Vascular Dementia

Vascular dementia

Topics covered:

  • Introduction
  • Aetiology and pathophysiology
    • Aetiology
    • Changes in the brain
    • Brain imaging findings
    • Pathophysiology
  • Classification and clinical criteria
    • Classification
    • Main subtypes
    • Clinical criteria
  • Clinical features
    • Cognitive syndrome
    • Neurological findings
    • Behavioural and psychological symptoms of dementia
  • Course and prognosis
  • Diagnosis and differential diagnosis
    • Clinical evaluation
    • Mental status examination
    • Brain imaging
    • Other investigations
    • Differential diagnosis of vascular dementia disease
  • Epidemiology
  • Treatment
  • Possibilities for prevention  
  • References


Vascular dementia is the second most frequent cause of dementia. (1,2) Because vascular causes of cognitive impairment are common, may be preventable, and the patients could benefit from therapy, early detection and accurate diagnosis of vascular dementia is desirable. (3)

Vascular dementia is not only multi-infarct dementia, but is related to other other vascular mechanisms and pathological changes in the brain, and has other causes and clinical manifestations. Vascular dementia is not a disease, but a syndrome. The origin of of this syndrome reflects complex interactions between vascular aetiologies (cerebrovascular disorders and vascular risk factors), changes in the brain (infarcts, white-matter lesions, atrophy), host factors (age, education), and cognition. (4,5,6,7 and 8)

Conceptual issues related to of vascular dementia include the definition of the cognitive syndrome (type, extent, and combination of impairments in different cognitive domains), and the vascular causes (vascular aetiologies and changes in the brain). Variations in these definitions has led to different estimates of point prevalence, to different groups of patients, and to reports of different types and distribution of brain lesions. (9,10 and 11) The cognitive syndrome of vascular dementia is characterized by predominate executive dysfunction rather than deficits in memory and language function. (12) Although the course of cognitive decline may be stepwise, it is often slowly progressive, and may include periods of stability or even some improvement. P>The relationship between vascular lesions in the brain and cognitive impairment is important, but which type, extent, side, site, and tempo of vascular lesions in the brain relates to different types of vascular dementia is not established in detail. (4,5 and 6,13)

Current criteria for vascular dementia are based on the concept of cerebral infarcts. For example the widely used NINDS-AIREN criteria include dementia, cerebrovascular disease, and a relationship between these two disorders. The main tools for the diagnosis include detailed history, neurological examination, mental state examination, relevant laboratory examinations, and preferably magnetic resonance imaging of the brain.

Vascular dementia research, until recently overshadowed by that into Alzheimer's disease, is now developing rapidly. There is great promise for intervention. Developments in classification, diagnosis, and treatment are likely.

Aetiology and pathophysiology


The main causes of vascular dementia are cerebrovascular disorders and their risk factors. The prevalent cerebrovascular disorders include large artery disease (artery-to-artery embolism, occlusion of an extra- or intracranial artery), cardiac embolic events, small vessel disease (lacunar infarcts, ischaemic white-matter lesions) and haemodynamic mechanisms. (13,14 and 15) Less frequent causes include specific arteriopathies, haemorrhage (intracranial haemorrhage, subarachnoidal haemorrhage), haematological factors, venous disease, and hereditary disorders. There may be as yet undiscovered causes.

In most patients diagnosed with vascular dementia, several aetiological factors are involved. However, the roles these factors play have not been identified in detail, and it is not certain which of these mechanisms distinguish vascular dementia from cerebrovascular disease without dementia. (4,5,7,16,17)

Risk factors for vascular dementia can be divided into vascular factors (e.g. arterial hypertension, atrial fibrillation, myocardial infarction, coronary heart disease, diabetes, generalized atherosclerosis, lipid abnormalities, smoking), demographic factors (e.g age, education), genetic factors (e.g. family history, individual genetic features), and stroke-related factors (e.g. type of cerebrovascular disease, site and size of stroke). (18,19) Hypoxic ischaemic events (cardiac arrhythmias, congestive heart failure, myocardial infarction, seizures, pneumonia) may be an important risk factor for incident dementia in patients with stroke. (20)

Changes in the brain

Vascular dementia is related to both ischaemic and non-ischaemic changes in the brain. (4,5,13,14) The ischaemic lesions include arterial territorial infarct, distal field (watershed) infarct, lacunar infarct, ischaemic white-matter lesions, and incomplete ischaemic injury. Incomplete ischaemic injury incorporates laminar necrosis, focal gliosis, granular atrophy, and incomplete white-matter infarction. (21,22) In addition, both focal (around the ischaemic lesion) and remote (disconnection, diaschisis) functional ischaemic changes relate to vascular dementia, and the volume of functionally inactive tissue exceeds that of focal ischaemic lesions in vascular dementia. (23) Limitation in current clinical methods have hampered the detection of both incomplete ischaemic injury and functional ischaemic changes related to vascular dementia. Atrophy is the non-ischaemic factor related to vascular dementia. However, there are no methods to distinguish between ischaemic and degenerative causes of atrophy.

Brain imaging findings

Work on the relationship between brain lesions and cognition in vascular dementia has used varying definitions and measures of cognitive impairment, varying techniques to reveal brain changes, and varying criteria for the selection of patients. (17)

CT and magnetic resonance imaging (MRI) studies on vascular dementia have shown that bilateral ischaemic lesions are important. (4,5,7,17) Some studies emphasize deep infarcts in the frontal and limbic areas, while others report cortical lesions especially in the temporal and parietal areas. There is disagreement about the number and volume of the infarcts, as well as the extent and location of atrophy. Diffuse and extensive white-matter lesions have been suggested as an important factor leading to functional disconnection of cortical brain areas. Some general conclusions on brain lesions in vascular dementia may be drawn.

  1. There is no single pathological feature, but a combination of infarcts, ischaemic white-matter lesions of varying size and type, and atrophy of varying degree and site.
  2. Infarcts associated with vascular dementia tend to be bilateral, multiple (more than two), and located in the dominant hemisphere and in the limbic structures (frontolimbic or prefrontal-subcortical and medial-limbic or medial-hippocampal circuits).
  3. White-matter lesions on CT or magnetic resonance imaging ( MRI) associated with vascular dementia are extensive, extending in periventricular white matter, and confluent to extending in the deep white matter.
  4. It is doubtful whether a single small lesion on imaging can be accepted as evidence for vascular dementia.
  5. Absence of cerebrovascular lesions on CT or MRI is contrary to a diagnosis of vascular dementia.


To what extent pathological changes in the brain cause, compound, or only coexist with the vascular dementia syndrome is still not known precisely. The vascular changes in the brain can be the main cause of cognitive impairment (as assumed in vascular dementia (24,25)), they can contribute to the clinical picture of other dementia syndromes including Alzheimer's disease, (7,26) or they may be coincidental. It is not certain which are the critical changes in the brain leading to the clinical picture of vascular dementia. the syndrome has been related to the volume of brain infarcts (with a critical threshold), the number of infarcts, the site of infarcts (bilateral, in strategic cortical or subcortical, or affecting white matter), to other ischaemic factors (incomplete ischaemic injury, delayed neuronal death, functional changes), to the atrophic changes (origin, location, extent), and finally to the additive effects of other pathologies (Alzheimer's disease, Lewy body dementia, frontal lobe dementias). But it is uncertain which type, extent, side, site, and tempo of vascular lesions in the brain, and which combinaton with other pathologies, relate to vascular dementia. (4,5 and 6,13)

Classification and clinical criteria


Vascular dementia has been divided into subtypes on the basis of clinical, radiological, and neuropathological features. It is uncertain whether these subtypes are distinct disorders, with separate pathological and clinical features, and responses to therapy. (27) If homogenous subtypes could be identified the comparability of research studies would be greater and multicentre studies easier. (28)

The subtypes of vascular dementia included in most classifications include multi-infarct dementia (cortical lesions), small-vessel dementia (subcortical deep lesions), and strategic infarct dementia. (12,14,27,29,30 and 31) Many include also hypoperfusion dementia. (12,14,30,33) Further suggested subtypes include haemorrhagic dementia, hereditary vascular dementia, and combined or mixed dementia (Alzheimer's disease with cerebrovascular disease).

DSM-IV (34) does not specify subtypes. ICD-10 (35) includes six subtypes (acute onset, multi-infarct, subcortical, mixed cortical and subcortical, other, and unspecified). The NINDS-AIREN criteria (30) include, without detailed description, cortical vascular dementia, subcortical vascular dementia, Binswanger's disease, and thalamic dementia.

Main subtypes

Multi-infarct dementia or cortical vascular dementia, and small-vessel dementia or subcortical vascular dementia are the two common subtypes, although their frequencies vary in different series. (12,14,31)

Cortical vascular dementia relates to large-vessel disease, cardiac embolic events, and hypoperfusion. Infarcts are predominantly in the cortical and corticosubcortical arterial territories, and their distal fields (watershed). Typical clinical features are lateralized sensimotor changes and the abrupt onset of cognitive impairment and aphasia. (31) A combination of different cortical neuropsychological syndromes has been suggested to occur in cortical vascular dementia. (36)

Subcortical vascular dementia, or small-vessel dementia, incorporates the entities ‘lacunar state' and ‘Binswanger's disease'. It relates to small-vessel disease and hypoperfusion, with predominately lacunar infarcts, focal and diffuse ischaemic white-matter lesions, and incomplete ischaemic injury. (31,36,37) Clinically, small-vessel dementia is characterized by pure motor hemiparesis, bulbar signs, dysarthria, depression, and emotional lability, and especially deficits in executive functioning. (36,37,38 and 39)

Clinical criteria

Since the 1970s several clinical criteria for vascular dementia have been published. (11,40,41) The most widely used include those in DSM-IV, (34) ICD-10, (35) and NINDS-AIREN. (30)

The two cardinal elements of any clinical criteria for vascular dementia are the definition of the cognitive syndrome (42) and the definition of the cause. (11,41,43) All clinical criteria are consensus criteria, derived neither from prospective community-based studies on vascular factors affecting the cognition, nor on detailed natural histories. (28,30,40,41) All these criteria are based on the concept of ischaemic infarcts. They are designed to have high specificity, but have been poorly validated. (40,44) An important consequence of the different definitions of the dementia syndrome, (9,42) and the vascular cause, (10,11) is that the different diagnostic criteria identify different populations.

The DSM-IV definition of vascular dementia requires focal neurological signs and symptoms or laboratory evidence of focal neurological damage clinically judged to be related to the disturbance. (34) The course is specified by sudden cognitive and functional losses. The DSM-IV criteria do not detail brain imaging requirements. The DSM-IV definition of vascular dementia is reasonably broad and lacks detailed clinical and radiological guidelines The ICD-10 criteria (35) require unequal distribution of cognitive deficits, focal signs as evidence of focal brain damage, and significant cerebrovascular disease judged to be aetiologically related to the dementia. The criteria do not detail brain imaging requirements.

The ICD-10 criteria specify six subtypes of vascular dementia. The ICD-10 criteria for vascular dementia have been shown to be highly selective and only some of those fulfilling the general criteria for ICD-10 vascular dementia can be classified into one of the subtypes. (11,43) The shortcoming of these criteria include lack of detailed guidelines (e.g. of unequal cognitive deficits and changes on neuroimaging), lack of aetiological criteria, and heterogeneity. (11,43) 

The NINDS-AIREN research criteria for vascular dementia (30) include a dementia syndrome, cerebrovascular disease, and a relationship between these. Cerebrovascular disease is defined by the presence of focal neurological lesions and brain imaging evidence of ischaemic changes in the brain. A relationship between dementia and cerebrovascular disorder is inferred from the onset of dementia within 3 months following a recognized stroke, or on abrupt deterioration in cognitive functions, or fluctuating stepwise progression of cognitive deficits. The criteria include a list of features consistent with the diagnosis, as well as a list of features that make the diagnosis uncertain or unlikely. Also, different levels of certainty of the clinical diagnosis (probable, possible, definite) are included.

The NINDS-AIREN criteria recognize heterogeneity (45) of the syndrome and variability of the clinical course in vascular dementia, and highlight detection of ischaemic lesions and a relationship between lesion and cognition, as well as stroke and dementia onset.

The NINDS-AIREN criteria are currently most widely used in clinical drug trials on vascular dementia. In a neuropathological series, sensitivity of the NINDS-AIREN criteria was 58 per cent and specificity 80 per cent. (47) The criteria successfully excluded Alzheimer's disease in 91 per cent of cases, and the proportion of combined cases misclassified as probable vascular dementia was 29 per cent. (47) The inter-rater reliability of the NINDS-AIREN criteria is moderate to substantial (k = 0.46–0.72). (48) These three sets of criteria for vascular dementia are not interchangeable; they identify different numbers and clusters of patients. The DSM-IV criteria are less restrictive than the ICD-10 and NINDS-AIREN criteria. (11,46)

Clinical features

Cognitive syndrome

The cognitive syndrome of vascular dementia is characterized by memory deficit, dysexecutive syndrome, slowed information processing, and mood and personality changes. These features are found especially among patients with subcortical lesions. Patients with cortical lesions often have additional cortical neuropsychological syndromes. (36)

The memory deficit in vascular dementia is often less severe than in Alzheimer's disease. It is characterized by impaired recall, relatively intact recognition, and more benefit from cues. (49) The dysexecutive syndrome in vascular dementia includes impairment in goal formulation, initiation, planning, organizing, sequencing, executing, set-sifting and set-maintenance, as well as in abstracting. (12,36,49) The dysexecutive syndrome in vascular dementia relates to lesions affecting the prefrontal subcortical circuit including prefrontal cortex, caudate, pallidum, thalamus, and the thalamocortical circuit (capsular genu, anterior capsule, anterior centrum semiovale, and anterior corona radiata). (50) Typically, personality and insight are relatively preserved in mild and moderate cases of vascular dementia.

Features that make the diagnosis of vascular dementia disease uncertain or unlikely include early and progressive worsening of memory, and other cognitive cortical deficits in the absence of corresponding focal lesions on brain imaging. (30)

Neurological findings

Frequent neurological findings indicating focal brain lesion early in the course of vascular dementia include mild motor or sensory deficits, decreased co-ordination, brisk tendon reflexes, Babinski's sign, visual field loss, bulbar signs including dysarthria and dysphagia, extrapyramidal signs (mainly rigidity and akinesia), disordered gait (hemiplegic, apraxic–ataxic, or small-stepped), unsteadiness, unprovoked falls, and urinary frequency and urgency. (30,31,37,38 and 39) Features that make the diagnosis of vascular dementia uncertain or unlikely include absence of focal neurological signs, other than cognitive disturbance. (30)

In cortical vascular dementia, typical clinical features are lateralized sensorimotor changes and abrupt onset of cognitive impairment and aphasia, and in subcortical vascular dementia disease pure motor hemiparesis, bulbar signs, and dysarthria. (31)

Behavioural and psychological symptoms of dementia

Depression, anxiety, emotional lability and incontinence, and other psychiatric symptoms are frequent in vascular dementia. Depression, abulia, emotional incontinence, and psychomotor retardation are especially frequent in subcortical vascular dementia disease. (12,36)

Ischaemic scores

Cardinal features of vascular dementia disease are incorporated in the Hachinski Ischaemia Score (Table 1) (51). In a recent neuropathological series, stepwise deterioration (odds ratio, 6.0), fluctuating course (odds ratio, 7.6), history of hypertension (odds ratio, 4.3), history of stroke (odds ratio, 4.3), and focal neurological symptoms (odds ratio, 4.4) differentiated patients with definite vascular dementia from those with definite Alzheimer's disease. (52) Nocturnal confusion and depression did not discriminate. However, the ischaemia score was unable to differentiate the Alzheimer's disease patients with cerebrovascular disease from those with vascular dementia.

Table 1 Hachinski Ischaemia Score

Purpose: The Hachinski Ischaemic Score (HIS) represents a brief clinical tool helpful in the “bedside” differentiation of the commonest dementia types, Dementia of Alzheimer’s Type (DAT) and Vascular Dememntia (VaD). It’s utility has been validated by meta-analysis in pathologically verified patients with dementia. A cut-off score ≤ 4 for DAT and ≥ 7 for VaD has a sensitivity of 89% and a specificity of 89% (Moroney 1997). It is not useful in determinations between mixed dementia and other dementia types.

Item No.




Abrupt onset



Stepwise deterioration



Fluctuating course



Nocturnal confusion



Preservation of personality






Somatic complaints



Emotional incontinence



History of hypertension



History of stroke



Associated atherosclerosis



Focal neurological symptoms



Focal neurological signs


HIS items distinguishing VaD from DAT were stepwise deterioration (odds ratio (OR), 6.06), fluctuating course (OR, 7.60), hypertension (OR, 4.30), history of stroke (OR, 4.30) and focal neurological symptoms (OR, 4.40). Reference Moroney, J.T., Meta-analysis of the Hachinski Ischaemic Score in pathologically verified dementias. Neurology, 49, 1096 – 1105.

Course and prognosis

Traditionally, vascular dementia has been characterized by a relative abrupt onset (days to weeks), a stepwise deterioration (some recovery after worsening), and fluctuating course (e.g. differences between days) of cognitive functions. These features are seen in patients with repeated lesions affecting cortical and corticosubcortical brain structures, i.e. large-vessel multi-infarct vascular dementia, and with watershed infarcts related to haemodynamic problems. However, in patients with small-vessel dementia, i.e. subcortical vascular dementia, the onset is more insidious and course more slowly progressive. (28,30,37,53) The mean duration of vascular dementia is around 5 years. (2) In most studies survival is less than for the general population or those with Alzheimer's disease. (54,55) Surprisingly little is known about the rate and pattern of cognitive decline, either overall or among different subgroups of vascular dementia. (56) This underlines the lack of studies detailing the natural history of vascular dementia.

Diagnosis and differential diagnosis

The clinical evaluation of patients with memory impairment has two stages, the symptomatic diagnosis, i.e. evaluation of the type and extent of cognitive impairment, and the aetiological diagnosis, i.e. evaluation of vascular cause(s) and related factors. The symptomatic categories other than dementia include delirium, circumscribed neuropsychological syndromes (e.g. aphasia) and functional psychiatric disorders (e.g. depression). (44) Stages of aetiological diagnosis include diagnosis of the specific causes, especially the potentially treatable conditions, evaluation of secondary factors able to affect the cognitive functioning, and more detailed differentiation between specific causes, especially that between vascular dementia disease and Alzheimer's disease.

Clinical evaluation

The cornerstone in the evaluation of a patient with suspected vascular dementia is detailed clinical and neurological history and examination, including interview of a close informant. Assessment of social functions, activities of daily living, as well as psychiatric and behavioural symptoms, is part of the basic evaluation. These patients are challenging and enough time should be allocated time for the consultation, often 40 to 60 min.

Mental status examination

Bedside mental status examination includes the Mini-Mental State Examination. (57) However, this has limitations as it emphasizes language, does not include timed elements and the recognition portion of the memory tests, is insensitive to mild deficits, and is influenced by education and age. Other proposed screening instruments for vascular dementia include a ten-word memory test with delayed recall, cube drawing test for copy, verbal fluency test (number of animals named in 1 min), Luria's alternating hand sequence, or finger rings and letter cancellation test (neglect). (30)

Frequently a more detailed neuropsychological test is needed. It should cover the main cognitive domains including memory functions (short- and long-term memory), abstract thinking, judgement, aphasia, apraxia, agnosia, orientation, attention, executive functions, and speed of information processing. (42,58)

Brain imaging

Brain imaging should be performed at least once during the initial diagnostic workout. MRI is preferred because it has high sensitivity and the ability to demonstrate medial temporal lobe and basal forebrain areas. Depending on the criteria of vascular dementia used, focal brain infarcts have been revealed in 70 to 100 per cent, and more extensive white-matter lesions in 70 to 100 per cent of cases. (13,25,30,59,60)

Single-photon emission CT and positron-emission tomography may reveal patchy reduction of regional blood flow and metabolism, as well as decreased white-matter flow and metabolism. (61)

Other investigations

Chest X-ray, elelectrocardiography, and screening laboratory tests are part of the basic evaluation. (15,62,63) In selected cases extended laboratory investigations, analysis of the cerebrospinal fluid, and EEG are performed, as well as examinations of the extra- and intracranial arteries and detailed cardiological investigations. (15,62,63)

In vascular dementia EEG is more often normal than in Alzheimer's disease, and if abnormal more frequently suggests a focal abnormality. Abnormalities increase with more severe intellectual decline both in vascular dementia disease and Alzheimer's disease. (53)

At present there is no specific laboratory test for vascular dementia. Tests may reveal risk factors and concomitant disorders such as hyperlipidaemia, diabetes, and cardiac abnormality.(53) Apolipoprotein E4 is a established risk factor for Alzheimer's disease, but its relationship to vascular dementia has not been consistent. (64) Determination of apolipoprotein E status is currently not part of clinical evaluation in vascular dementia.

Differential diagnosis of vascular dementia disease

Alzheimer's disease

Typical Alzheimer's disease is characterized by insidious onset and slowly progressive intellectual deterioration, absence of symptoms and signs indicating focal brain damage, and absence of any other specific disease affecting the brain. (65) Alzheimer's disease has typical clinical stages ranging from early changes to profound dementia. (66,67)

When patients with vascular dementia have a clinical history, neurological examination, and brain imaging findings compatible with ischaemic changes of the brain, the differentiation from Alzheimer's disease can be made clinically. (25)

Diagnostic problems arise when Alzheimer's disease is combined with cerebrovascular disease. Difficult clinical problems include stroke unmasking Alzheimer's disease in patients with post-stroke dementia, insidious onset, and/or slow progressive course in vascular dementia patients, and cases where it is difficult to assess the role of white-matter lesions or of infarcts found on neuroimaging. This clinical challenge may be solved when a sensitive and specific ante-mortem marker for Alzheimer's disease is available. The distinction would be less difficult if there were more detailed knowledge of the sites, type, and extent of ischaemic brain changes critical for vascular dementia, and the extent and type of medial temporal lobe atrophy critical for Alzheimer's disease.

Other important conditions to be diffentiated from vascular dementia include normal pressure hydrocephalus, (68) white-matter lesions and dementia, (17,30) frontal lobe tumours and other intracranial masses, (15) Lewy body dementia, (69) frontotemporal dementia, (70) Parkinsons's disease and dementia, (71) progressive supranuclear palsy, (72) and multisystem atrophy. (73)


Vascular dementia is the second most common cause of dementia accounting for 10 to 50 per cent of cases, depending on the geographic location, patient population, and clinical methods used. (1,2) The prevalence of vascular dementia is from 1.2 to 4.2 per cent of persons aged 65 years and older, and the incidence is 6 to 12 cases per 1000 persons aged over 70 years per year. (2) The prevalence and the incidence of vascular dementia disease increases with increasing age, and men seem to have a higher prevalence of vascular dementia than women. Epidemiology of vascular dementia has been affected by variations in the definition of the disorder, the clinical criteria used, and the clinical methods applied. (18,74,75)

The frequency of vascular dementia disease has been higher than previously reported in recent series comprising older subjects. (10) Stroke and cerebrovascular disorders relate also to a high risk of cognitive impairment and dementia. (24,76) Finally, vascular factors such as stroke and white-matter lesions have a clinical effect on Alzheimer's disease. (26) Thus, vascular factors may even be the leading cause of cognitive impairment worldwide. (77)


The objectives of targeted treatment of vascular dementia include symptomatic improvement of core symptoms (e.g. cognitive, behavioural), slowing progression of the disorder, and treatment of secondary factors affecting cognition (e.g. depression, anxiety, agitation).

A number of drugs have been studied in the symptomatic treatment of vascular dementia including cerebro- and vasoactive drugs, nootropics, and some calcium antagonists, but largely these studies have shown negative results. (78) Studies on symptomatic improvement in vascular dementia have mostly had small numbers, short treatment periods, variations in diagnostic criteria and tools, mixed populations, and have had variation in clinical endpoints applied.

Recently nimodipine, (79) memantine, (80) and propentofylline (81) have raised expectations for a symptomatic treatment of vascular dementia. A number of phase 3 double-blind randomized placebo-controlled trials in patients with vascular dementia using these compounds are in progress. (82)

Possibilities for prevention

For primary prevention the target is the brain at risk of cerebrovascular disease and cognitive impairment. The methods relate to the treatment of putative risk factors of vascular dementia, and the promotion of potential protective factors. Risk factors include those related to cerebrovascular disorders and stroke, to vascular dementia, to post-stroke dementia, to white-matter lesions, and to cognitive impairment or dementia, and also those related to Alzheimer's disease. (8) The vascular risk factors include arterial hypertension, atrial fibrillation, myocardial infarction, coronary heart disease, diabetes, generalized atherosclerosis, lipid abnormalities, and smoking. The demographic factors include age and education. One putative protective factor is oestrogen. (83)

Knowledge of effects of primary prevention on these risk factors in populations free of cognitive impairment is still scant. (8,84) In a European study, treatment of mild systolic hypertension decreased the incidence of dementia. (85) Positive effects in primary prevention of stroke support the idea that action on vascular risk factors could reduce the numbers of patients with vascular dementia.

For secondary prevention the target is the brain already affected by cerebrovascular disease and at risk of vascular dementia. Actions include diagnosis and treatment of acute stroke in order to limit the extent of ischaemic brain changes, prevention of recurrence of stroke, and treatment of risk factors. Treatment is guided by the aetiology of cerebrovascular disorder such as large artery disease (e.g. aspirin, dipyridamole, carotid endarterectomy), cardiac embolic events (e.g. anticoagulation, aspirin), small-vessel disease (e.g. antiplatelet therapy), and haemodynamic mechanisms (e.g. control of hypotension and cardiac arrhythmias).(15,29,44) Hypoxic ischaemic events (cardiac arrhythmias, congestive heart failure, myocardial infarction, seizures, pneumonia) are an important risk factor for incident dementia in patients with stroke and should be taken into account in the secondary prevention of vascular dementia. (20)

Detailed knowledge of the effects of secondary prevention of vascular dementia is lacking. In a small series of patients with established vascular dementia, control of high arterial blood pressure, (86) cessation of smoking, (86) and use of aspirin (87) improved or stabilized cognition. It has been suggested that lowering of plasma viscosity could also have an effect in vascular dementia. (88) The absence of progressive cognitive decline in patients receiving placebo in treatment trials of vascular dementia may also reflect an effect of intensified risk factor control. (81) 


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