Fortschr Neurol Psychiatr 2013; 81(5): 250-259
DOI: 10.1055/s-0033-1335253
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Schizophrenie – eine milde Enzephalitis?

Schizophrenia – a Mild Encephalitis?
K. Bechter
Further Information

Publication History

Publication Date:
29 April 2013 (online)

Zusammenfassung

Die Milde-Enzephalitis (ME)-Hypothese beschreibt eine Subgruppe schwerer psychiatrischer Erkrankungen, insbesondere eine Subgruppe von Schizophrenien, bei denen Kern der Pathogenese eine geringfügige Neuroinflammation darstellt. Low Level Neuroinflammation wird in der experimentellen Neuroimmunologie zunehmend beschrieben und kann prinzipiell verschiedenartige Psychopathologien erklären. Epidemiologie und Krankheitsverlauf von Schizophrenien sind gut kompatibel mit der ME-Hypothese, was bedeuten könnte, dass eine relativ große Subgruppe mit ME assoziiert ist. Zum ME-Modell gehören folgende wesentliche Bedingungsfaktoren: Gene, Umweltfaktoren (hierbei insbesondere infektiöse Erreger) und Immunsystem. Die Typizität der beim Individuum auftretenden Symptomatik mag wesentlich auf anderen Bedingungsfaktoren, z. B. präexistierenden Vulnerabilitäten beruhen. Die erste Large Scale Epidemiological Study der Psychiatrie identifizierte schwere Infektionskrankheiten und Autoimmunkrankheiten, welche im Laufe des Lebens auftreten, als Risikofaktoren. Dies und klinische Befunde unterstützen zunehmend die ME-Hypothese, z. B. aktivierte Monozyten oder Proteomveränderungen im Blut und diskrete Liquorpathologien in über 60 % therapieresistenter schizophrener Psychosen oder aktivierte Mikroglia und Dyskonnektivität in bildgebenden Verfahren.

Abstract

The mild encephalitis (ME) hypothesis describes a subgroup of severe psychiatric disorders, with a focus on a subgroup of schizophrenias, in which low-level neuroinflammation (LLNI) represents the core in pathogenesis. LLNI is increasingly recognised in experimental neuroimmunology and is in principle able to explain various types of psychopathology. Epidemiology and course of schizophrenia are well compatible with the ME hypothesis, indirectly indicating that the ME subgroup may be rather large. With the ME model connected is a set of three contributing factors: genes, environment (especially infectious agents) and the immune system. The type of psychopathology observed in the individual case may heavily depend upon other conditions, e. g. pre-existing vulnerabilities. The first large-scale epidemiological study in psychiatry identified two factors during lifetime, severe infectious diseases and autoimmune diseases, as risk factors. This and clinical findings more and more support the ME hypothesis, e. g., activated monocytes or proteome changes in blood and slight CSF pathologies in more than 60 % of therapy-resistant schizophrenia, or activated microglia and dysconnectivity in neuroimaging.

 
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