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71. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
9. Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

21.06. - 24.06.2020

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Hippocampal mossy fibre sprouting into CA2 in temporal lobe epilepsy

Hippocampale Moosfasersprossung in die CA2 Region bei Temporallappenepilepsie

Meeting Abstract

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  • presenting/speaker Barbara Puhahn-Schmeiser - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Ute Häussler - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Josef Zentner - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Soroush Dooskamp - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Marco Prinz - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Jürgen Beck - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Carola Haas - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland
  • Thomas Freiman - Universitätsklinikum Freiburg, Neurochirurgie, Freiburg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 71. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 9. Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. sine loco [digital], 21.-24.06.2020. Düsseldorf: German Medical Science GMS Publishing House; 2020. DocV062

doi: 10.3205/20dgnc066, urn:nbn:de:0183-20dgnc0663

Veröffentlicht: 26. Juni 2020

© 2020 Puhahn-Schmeiser et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.

Gliederung

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Objective: Hippocampal sclerosis (HS) in Temporal Lobe Epilepsy (TLE) is characterized by selective neuronal death in the hippocampal subregions of the cornu ammonis (CA) CA1, CA3 and CA4. Granule cells (GC) and CA2 neurons are less affected. It is assumed that GC axons, the mossy fibers (MF), loose targets in CA3 and CA4 and sprout to the surviving GC layer (GCL), the so-called MF sprouting (MFS). We examined in TLE whether MF sprout only to the GCL or also to CA2 and whether MFS is associated with the death of the CA3 and CA4 target neurons.

Methods: In total, 319 hippocampal specimens of patients with TLE were analyzed. Immunohistochemical stainings for neuronal nuclei (NeuN) were used to determine neuronal loss and for synaptorin (SPO) to localize MF terminals. Cell death was analyzed according to two HS classifications, the Wyler grade and the International League against Epilepsy (ILAE) types. Clinical patient records were compared.

Results: The hippocampal subregions CA1 and CA2 are normal, absent of SPO-positive background. In HS Wyler III and IV as well as ILAE 1, 2, 3, CA2 and to a lesser extent CA1 was significantly correlated with SPO-positive axon terminals and granule cell dispersion (GCD). In addition, SPO-positive axon terminals were associated with cell death in CA3 and CA4 in the classical severe HS ILAE type 1, whereas this was not the case inatypical HS ILAE type 2.

Conclusion: These SPO-positive axon terminals were interpreted as atypical MFS into CA1 and CA2 in patients with TLE. The sprouting process also seems to appear without cell death of target neurons in CA3 and CA4 and seems to be directed to the surviving cell populations of GCL and CA2 even if it was also observed to a lesser extent in CA1, where cell death was most severe