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@ARTICLE{Stegmayr:875458,
      author       = {Stegmayr, Carina and Surges, Rainer and Choi, Chang-Hoon
                      and Burda, Nicole and Stoffels, Gabriele and Filß,
                      Christian and Willuweit, Antje and Neumaier, Bernd and
                      Heinzel, Alexander and Shah, N. Jon and Mottaghy, Felix M.
                      and Langen, Karl-Josef},
      title        = {{I}nvestigation of {C}erebral
                      {O}-(2-[$^{18}${F}]{F}luoroethyl)-{L}-{T}yrosine {U}ptake in
                      {R}at {E}pilepsy {M}odels},
      journal      = {Molecular imaging $\&$ biology},
      volume       = {22},
      issn         = {1860-2002},
      address      = {New York [u.a.]},
      publisher    = {Springer},
      reportid     = {FZJ-2020-02050},
      pages        = {1255–1265},
      year         = {2020},
      abstract     = {A recent study reported on high, longer lasting and finally
                      reversible cerebral uptake of
                      O-(2-[18F]fluoroethyl)-L-tyrosine ([18F]FET) induced by
                      epileptic activity. Therefore, we examined cerebral [18F]FET
                      uptake in two chemically induced rat epilepsy models and in
                      patients with focal epilepsy to further investigate whether
                      this phenomenon represents a major pitfall in brain tumor
                      diagnostics and whether [18F]FET may be a potential marker
                      to localize epileptic foci.Five rats underwent kainic acid
                      titration to exhibit 3 to 3.5 h of class IV–V motor
                      seizures (status epilepticus, SE). Rats underwent 4×
                      [18F]FET PET and 4× MRI on the following 25 days. Six rats
                      underwent kindling with pentylenetetrazol (PTZ) 3 to
                      8×/week over 10 weeks, and hence, seizures increased from
                      class I to class IV. [18F]FET PET and MRI were performed
                      regularly on days with and without seizures. Four rats
                      served as healthy controls. Additionally, five patients with
                      focal epilepsy underwent [18F]FET PET within 12 days after
                      the last documented seizure.No abnormalities in [18F]FET PET
                      or MRI were detected in the kindling model. The SE model
                      showed significantly decreased [18F]FET uptake 3 days after
                      SE in all examined brain regions, and especially in the
                      amygdala region, which normalized within 2 weeks.
                      Corresponding signal alterations in T2-weighted MRI were
                      noted in the amygdala and hippocampus, which recovered 24
                      days post-SE. No abnormality of cerebral [18F]FET uptake was
                      noted in the epilepsy patients.There was no evidence for
                      increased cerebral [18F]FET uptake after epileptic seizures
                      neither in the rat models nor in patients. The SE model even
                      showed decreased [18F]FET uptake throughout the brain. We
                      conclude that epileptic seizures per se do not cause a
                      longer lasting increased [18F]FET accumulation and are
                      unlikely to be a major cause of pitfall for brain tumor
                      diagnostics.},
      cin          = {INM-11 / INM-4 / INM-5 / JARA-BRAIN},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-11-20170113 / I:(DE-Juel1)INM-4-20090406 /
                      I:(DE-Juel1)INM-5-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32409931},
      UT           = {WOS:000532879300001},
      doi          = {10.1007/s11307-020-01503-x},
      url          = {https://juser.fz-juelich.de/record/875458},
}