Differential Diagnostic Schedule of Mild Encephalitis (ME)/Mild Neuroinflammatory Subtypes – A Proposal from a clinical perspective Autoimmune mild neuroinflammation -Autoimmune Psychosis (AP) with presence of CNS antibodies according to recent international consensus criteria (20). A distinction is made between possible AP (clinical syndrome which should lead to a broad organic diagnostic work-up), probable AP (with additional diagnostic findings such as pleocytosis in cerebrospinal fluid), and definite AP (with detection of antineuronal IgG antibodies in cerebrospinal fluid). -Poorly defined psychiatric cases of autoimmune origin without detection of (known) CNS antibodies, based on different diagnostic findings including brain biopsy pathologies or plausibility from therapy response on immune modulatory treatments (24, 28) Infectious mild neuroinflammation -Low-grade “encephalitis” caused by various neurotropic viruses or other infectious agents presenting with acute though mild neuroinflammation without neurological hard signs but prominent or exclusive psychiatric syndromes in context with paraclinical, especially intrathecal signs of specific infections (using PCR, antibody index, and culture). Historical examples are late-stage syphilis or influenza-associated severe mental disorders; recent examples include acute Lyme Neuroborreliosis, Bartonellosis, mild cerebral Whipple's disease, or potentially acute BDV infection [compare, for example, (39)] Combined infectious-autoimmune mild neuroinflammation -Persistent infection having induced in parallel an autoimmune response, pathology from both mechanisms can be involved in the pathogenesis of clinical syndrome observed in the diseased individual, paradigmatic cases represented by pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection (PANDAS)/pediatric acute-onset neuropsychiatric syndrome (PANS), implicating requirement of primary agent-focused (elimination) and/or immune modulatory treatment (67). Besides PANDAS/PANS, the concept is also well established for anti-NMDAR encephalitis after herpes encephalitis (53, 56). Multiconditional mild neuroinflammation -Various risk factors acting together in rather balanced weight of each single factor, e.g., ubiquitous persistent infections plus social stress in context with genetic factors, and other variant endogenous factors (e.g., endocrine and immune status), age, etc. (18).