Zusammenfassung
Die subkortikale vaskuläre Enzephalopathie (SVE) ist eine zunehmend häufiger diagnostizierte Erkrankung des höheren Lebensalters, die eine hohe gesundheitsökonomische Bedeutung hat. Dies liegt zum einen an einer fortschreitenden Behinderung und Immobilisierung durch Gang- und Posturalkontrollstörung sowie zum anderen an einem progredienten Demenzsyndrom mit kognitiver Verlangsamung, Initiativmangel und Vergesslichkeit. Eine valide klinische Diagnosestellung wurde erst durch die deutliche Verbesserung der zerebralen Bilddiagnostik in den 80er-Jahren möglich. Dies erklärt auch die bis vor kurzem verwirrende Vielfalt von unterschiedlichen Begriffen. Pathophysiologische Grundlage ist die zerebrale Mikroangiopathie, die zu lakunären Infarkten und diffusen ischämischen Läsionen der weißen Hirnsubstanz führt, die häufig in Kombination vorkommen. In ihrer Summe führen solche Läsionen zur Unterbrechung parallel geschalteter präfrontal-subkortikaler Schaltkreise, auf deren Intaktheit die physiologische psychomotorische Funktion beruht. Zur Diagnosestellung sind neuroradiologische bildgebende Verfahren (Computertomographie, Magnetresonanztomographie) essenziell. Die Prognose ist eher ungünstig. Mehrere Konsensusgespräche haben versucht, klinische und diagnostische Kriterien zu etablieren, auf deren Boden inzwischen erste therapeutische Optionen zur Verfügung stehen. Dieser Artikel soll das Syndrom der SVE klinisch beschreiben, ätiologische und pathophysiologische Mechanismen diskutieren und Therapiemöglichkeiten aufzeigen.
Abstract
Subcortical Vascular Encephalopathy (SVE) is an increasingly diagnosed disease with an enormous socio-economic impact. This is mainly due to a progressive disability with immobilisation because of gait- and postural disturbances and with a progressive subcortical vascular dementia which is composed of cognitive slowing, loss of initiative and forgetfulness. A valid diagnosis has become possible only through clear improvements in cerebral imaging techniques in the eighties. This explains why so many different and confusing terms exist to describe the syndrome. The pathophysiological basis is a cerebral microangiopathy leading to lacunar infarcts and to diffuse ischemic white matter lesions, often occurring side by side. Taken together, such lesions lead to an interruption of parallel functional prefrontal-subcortical circuits, which are essential for psychomotor function. Neuroradiological methods like computed tomography (CT) and magnetic resonance imaging (MRI) are essential for the diagnosis. The prognosis is rather unfavourable. Several consensus meetings have established clinical and diagnostic criteria, which can serve as a basis for therapeutical trials. This review wants to delineate diagnostic milestones, to discuss etiological and pathophysiological mechanisms, and to display therapeutical options.
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