Subcortical ischaemic vascular dementia

doi:10.1016/S1474-4422(02)00190-4

The Lancet Neurology

Volume 1, Issue 7, November 2002, Pages 426-436

https://doi.org/10.1016/S1474-4422(02)00190-4 Get rights and content

Summary

Vascular dementia is the second most common type of dementia. The subcortical ischaemic form (SIVD) frequently causes cognitive impairment and dementia in elderly people. SIVD results from small-vessel disease, which produces either arteriolar occlusion and lacunes or widespread incomplete infarction of white matter due to critical stenosis of medullary arterioles and hypoperfusion (Binswanger's disease). Symptoms include motor and cognitive dysexecutive slowing, forgetfulness, dysarthria, mood changes, urinary symptoms, and short-stepped gait. These manifestations probably result from ischaemic interruption of parallel circuits from the prefrontal cortex to the basal ganglia and corresponding thalamocortical connections. Brain imaging (computed tomography and magnetic resonance imaging) is essential for correct diagnosis. The main risk factors are advanced age, hypertension, diabetes, smoking, hyperhomocysteinaemia, hyperfibrinogenaemia, and other conditions that can cause brain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, and orthostatic hypotension. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) and some forms of cerebral amyloid angiopathy have a genetic basis. Treatment is symptomatic and prevention requires control of treatable risk factors.

Section snippets

Definitions and terminology

The term subcortical refers to lesions, and their manifestations, that predominantly involve the basal ganglia, cerebral white matter, and the brainstem (as opposed to cortical dementias). Dementia in SIVD is caused by ischaemic injury, which includes both complete infarction (lacunar infarcts and microinfarcts) and incomplete infarction of deep cerebral white matter. Lacunar infarcts or lacunes are small cavitated ischaemic infarcts of less than 15 mm in diameter. They are typically located in

Magnitude of the problem

In clinical studies, the proportion of vascular dementia caused by small-vessel disease ranges from 36% to 67%.⁴ Lacunar infarcts are found in 10% to 31% of symptomatic strokes, with a population-based prevalence of 13·4 per 100 000 in white people,⁵ although the prevalence is higher in oriental (Japanese and Korean), hispanic, and black populations and mixed ethnic groups.4, 6, 7

A significant proportion of subcortical lacunes are clinically silent.8, 9 In the population-based Cardiovascular

Pathophysiology of ischaemic brain injury

Figure 1 shows the two main pathophysiological pathways involved in SIVD. In the first, occlusion of the arteriolar lumen due to arteriolosclerosis leads to the formation of lacunes, which results in a lacunar state (état lacunaire). In the second, critical stenosis and hypoperfusion of multiple medullary arterioles causes widespread incomplete infarction of deep white matter²² with a clinical picture of Binswanger's disease.²³ In practice, the two clinical pathways can overlap; lacunes and

Determinants of ischaemia

Ischaemia develops when tissue perfusion and the supply of essential nutrients such as oxygen and glucose become inadequate for the support of cell metabolism. The balance between supply and demand is influenced by differences in the oxygen and glucose requirements of different brain cells, regional differences in cerebral blood flow (CBF), and duration of hypoperfusion. Energy requirements are considered higher for neurons than for glia (neurons> oligodendrocytes>astrocytes>endothelial cells).

Incomplete infarction

Below a critical perfusion threshold, selective cell loss may occur without pronounced infarction or cystic necrosis. Selective neuronal loss occurs in the penumbra surrounding acute infarcts,²⁵ whereas selective loss of oligodendrocytes, myelin, and axons occurs in deep white matter of patients with severe stenosis of medullary arterioles.27, 28 This selective loss of tissue elements due to ischaemia is known as incomplete infarction22, 25, 29 and may occur when systemic blood pressure drops

Haemorheological factors

As summarised in panel 2, oxygen delivery to tissues depends on blood flow and the concentration of red blood cells. A high concentration of red blood cells and raised plasma viscosity are important in the pathogenesis of Binswanger's disease.³⁶ Other clinically relevant haemorheological factors in SIVD include hyperglycaemia, hyper-fibrinogenaemia, polycytaemia, hyperlipidaemia, and hyperviscosity.36, 37

Decreased autoregulatory reserve in SIVD

Under normal conditions, autoregulatory mechanisms compensate for variations in mean arterial pressure of 60–150 mm Hg. In patients with chronic hypertension, the curve is shifted upwards—ie, these individuals are unable to compensate for rapid decreases in blood pressure.38, 39 In patients with Binswanger's disease, the range is narrowed and vasodilator capacity is impaired in response to carbon dioxide or acetazolamide.40, 41 Patients with small-artery disease and compromised autoregulatory

Increased oxygen extraction fraction (OEF) in SIVD

Increased OEF is a marker of ongoing ischaemia and pending infarction. By use of ¹⁵O-PET, Yao and colleagues⁴² found that patients with Binswanger's dementia had reduced CBF and cerebral metabolic rate for oxygen (CMRO₂; 20–30% lower than normal in grey matter and 30–40% lower in white matter). Non-demented patients with Binswanger's disease had no significant changes in CBF and CMRO₂ in grey matter; however, a 30% reduction in CBF and a 130% increase in OEF were found in white matter. In a

Relationship between ischaemia and dementia

Severity of dementia in SIVD correlates more strongly with the degree of hippocampal and cerebral atrophy than with severity of white-matter hyperintensities.44, 45, 46 Nonetheless, cerebral atrophy and white-matter lesions are related. Quantitative MRI reveals widespread atrophy in SIVD that is not solely due to focal infarction. Possible causes include concomitant Alzheimer's disease, deafferentation or metabolic idling, and hypoperfusion.

Microangiopathy

SIVD has been called small-vessel dementia because changes in cerebral microcirculation have a central role in its pathogenesis.²⁹ Microangiopathy is mainly related to ageing,⁴⁷ arterial hypertension,²⁹ and diabetes mellitus⁴⁸ but other conditions, such as hyper-homocysteinaemia,⁴⁹ may also be important.

Clinical features

The clinical manifestations of SIVD include psychomotor slowness due to loss of control of executive cognitive functioning, forgetfulness, and changes in speech, affect, and mood.⁹¹ Symptoms are caused by the interruption of prefrontal-subcortical circuits by ischaemic lesions.92, 93 These circuits are known to be involved in executive control of working memory, organisation, language, mood, regulation of attention, constructional skills, motivation, and socially responsive behaviours.94, 95, 96

Populations at risk

Clinicians should suspect SIVD in patients who have behavioural changes suggestive of executive dysfunction, particularly in elderly patients with a history of hypertension, diabetes, cigarette smoking, hyperfibrinogenaemia, or obstructive sleep apnoea.¹¹³ The presence of congestive heart failure,114, 115 cardiac arrhythmias,¹¹⁶ or orthostatic hypotension¹¹⁷ is also important in elderly patients. Hypoperfusion due to congestive heart failure is increasingly recognised as a significant risk

Alzheimer's disease and vascular dementia

The clinical differentiation of vascular dementia from Alzheimer's disease with cerebrovascular disease can be difficult.¹³⁴ Over 60% of older patients with Alzheimer's disease present with incomplete white-matter infarction²² and patients with anterior-choroidal-artery stroke may meet criteria for Alzheimer's disease.¹³⁵ The ischaemic score may provide additional elements for the diagnosis of the multi-infarct form of vascular dementia.¹³⁶ Stepwise deterioration, fluctuating course, history of

Diagnostic criteria

Current criteria for vascular dementia are not interchangeable and their sensitivity and specificity are variable. Furthermore, none of them can distinguish mixed forms of dementia, such as Alzheimer's disease plus cerebrovascular disease, and prospective validation is missing. Panel 3 summarises the proposed clinical criteria for the diagnosis of patients with SIVD143 based on a modification of the National Institute of Neurological Disorders and Stroke and the Assocation Internationale pour

Prognosis, prevention, and treatment

Older age, fewer years of education, lacunar strokes, larger white-matter lesions, and possibly race are all risk factors for the development of dementia after ischaemic stroke. In patients with lacunar stroke, the presence of extensive white-matter lesions is a poor prognostic sign and increases the risk of recurrent stroke (odds ratio=6·4), dementia (odds ratio=11·1), and death (odds ratio=4·6).¹⁰ Prospective, community-based studies and short-term clinical trials indicate that control of

Conclusion

The subcortical form of vascular dementia is one of the commonest causes of cognitive decline in elderly people. SIVD is commonly not recognised and remains undiagnosed, but it accounts for a significant number of cases of dementia, recurrent falls in old age (and subsequent hip fractures), and incontinence and results in many admissions to nursing homes. It is therefore a heavy burden on public health; better recognition of the disease is necessary for maximum benefit to be derived from

Search strategy and selection criteria

Articles were identified by searches of Medline, Current Contents, and from relevant books and the authors' extensive files. The search terms “vascular dementia”, “subcortical dementia”, “vascular cognitive impairment”, “lacunar stroke”, and “Binswanger's disease” were used. Recent articles were preferentially selected.

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ReviewSubcortical ischaemic vascular dementia

Summary

Section snippets

Definitions and terminology

Magnitude of the problem

Pathophysiology of ischaemic brain injury

Determinants of ischaemia

Incomplete infarction

Haemorheological factors

Decreased autoregulatory reserve in SIVD

Increased oxygen extraction fraction (OEF) in SIVD

Relationship between ischaemia and dementia

Microangiopathy

Clinical features

Populations at risk

Alzheimer's disease and vascular dementia

Diagnostic criteria

Prognosis, prevention, and treatment

Conclusion

Search strategy and selection criteria

Clin Cornerstone

J Neurol Sci

Brain Res

J Neurosci Methods

Brain Res Bull

J Neurol Sci

Neurobiol Aging

Lancet

Lancet

J Psychiatr Res

The incidence of vascular dementia in Canada: a comparison with Europe and East Asia.

Neuroepidemiology

The neuropathology of vascular dementia

Companion to clinical neurology.

Epidemiological characteristics of lacunar infarcts in a population.

Stroke

Southern Buenos Aires stroke project.

Acta Neurol Scand

Yonsei Stroke Registry: analysis of 1000 patients with acute cerebral infarctions.

Cerebrovasc Dis

Lacunes: small deep cerebral infarcts.

Neurology

Silent cerebral infarction in a community-based autopsy series in Japan: the Hisayama Study.

Stroke

Lacunar infarcts defined by magnetic resonance imaging of 3660 elderly people: the Cardiovascular Health Study.

Arch Neurol

Prevalence of silent stroke in patients presenting with initial stroke: the Framingham Study.

Stroke

Natural history of lacunar syndromes: contribution of the Dijon registry of cerebrovascular complications.

Rev Neurol (Paris)

Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study.

Stroke

Clinical correlates of white matter findings on cranial magnetic resonance imaging of 3301 elderly people: the Cardiovascular Health Study.

Stroke

Cerebral white matter lesions, vascular risk factors, and cognitive function in a population-based study: the Rotterdam Study.

Neurology

White matter hyperintensities on the MRI in the neurologically non-demented elderly: analysis of cohorts of consecutive subjects aged 65 to 85 years living at home.

Stroke

Cerebral lesions on magnetic resonance imaging, heart disease, and vascular risk factors in subjects without stroke: a population-based study.

Stroke

The prevalence and severity of white matter lesions, their relationship with age, ethnicity, gender, and cardiovascular risk factors: the ARIC study.

Neuroepidemiology

From UBOs to Binswanger's disease: impact of magnetic resonance imaging on vascular dementia research.

Stroke

Cerebral white matter lesions and subjective cognitive dysfunction: the Rotterdam Scan Study.

Neurology

A population-based study on motor performance and white matter lesions in older women.

J Am Geriatr Soc

Correlations between histopathologic white matter changes and proton MR relaxation times in dementia.

Alzheimer Dis Assoc Disord

Senile dementia of the Binswanger type: a vascular form of dementia in the elderly.

JAMA

Neuropathological substrate of ischemic vascular dementia.

J Neuropathol Exp Neurol

Ischemic stroke and incomplete infarction.

Stroke

Cerebral white matter is highly vulnerable to ischemia.

Stroke

Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly.

J Am Geriatr Soc

Review
Subcortical ischaemic vascular dementia

Time dependency of the acetazolamide effect on cerebral hemodynamics in patients with chronic occlusive cerebral arteries: early steal phenomenon demonstrated by ¹⁵O-H₂O positron emission tomography.