Vascular dementia

Vascular dementia (VaD) is common; it frequently co-exists with AD. Epidemiology

VaD usually starts between the ages of 60 and 70 but sometimes earlier. Men are affected slightly more often than women.


The cause is focal infarction of the brain due to haemorrhage, thrombosis, or embolism, usually associated with cerebral arteriosclerosis. There may be a single cerebral vascular accident, multiple small infarcts, or small vessel disease causing white matter damage. Most patients have hypertension, focal neurological signs, and evidence of arteriosclerosis in other organs.


Loss of memory, intellectual deterioration, and mood changes occur. Insight and personality are retained longer than in AD, and the continued insight may contribute to the depression that is often present. Deterioration is stepwise rather than gradual, as repeated small strokes or episodes of hypertensive encephalopa-thy occur and leave residual damage.

Prevention and treatment

Some cases might be prevented by control of hypertension in its early stages, and by attention to potential sources of emboli in the brain. Some improvement in the established condition may be achieved by treatment of very high blood pressure levels, cessation of smoking, and regular low-dose aspirin.


Average survival time is about 5 years; the usual causes of death are ischaemic heart disease and stroke.

Lewy body dementia Definition and neuropathology

Comparatively recently, in fact since the last edition of this book, Lewy body dementia (LBD) has been recognized as a distinct condition. This is a type of dementia in which Parkinsonian features are prominent. Conscious level and cognitive function tend to fluctuate; and visual illusions or hallucinations may occur, as may frank psychotic symptoms.

It has been recognized that Parkinson's disease can sometimes proceed to dementia. Patients with LBD seem to be on a continuum between pure Parkin-sonism, on the one hand, and dementia on the other hand.

Lewy bodies are oval structures that are in fact eosinophilic inclusion bodies within degenerating dopamine-bearing cells in the substantia nigra and related areas; they are the neuropathological basis of Parkinson's disease. The presence of such Lewy bodies (which are morphologically similar but distinct) in other areas of the brain appears at least partly to underlie the clinical syndrome of LBD.


It is not yet clear what proportion of dementia cases overall should be classified as LBD. Clearly, this would depend on how a case should be defined. It has, however, been suggested that it is the second commonest cause of dementia after AD.

Clinical features

LBD is marked by fluctuating cognitive performance and conscious level, Parkinsonism (in the majority of cases), and psychiatric symptoms including visual hallucinations.


Treatment is inherently difficult. Drugs used to help Parkinsonian features tend to exacerbate any psychotic symptoms present. Parkinsonian treatment should be reviewed and reduced if possible, beginning probably with any anticholinergics.

Conversely, antipsychotic drugs, if employed for psychotic symptoms -whether inherent or due to side-effects of anti-Parkinson drugs - will make Parkinsonian symptoms worse. Patients are often very sensitive to neuroleptics, both typical and atypical, and they should be avoided if at all possible. A difficult balance has to be struck.

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