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57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

12. - 15.09.2012, Erlangen

57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

Unilateral cerebellar hypoplasia and mesencephalic malformation in a Hanoverianthoroughbred foal

Meeting Abstract

  • Sabrina Schroeder - Institute of Veterinary Pathology, Justus-Liebig-University, Gießen, Germany
  • Martin Schmidt - Clinic for Small Animals, Surgery - Neurology, Giessen, Germany
  • Sandra Preis - Institute of Veterinary Pathology, Justus-Liebig-University, Gießen, Germany
  • Stephan Klumpp - Clinic for Small Animals, Surgery - Neurology, Giessen, Germany
  • Kernt Koehler - Institute of Veterinary Pathology, Justus-Liebig-University, Gießen, Germany
  • Klaus Kuchelmeister - Institute for Neuropathology, Universitätsklinikum, Bonn, Germany
  • presenting/speaker Christiane Herden - Institute of Veterinary Pathology, Justus-Liebig-University, Gießen, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP4.13

DOI: 10.3205/12dgnn090, URN: urn:nbn:de:0183-12dgnn0903

Published: September 11, 2012

© 2012 Schroeder et al.
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Outline

Text

Unilateral absence of a cerebellar hemisphere and vermis accompanied by contralateral malformation of the mesencephalon was diagnosed in a Hanoverian foal. The missing areas of the right cerebellar hemisphere were replaced by a cystic formation. The left part of the mesencephalic lamina quadrigemina was reduced in size and the corpus callosum was hypoplastic. Additional microscopical findings were most obvious near the cyst formation and include angiofibrosis in remaining cerebellar and mesencephalic parenchyma and leptomeninges, heterotopia of cerebellar neurons, sclerosis in cerebellar cortex, focal proliferation of meningeal cells and mild mononuclear perivascular infiltrates. Occassional irregular neuronal arrangement in the mesencephalon was also present. Infectious agents such as Borna disease virus, rabies virus, and equine herpesvirus were not detected. Therefore, the complex malformation in this foal might have been caused by a destructive, possibly ischemic event, or could represent a sequel of a primary retrocerebellar cyst with accompanying compression of adjacent parenchyma.