Also prolonged cerebral transit time (CCT) in CADASIL patients was recorded by measuring the time that a contrast agent needs to pass from a cerebral artery to its corresponding vein with transcranial color-coded duplex sonography (12). The prolonged CTT reflect microvascular changes in CADASIL, as well in other vascular dementia (13), to disclose small vessel disease. Although neurosonology is widely applied in management and prevention of stroke, its use in vascular dementia in only at the beginning. Hypoperfusion as a result of microvascular changes in different vascular types may be obtained. Still the differentiation of various types of vascular dementia is initial.

ultrasound; vascular dementia; diagnostics

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