• Open Access

Necrosis of Hippocampus and Piriform Lobe in 38 Domestic Cats with Seizures: A Retrospective Study on Clinical and Pathologic Findings

Authors

  • R. Fatzer,

    Corresponding author
    1. Swiss Reference Lab for Spongiform Encephalopathies, Institute of Animal Neurology, University of Bern, Bern, Switzerland
      Institute of Animal Neurology, Faculty of Veterinary Medicine, University of Bern, Bremgartenstrasse 109a, CH-3012 Bern, Switzerland; e-mail: rosmarie.fatzer@ itn.unibe.ch.
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  • G. Gandini,

    1. Department of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, University of Bologna, Bologna, Italy
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  • A. Jaggy,

    1. Swiss Reference Lab for Spongiform Encephalopathies, Institute of Animal Neurology, University of Bern, Bern, Switzerland
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  • M. Doherr,

    1. IVI, Institute for Virus Diseases and Im-munoprophylaxis, Mittelhäusern, Switzerland
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  • M. Vandevelde

    1. Swiss Reference Lab for Spongiform Encephalopathies, Institute of Animal Neurology, University of Bern, Bern, Switzerland
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Institute of Animal Neurology, Faculty of Veterinary Medicine, University of Bern, Bremgartenstrasse 109a, CH-3012 Bern, Switzerland; e-mail: rosmarie.fatzer@ itn.unibe.ch.

Abstract

The clinical records of 38 cats (1985–1995) with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and occasionally the lobus piriformis were evaluated retrospectively. There was no sex or breed predisposition. Most cats were between 1 and 6 years of age (mean age = 35 months) and had either generalized or complex-partial seizures of acute onset and rapid progression. The seizures had a tendency to become recurrent and to present as clusters or even status epilepticus later in the course of the disease. Fourteen cats died spontaneously, and 24 were euthanized. Histopatologic examination revealed bilateral lesions restricted to the hippocampus and occasionally the lobus piriformis. The lesions seemed to reflect different stages of the disease and consisted of acute neuronal degeneration to complete malacia, affecting mainly the layer of the large pyramidal cells but sometimes also the neurons of the dentate gyrus and the piriform lobe. The clinical, neuropathologic, and epidemiologic findings suggest that the seizures in these cats were triggered by primary structural brain damage, perhaps resulting from exitotoxicity. The cause remains unknown, but epidemiologic analysis suggests an environmental factor, probably a toxin.

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