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@ARTICLE{vonZedtwitz:281364,
      author       = {von Zedtwitz, Katharina and Weiser, Judith and Dressle,
                      Raphael J and Maier, Simon J and Feige, Bernd and Nickel,
                      Kathrin and Venhoff, Nils and Domschke, Katharina and
                      Brumberg, Joachim and Rauer, Sebastian and Tebartz van Elst,
                      Ludger and Hannibal, Luciana and Prüss, Harald and Rau,
                      Alexander and Endres, Dominique},
      title        = {{C}ase {R}eport: {A}cute polymorphic psychosis and
                      {NMDA}-{R} {I}g{G} antibodies in serum: a follow-up case
                      study.},
      journal      = {Frontiers in immunology},
      volume       = {16},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DZNE-2025-01111},
      pages        = {1630357},
      year         = {2025},
      abstract     = {Anti-N-methyl-D-aspartate receptor (NMDA-R) encephalitis is
                      a neuropsychiatric disorder with additional psychiatric
                      features caused by NMDA-R immunoglobulin G (IgG) antibodies
                      in cerebrospinal fluid (CSF). This report presents the
                      follow-up of a patient in whom we assumed mild NMDA-R
                      encephalitis in the first psychotic episode.A patient with a
                      prior episode of an acute polymorphic psychotic syndrome
                      relapsed five and a half years later following a severe
                      COVID-19 infection. Serum NMDA-R antibodies were again
                      detected with a titer of max. 1:320 using fixed-cell-based
                      assays, but conventional magnetic resonance imaging (MRI),
                      electroencephalography (EEG), and CSF findings were largely
                      normal. NMDA-R antibody levels in serum decreased to 1:80
                      after approximately one month without immunotherapy.
                      [18F]fluorodeoxyglucose positron emission tomography
                      (FDG-PET) still revealed pronounced metabolism of the
                      association cortices (clearly more pronounced in the first
                      episode with an encephalitis-like pattern at that time).
                      Advanced MRI analyses including diffusion microstructure
                      imaging (DMI) showed frontal and thalamic microstructural
                      alterations compatible with edematization (but also far less
                      accentuated than in the first episode). Further advanced
                      antibody tests of CSF (approx. 1 month after symptom onset)
                      using a live-cell-based and different tissue-based assays
                      were negative for NMDA-R IgG antibodies. Research mass
                      spectrometry of the CSF identified
                      neurotransmitter-precursor shortages, increased turnover of
                      tryptophan into quinolinic acid, and low-glucose/lactate
                      levels. Immunotherapy (performed after the initial
                      assumption of an autoimmune cause) with steroids led to
                      clinical improvement of residual symptoms. After
                      approximately three months, NMDA-R IgG serum antibodies were
                      no longer detectable; however, FDG-PET/DMI follow-up
                      revealed no relevant changes.The international consensus
                      criteria for a probable/definite diagnosis of NMDA-R
                      encephalitis or autoimmune psychosis were not fulfilled,
                      especially as no NMDA-R IgG antibodies were identified in
                      CSF using different antibody assays and EEG/CSF routine
                      findings were inconspicuous. NMDA-R encephalitis was
                      therefore not diagnosed (as initially suspected).
                      Independent of the NMDA-R IgG antibodies, there were
                      possible signs of an autoimmune process. For a better
                      understanding of similar patients, multimodal diagnostic
                      approaches including complementary antibody tests could be
                      promising.},
      keywords     = {Humans / Anti-N-Methyl-D-Aspartate Receptor Encephalitis:
                      immunology / Anti-N-Methyl-D-Aspartate Receptor
                      Encephalitis: diagnosis / Anti-N-Methyl-D-Aspartate Receptor
                      Encephalitis: blood / Autoantibodies: blood /
                      Autoantibodies: immunology / COVID-19: complications /
                      COVID-19: immunology / Follow-Up Studies / Immunoglobulin G:
                      blood / Immunoglobulin G: immunology / Magnetic Resonance
                      Imaging / Positron-Emission Tomography / Psychotic
                      Disorders: immunology / Psychotic Disorders: blood /
                      Psychotic Disorders: diagnosis / Psychotic Disorders:
                      etiology / Receptors, N-Methyl-D-Aspartate: immunology /
                      autoimmune (Other) / autoimmune encephalitis (Other) / brain
                      (Other) / immunotherapy (Other) / inflammation (Other) /
                      Autoantibodies (NLM Chemicals) / Immunoglobulin G (NLM
                      Chemicals) / Receptors, N-Methyl-D-Aspartate (NLM
                      Chemicals)},
      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:40927716},
      pmc          = {pmc:PMC12414783},
      doi          = {10.3389/fimmu.2025.1630357},
      url          = {https://pub.dzne.de/record/281364},
}