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Aktuelle Neurologie 2002; 29(10): 483-489
DOI: 10.1055/s-2002-36013
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© Georg Thieme Verlag Stuttgart · New York

Aktuelles über die vaskulären Demenzen

Update on Vascular DementiasJ.  Diehl1 , A.  Kurz1
  • 1Klinik für Psychiatrie und Psychotherapie, Technische Universität München
Wir danken Frau Prof. Gräfin von Einsiedel, Neurologische Klinik der TU München, für die Überlassung der Aufnahmen
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Publication History

Publication Date:
09 December 2002 (online)

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Zusammenfassung

Die vaskulären Demenzen sind eine ätiologisch, pathogenetisch, histopathologisch und klinisch höchst heterogene Gruppe von Krankheiten. In der Mehrzahl der Fälle werden die kognitiven Leistungseinschränkungen nicht durch größere kortikale und subkortikale Territorial- und Grenzlinieninfarkte hervorgerufen (Multi-Infarkt-Demenz), sondern durch die Kombination aus subkortikalen Mikroinfarkten (Lakunen) und ausgedehnten ischämischen Marklagerveränderungen. Beide sind Ausdruck einer subkortikalen zerebralen Mikroangiopathie. Die subkortikalen Varianten der vaskulären Demenz sind psychopathologisch vor allem charakterisiert durch Einschränkungen der Exekutivfunktionen und Veränderungen der Persönlichkeit. Sie entsprechen also meist nicht dem klinischen Bild der Alzheimer-Krankheit. Andererseits zeigen sie häufig weder den plötzlichen Beginn noch die schrittweise Verschlechterung der Multi-Infarkt-Demenz. Zur Klärung der ursächlichen Verknüpfungen zwischen vaskulären Läsionen und kognitiven Leistungseinschränkungen haben Verfahren der funktionellen Bildgebung beigetragen. Sie weisen nach, dass die Unterbrechung von subkortiko-kortikalen Verbindungsbahnen und interkortikalen Assoziationsfasern eine wesentliche pathogenetische Rolle spielen. Das bisher äußerst unbefriedigende Repertoire an symptomatischen Behandlungsmöglichkeiten könnte sich in naher Zukunft erweitern. Positive Ergebnisse klinischer Prüfungen liegen für Galantamin, Donepezil und Memantine vor.

Abstract

The vascular dementias are a heterogeneous group of disorders in terms of aetiology, histopathology, pathogenetic mechanisms, and clinical appearance. In the majority of cases cognitive impairment is not caused by large cortical and subcortical territorial and watershed infarcts (multi-infarct dementia), but are due to a combination of subcortical microinfarcts (lacunes) and severe ischemic white matter changes, both indicating cerebral small-vessel disease. The subcortical variants of vascular dementia are clinically characterised by impairment of executive function and by changes in personality. Hence they are dissimilar to the clinical picture of Alzheimer's disease. On the other hand they often lack the abrupt onset and stepwise deterioration seen in multi-infarct dementia. Functional brain imaging has significantly contributed to unveiling the causal relationships between vascular lesions and cognitive deficits. It has been demonstrated that disruption of subcortico-cortical connections and of intercortical association pathways play a major pathogenetic role. The repertoire of symptomatic treatments for vascular dementias is extremely limited to date but may improve in the near future. Positive results are available from clinical trials with galantamine, donepezil, and memantine.

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Dr. Janine Diehl

Klinik für Psychiatrie und Psychotherapie · Technische Universität München

Möhlstraße 26

81675 München

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