[Autoimmune encephalitis-An update]. / Autoimmunenzephalitis ­ ein Update.

Detection of autoantibodies against neurons and glia cells has brought about the early and specific diagnosis of autoimmune encephalitis in patients with variable neurological and psychiatric symptoms. Growing knowledge not only resulted in profound changes in treatment algorithms including immunotherapy but also in the understanding of disease mechanisms and etiological factors. The still increasing numbers of new autoantibodies calls for continuous updates on the state of the art in antibody diagnostics, frequencies of associated tumors and the clinical spectrum linked to each antibody, which can range from mood changes, cognitive impairment and epileptic seizures to abnormal movements, autonomic dysfunction and impaired levels of consciousness. This article summarizes the recent developments in the predominant clinical presentations of autoimmune encephalitis patients in imaging and cerebrospinal fluid diagnostics and also in prognostic markers, in the establishment of innovative immunotherapies, in the use of diagnostic pathways even before the results of the antibody tests are available and the understanding of the autoimmune etiology.

Dysregulated autoantibodies targeting vaso- and immunoregulatory receptors in Post COVID Syndrome correlate with symptom severity.

Most patients with Post COVID Syndrome (PCS) present with a plethora of symptoms without clear evidence of organ dysfunction. A subset of them fulfills diagnostic criteria of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Symptom severity of ME/CFS correlates with natural regulatory autoantibody (AAB) levels targeting several G-protein coupled receptors (GPCR). In this exploratory study, we analyzed serum AAB levels against vaso- and immunoregulatory receptors, mostly GPCRs, in 80 PCS patients following mild-to-moderate COVID-19, with 40 of them fulfilling diagnostic criteria of ME/CFS. Healthy seronegative (n=38) and asymptomatic post COVID-19 controls (n=40) were also included in the study as control groups. We found lower levels for various AABs in PCS compared to at least one control group, accompanied by alterations in the correlations among AABs. Classification using random forest indicated AABs targeting ADRB2, STAB1, and ADRA2A as the strongest classifiers (AABs stratifying patients according to disease outcomes) of post COVID-19 outcomes. Several AABs correlated with symptom severity in PCS groups. Remarkably, severity of fatigue and vasomotor symptoms were associated with ADRB2 AAB levels in PCS/ME/CFS patients. Our study identified dysregulation of AAB against various receptors involved in the autonomous nervous system (ANS), vaso-, and immunoregulation and their correlation with symptom severity, pointing to their role in the pathogenesis of PCS.