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@ARTICLE{Skripuletz:164145,
      author       = {Skripuletz, Thomas and Möhn, Nora and Franke, Christiana
                      and Prüß, Harald},
      title        = {{N}euroimmunologie von {COVID}‑19.},
      journal      = {Der Nervenarzt},
      volume       = {92},
      number       = {6},
      issn         = {0028-2804},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2022-00801},
      pages        = {521 - 530},
      year         = {2021},
      abstract     = {Many neuroimmunological diseases, such as encephalopathy,
                      encephalitis, myelitis and acute disseminated
                      encephalomyelitis (ADEM) have occurred more frequently after
                      infections with severe acute respiratory syndrome
                      coronavirus 2 (SARS-CoV-2), which indicates a parainfectious
                      or postinfectious association. The most likely underlying
                      mechanisms include virus-triggered overactivation of the
                      immune system with hyperinflammation and cytokine storm but
                      potentially also the development of specific autoantibodies
                      against central nervous system (CNS) tissue. These were
                      predominantly detected in the cerebrospinal fluid of
                      severely ill coronavirus disease 2019 (COVID-19) patients.
                      In contrast, direct damage after invasion of SARS-CoV‑2
                      into the brain and spinal cord does not seem to play a
                      relevant role. Susceptibility to infection with SARS-CoV‑2
                      in patients with multiple sclerosis, myasthenia or other
                      neuroimmunological diseases including the risk for severe
                      disease courses, is not determined by the administered
                      immunotherapy but by known risk factors, such as age,
                      comorbidities and the disease-related degree of disability.
                      Therefore, immunotherapy in these patients should not be
                      delayed or discontinued. The contribution of
                      neuroimmunological mechanisms to long-term sequelae after
                      survival of a COVID-19 illness, such as fatigue, impairment
                      of memory, sleep dysfunction or anxiety, will require
                      long-term clinical follow-up, preferentially in COVID-19
                      register studies.},
      keywords     = {Brain Diseases / COVID-19 / Encephalitis / Humans /
                      Neuroimmunomodulation / SARS-CoV-2 / Autoantibodies (Other)
                      / Encephalitis (Other) / Hyperinflammation (Other) /
                      Immunotherapy (Other) / Myelitis (Other)},
      cin          = {AG Prüß},
      ddc          = {610},
      cid          = {I:(DE-2719)1810003},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33651117},
      pmc          = {pmc:PMC7923405},
      doi          = {10.1007/s00115-021-01077-1},
      url          = {https://pub.dzne.de/record/164145},
}