Vaskuläre Demenzen
Martin
Dichgans,
Neurologische Klinik, Ludwig-Maximilians-Universität München
Vascular
Dementia (VaD) is the second most frequent cause of dementia following Alzheimers’ disease.
Mixed pathologies are common but the interaction between AD and vascular
pathology is not recognized by current diagnostic systems.
Diagnostic criteria for VaD vary and there is no uniform classification system
of VaD, which is heterogeneous both in terms of underlying vascular causes
and dementia mechanisms (e.g. strategic infarcts vs. multi-infarct dementia).
Early stages of vascular cognitive impairment (VCI) are still poorly defined.
The impact of ischemic lesions and cognition depends on multiple lesion variables
(location, volume, depth, type of lesion) and the interaction between single
lesions. Multimodal approaches are needed to explore these interactions and
the role of brain atrophy. Validation of imaging endpoints and other surrogate
markers for use in long term preventive trials remains another challenge. There
is reason to believe that aggressive treatment of elevated arterial blood pressure
will reduce the load of ischemic lesions and rate of cognitive decline. However,
trials in VCI are still in their infancy. CADASIL has emerged as a model for
pure subcortical ischemic vascular dementia (SIVD). A recent randomized trial
showed no treatment effect of donepezil on overall cognition as assessed by
the V-ADAS-cog (primary endpoint). However, significant improvements were noted
on various executive function tests which are typical for SIVD. These results
illustrate the importance of focusing on aetiological subgroups of VaD. They
further emphasize the need to develop targeted neuropsychological test batteries
for use in VCI. Recently proposed standards for identifying and describing
patients with VCI mark an important step toward a better understanding of VaD
and earlier stages of VCI.