The diagnosis of vascular dementia

Vascular dementia is under-researched, meaning less is known about effective therapeutic options.

MRI of patient with CADASIL, which is a hereditary cerebrovascular disorder (Photograph: SPL)
MRI of patient with CADASIL, which is a hereditary cerebrovascular disorder (Photograph: SPL)

An MRI report appears on your desk. It states that: 'Cortical atrophy is present, in keeping with the patient's age. In addition there are scattered deep white matter and periventricular hyperintensities, perhaps concentrated in the frontal regions. In view of the patient's age these are likely to be ischaemic in nature.'

What is the diagnosis - Alzheimer's disease (AD), vascular dementia, or a mixture of the two? The short answer is that a diagnosis of dementia cannot be made on a scan result. This result can only be used to support clinical findings.

Neuropathological changes
Among an elderly population such findings on neuroimaging are not unusual. A population-based study in Rotterdam showed that 24 per cent of people without dementia, aged 60 to 90 years, had one or more focal infarcts, with silent infarcts being five times more common than in those showing symptoms of dementia.1

Extensive deep white matter lesions were present in 14 per cent of people (mean age 62 years) in the Framingham offspring study. In themselves, these may not be causing dementia although people with white matter lesions are at higher risk.2

The Nun study showed that neuropathological changes of AD are not necessarily associated with dementia, but dementia was found to be more prevalent when comorbid stroke was present.3 Conversely, the presence of stroke without neuropathological changes of AD was only weakly associated with presence of dementia.

People developing dementia after a stroke frequently have pre-morbid mild cognitive impairment. Both vascular dementia and AD shorten life expectancy and although vascular dementia is traditionally associated with stepwise progression, recurring delirium can have the same effect in a patient with AD.

Cerebrovascular disease
Traditionally people have talked about AD and vascular dementia as two separate entities. Syndromes such as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) are genetically inherited, and an acute syndrome of vascular dementia is described in the NINDS-AIREN criteria,4 where there is a relationship between dementia and cerebrovascular disease, manifested or inferred by the presence of one or more of the following:

  • Onset of dementia within three months following a recognised stroke.
  • Abrupt deterioration in cognitive function.
  • Fluctuating, stepwise progression of cognitive deficits.

However, focal neurological symptoms and signs occur as a result of discrete infarcts, whereas a syndrome of headache, dizziness, nausea, balance problems, reduced step length with or without a wider gait base, falling, urinary frequency and urgency can all occur when cerebrovascular disease without infarct is present,5 although changes can be fairly extensive without any of these symptoms appearing.

Hypertension and cardiac failure are more common in this group than in the general population.

Pharmacological treatment
The blurring of the distinction between AD and cerebrovascular disease has clinical implications. Cholinesterase inhibitors are only licensed for the treatment of AD in the UK, yet our increasing understanding of neuropathological interactions makes finding 'pure' cases increasingly difficult.

Studies of 'mixed AD with cerebrovascular disease' do not discriminate those with peripheral symptoms of cerebrovascular disease from those without when describing response. In clinical practice, the more obvious peripheral symptoms are, the less likely a patient is to tolerate these drugs without increased side-effects.

Whether or not people with vascular dementia show an improved clinical response is controversial.

Vascular dementia remains an under-researched area by comparison with AD and as a consequence less is known about effective therapeutic interventions. Comorbid vascular risk factors are common in people with vascular dementia although these are also risk factors for AD.

Evidence for the treatment of individual vascular risk factors is limited when the patient has already progressed to dementia. No good evidence exists for the benefits of aspirin or statins in treating patients with established vascular dementia, but reduced decline was associated with perindopril and indapamide treatment of patients with mild impairment in whom stroke was present.6

Stroke increases the rate of decline in AD, therefore stroke prevention and reduction of vascular comorbidity is likely to lead to more stable physical health even if cognition is not improved. Intensive treatment of all vascular risk factors versus no treatment was found to reduce cognitive decline in an observational study of people with AD without cerebrovascular disease, though the effect size was modest.7

Behaviour changes
Behavioural complications are as common in vascular dementia as in AD. Particular caution is required when using antipsychotic drugs, which may be more toxic in vascular dementia.8

However, there is no reason to assume that non-pharmacological treatments and psychological interventions are less effective for people with vascular dementia than for those with AD, and these should continue to be provided where possible.

  • Dr Connelly is a consultant old age psychiatrist at Murray Royal Hospital, Perth, Scotland, and the current chairman of the Old Age Faculty of the Royal College of Psychiatrists.
  • The views expressed in the article are his own and not necessarily those of the Royal College of Psychiatrists.

1. Poels MMF, Arfan Ikram, Van der Lugt A, et al. Incidence of cerebral microbleeds in the general population. Stroke 2011; 42: 656-61.

2. Debette S, Markus HS. The clinical importance of white matter hyperintensities on brain magnetic resonance imaging. BMJ 2010; 341: c3666.

3. Snowdon DA, Greiner LH, Mortimer JA, et al. Brain infarction and the clinical expression of Alzheimer disease. The Nun study. JAMA 1997; 277: 813-7.

4. Roman GC, Tatemichi TK, Erkinjuntti T, et al. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology 1993; 43(2): 250-60.

5. Tarvonen-Schroder S, Roytta M, Raiha I, et al. Clinical features of leuko-araiosis. J Neurol Neurosurg Psychiatry 1996; 60(4): 431-6.

6. Tzourio C, Anderson C, Chapman N, et al. Effects of blood pressure lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease. Arch Intern Med 2003; 163(9): 1069-75.

7. Deschaintre Y, Richard F, Leys D, et al. Treatment of vascular risk factors is associated with slower decline in Alzheimer disease. Neurology 2009; 73 (9): 674-80.

8. Barnett MJ, Wehring H, Perry PJ. Comparison of risk of cerebrovascular events in an elderly VA population with dementia between antipsychotic and nonantipsychotic users. J Clin Psychopharmacol 2007; 27(6): 595-601.

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