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@ARTICLE{Krohn:276321,
      author       = {Krohn, Stephan and Müller-Jensen, Leonie and Kuchling,
                      Joseph and Romanello, Amy and Wurdack, Katharina and Rekers,
                      Sophia and Bartsch, Thorsten and Leypoldt, Frank and Paul,
                      Friedemann and Ploner, Christoph J and Prüss, Harald and
                      Finke, Carsten},
      title        = {{C}ognitive {D}eficits in {A}nti-{LGI}1 {E}ncephalitis
                      {A}re {L}inked to {I}mmunotherapy-{R}esistant {W}hite
                      {M}atter {N}etwork {C}hanges.},
      journal      = {Neurology: Neuroimmunology $\&$ Neuroinflammation ;
                      official journal of the American Academy of Neurology},
      volume       = {12},
      number       = {2},
      issn         = {2332-7812},
      address      = {Philadelphia, Pa.},
      publisher    = {Wolters Kluwer},
      reportid     = {DZNE-2025-00284},
      pages        = {e200360},
      year         = {2025},
      abstract     = {Cognitive deficits represent a major long-term complication
                      of anti-leucine-rich, glioma-inactivated 1 encephalitis
                      (LGI1-E). Although severely affecting patient outcomes, the
                      structural brain changes underlying these deficits remain
                      poorly understood. In this study, we hypothesized a link
                      between white matter (WM) networks and cognitive outcomes in
                      LGI1-E.In this cross-sectional study, we combined clinical
                      assessments, comprehensive neuropsychological testing,
                      diffusion tensor MRI, probabilistic WM tractography, and
                      computational network analysis in patients with LGI1-E
                      referred to Charité-Universitätsmedizin Berlin. Healthy
                      individuals were recruited as control participants and
                      matched to patients for age and sex with logistic regression
                      propensity scores.Twenty-five patients with LGI1-E (mean age
                      = 63 ± 12 years, $76\%$ male) and 25 healthy controls were
                      enrolled. Eighty-eight percent of patients presented
                      persistent cognitive symptoms at postacute follow-up
                      (median: 12 months from onset, interquartile range: 6-23
                      months)-despite treatment with immunotherapy and good
                      overall recovery (modified Rankin Scale [mRS] score at peak
                      illness vs postacute: z = -4.1, p < 0.001, median mRS score
                      at postacute visit: 1). Neuroimaging revealed that WM
                      networks in LGI1-E are characterized by (1) a systematic
                      reduction in whole-brain connectivity (t = -2.16, p = 0.036,
                      d = -0.61), (2) a cortico-subcortical hypoconnectivity
                      cluster affecting both limbic and extralimbic brain systems,
                      and (3) a 'topological reorganization' marked by a
                      bidirectional shift in the relative importance of individual
                      brain regions in the WM network. The extent of this WM
                      reorganization was strongly associated with long-term
                      deficits of verbal memory (r = -0.56), attention (r =
                      -0.55), and executive functions (r = -0.60, all pFDR =
                      0.017).Although traditionally viewed as a form of limbic
                      encephalitis, our study characterizes LGI1-E as a 'network
                      disorder' that affects the whole brain. Structural
                      reorganization of WM networks was linked to long-term and
                      multidomain cognitive impairment, which was not prevented by
                      immunotherapy. These findings highlight the need for closer
                      monitoring and improved treatment strategies to mitigate
                      long-term cognitive impairment in LGI1-E.},
      keywords     = {Humans / Male / Female / Middle Aged / White Matter:
                      diagnostic imaging / White Matter: pathology / Cognitive
                      Dysfunction: etiology / Cognitive Dysfunction:
                      physiopathology / Cognitive Dysfunction: diagnostic imaging
                      / Aged / Cross-Sectional Studies / Immunotherapy: methods /
                      Nerve Net: diagnostic imaging / Nerve Net: physiopathology /
                      Nerve Net: pathology / Encephalitis: diagnostic imaging /
                      Encephalitis: immunology / Intracellular Signaling Peptides
                      and Proteins / Autoantibodies: blood / Diffusion Tensor
                      Imaging / LGI1 protein, human (NLM Chemicals) /
                      anti-leucine-rich glioma-inactivated 1 autoantibody (NLM
                      Chemicals) / Intracellular Signaling Peptides and Proteins
                      (NLM Chemicals) / Autoantibodies (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:39879565},
      doi          = {10.1212/NXI.0000000000200360},
      url          = {https://pub.dzne.de/record/276321},
}