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Tesi etd-02172016-122820


Tipo di tesi
Tesi di laurea specialistica LC5
Autore
MIKOVSKI, MATAN
URN
etd-02172016-122820
Titolo
Neuropathological findings in feline Hippocampal necrosis
Dipartimento
SCIENZE VETERINARIE
Corso di studi
MEDICINA VETERINARIA
Relatori
relatore Prof. Cantile, Carlo
correlatore Dott. Pirone, Andrea
Parole chiave
  • cat
  • epilepsy
  • Hippocampus
  • ischemic
  • limbic system
  • necrosis
  • neurodegeneration
Data inizio appello
04/03/2016
Consultabilità
Tesi non consultabile
Data di rilascio
04/03/2086
Riassunto
The present study reports the neuropathological changes of the hippocampus and contiguous structures in the condition known as Feline Hippocampal Necrosis. The disease is a well-recognized but poorly understood entity and may result from several different pathologic processes. It is clinically characterized by acute onset of complex partial cluster seizures with orofacial involvement and behavioral changes (such as aggression), which are non-responsive to treatment. Nine cases of FHN were examined with histological and immunohistochemical methods. Selected brain sections were mounted on treated glass slides and stained with Hematoxylin and Eosin (H&E) and labeled with Fluoro-Jade C (FJC), NeuN and glial fibrillary acidic protein (GFAP) markers, in order to detect the morphological changes of neurons and glial cells in the affected brain areas. The results were consistent with the development of degenerative processes at various stages with different involvement of the structures of the limbic system, from initial signs of inflammation and degeneration to a complete tissue necrosis. The neuropathological findings reported here are identical to what has been reported earlier in cats with necrosis of the hippocampus and piriform lobe. However, in some cases of our series, neuronal degeneration and necrosis was observed in additional areas of the limbic system such as septal nuclei. These findings could suggest a selective involvement of specific areas of the limbic system and hence a possible pathological mechanism such as excitotoxicity-mediated neuronal injury.
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