Abstract

The Mild Encephalitis (ME) hypothesis describes a subgroup of low level neuroinflammation (LLNI) associated psychiatric disorders, LLNI representing the core of the underlying pathophysiology (Bechter, 2001). A model for ME was infections with the highly neurotropic Borna Disease Virus (BDV). In general, various infections have the potential to induce ME and non-specific symptoms explaining overlap with regard to diagnostic categories, though mainly affective and schizophrenic spectrum disorders and some other psychiatric syndromes. Such view is now supported by many findings especially the first large scale epidemiological study in psychiatry (Benros et al., 2011; Benros et al., 2012): infectious agents and autoimmunity acquired during lifetime increase significantly and additively the risk of schizophrenia and spectrum disorders. A most important step is to further improve ME diagnostics at the clinical case level: with advanced cerebrospinal fluid diagnostics, we identified in more than 50% of cases with therapy-resistant schizophrenic or affective spectrum disorders at least some CSF pathology, directly or probably indicating LLNI according to established classification (Bechter et al., 2010; Kuehne et al., 2013). Bechter K. et al. (2010). J Psychiatr Res 44, 321–30; Bechter K. (2012). Updating the Mild Encephalitis Hypothesis of Schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry in press: doi: 10.1016/j.pnpbp.2012.1006.1019; Benros M. et al. (2012). Ann N Y Acad Sci 1262: 56–66; Maxeiner H.G. et al. (2009). Brain Behav Immun 23(1):134–142.

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