The past decade has seen a renewed interest in
vascular dementia. The search for a causal relationship between a vascular event or a vascular cerebral lesion and
dementia has led to new classification schemes which no longer consider
vascular dementia a homogeneous entity but acknowledge the diversity of the clinical and morphological substrates of this syndrome. Deviation from the term "
multi-infarct dementia" is only one but many consequencies of these recent developments. Etiologically,
vascular dementia may result from
cerebral small vessel disease leading to extensive leucencephalopathy or lacunes or may be the consequence of strategically located
infarcts or multiple
infarcts in large vessel territories. It may also be the consequence of global cerebral hypoperfusion,
intracerebral hemorrhage or other mechanisms such as
vasculitis. There is no definitive medical or surgical treatment for
vascular dementia. Thus, it appears that
stroke prevention offers the most immediate and substantial
solution to reduce the morbidity and mortality. This is best substantiated for treatment of arterial
hypertension. Once
vascular dementia occurs control of vascular risk factors may be useful but this contention will require larger scale studies to provide more definite proof. A number of metabolically active drugs has been used for the treatment of
cognitive symptoms in
vascular dementia. Yet, the data are conflicting und the effects described modest at most. There is epidemiological evidence for a more than incidental co-existence between vascular and primary degenerative
dementia which suggests that
therapies found to be effective in
Alzheimer's disease may also prove beneficial at least in subgroups of
vascular dementia. Lately, this concept is tested by several studies on the efficacy of
acetylcholinesterase inhibitors in
vascular dementia.