Fortschr Neurol Psychiatr 2012; 80(11): 618-626
DOI: 10.1055/s-0032-1313218
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Zerebrale Amyloidangiopathie – ein Update

Cerebral Amyloid Angiopathy – An Update
M. Gahr
1   Klinik für Psychiatrie und Psychotherapie III, Universitätsklinikum Ulm
,
D. A. Nowak
2   Neurologische Fachklinik, Klinik Kipfenberg
,
B. J. Connemann
1   Klinik für Psychiatrie und Psychotherapie III, Universitätsklinikum Ulm
,
C. Schönfeldt-Lecuona
1   Klinik für Psychiatrie und Psychotherapie III, Universitätsklinikum Ulm
› Author Affiliations
Further Information

Publication History

Publication Date:
08 November 2012 (online)

Zusammenfassung

Die zerebrale Amyloidangiopathie (ZAA), welche am häufigsten sporadisch, jedoch auch hereditär vorkommen kann, gehört zu den Amyloidosen und ist durch die Deposition und Akkumulation von beta-Amyloid (Aβ) in kleineren arteriellen Gefäßen des Gehirns charakterisiert. Die Ablagerung von Aβ führt zu degenerativen Veränderungen im zerebralen Gefäßsystem (Gefäßwandverdickungen, Mikroaneurysmen, Lumeneinengung, Dissektion), welche die Entwicklung der häufigsten ZAA-assoziierten klinischen Manifestationen (spontane intrazerebrale Blutungen) begünstigen. Neben Hämorrhagien können auch zerebrale Ischämien, transiente neurologische Symptome, Leukenzephalopathie sowie kognitive Einschränkungen bis hin zur Demenz im Zusammenhang mit der ZAA auftreten. Die sichere Diagnose einer ZAA kann nur auf der Grundlage einer pathologischen Beurteilung erfolgen, wenngleich Befunde der zerebralen Bildgebung und klinische Symptome eine wahrscheinliche ZAA diagnostizieren lassen. Kausale Therapieoptionen bestehen gegenwärtig nicht. Obwohl die ZAA in das Spektrum der neurologischen Erkrankungen verortet wird, können psychiatrische Symptome auftreten. In der Übersichtsarbeit werden neben epidemiologischen, pathogenetischen, klinischen und diagnostischen Aspekten mögliche psychiatrische Implikationen diskutiert.

Abstract

Cerebral amyloid angiopathy (CAA) belongs to the group of amyloidoses and is characterised by the deposition and accumulation of beta-amyloid (Aβ) in small arterial vessels of the brain. Hereditary forms of CAA exist but sporadic CAA is much more frequent. Deposition of Aβ induces degenerative changes of the cerebral vascular system (thickening of the vessel wall, constriction of vascular lumen, microaneurysms, dissection) that trigger the development of the typical clinical presentation of CAA, that is spontaneous intracerebral haemorrhage. Apart from haemorrhages, also cerebral ischaemia, transient neurological symptoms, leukencephalopathy as well as cognitive decline and dementia can occur in association with CAA. The definite diagnosis of CAA is only possible by means of pathological examination, even though neuroimaging and clinical findings allow the diagnosis of a probable CAA. Currently, no specific causal therapy exists. Although CAA is located in the range of neurological diseases psychiatric symptoms might occur. In the review, we discuss epidemiological, pathogenetic, clinical and diagnostic aspects and possible psychiatric implications of CAA.

 
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