Zusammenfassung
Unterschieden werden die durch Erregertoxine vermittelten Syndrome, bei denen nicht die Erreger selbst in das ZNS eindringen (z.B. Legionellose, EHEC), von den neuro-invasiven infektiösen Prozessen, bei denen Keime oder Prionen im ZNS präsent sind und replizieren. Dabei können die entzündlichen Gewebereaktionen sehr gering ausfallen, z.B. bei Immun-schwäche und progressiver multifokaler Leukenzephalopathie durch das JC-Virus. So ist die Grenze zu den Enzephalitiden fließend, da Abräumreaktionen dominieren und Mikroglia-aktivierungen in ähnlicher Weise auch bei metabolischen Enzephalopathien (septisch, hepatisch, urämisch) zu finden sind. Die Creutzfeldt-Jakob-Erkrankung (CJD) weist trotz Ausbreitung pathologisch veränderter, sich virusartig verhaltender Proteine (Prione) keine entzündlichen Reaktionen auf. Fragen der Infektiosität, der Diagnostik und Therapiemöglich-keiten werden im Hinblick auf die Laborbefunde, Neurophysiologie und Bildgebung bespro-chen. Typische Komponenten des zerebralen Allgemeinsyndroms dieser Enzephalopathien sind Krampfanfälle und Myoklonien, die aber weder früh noch obligat auftreten müssen und einige bildgebende und neurophysiologische Befunde sind pathognomonisch (EEG).
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Friese, M., Gerloff, C., Weber, T. (2013). Enzelphalopathien bei Infektionserkrankungen . In: Hansen, HC. (eds) Bewusstseinsstörungen und Enzephalopathien. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-36915-5_21
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