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  • Author or Editor: Ákos Pákozdy x
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Authors: Pákozdy Ákos, Johann Thalhammer, Michael Leschnik and Péter Halász

The main aim of this study was to identify interictal epileptiform discharges in a group of dogs with seizures of known aetiology (symptomatic epilepsy, SE) and in dogs with idiopathic epilepsy (IE). Propofol was used for chemical restraint in all dogs. We found electroencephalographic (EEG) changes that could be considered epileptiform discharges (EDs) in 5 out of 40 dogs (12.5%). The EEG changes identified were spikes in four cases and periodic epileptiform discharges in one case. All EDs were seen in the SE group. We conclude that the interictal electroencephalographic examinations of propofolanaesthetised dogs suffering from IE and SE rarely show epileptic discharges and that the diagnostic value of such EEGs in the work-up for epilepsy seems to be low as epileptic discharges were unlikely to be detected. However, positive findings are more likely to be connected with SE. We found frequent, transient EEG phenomena (spindles, K-complexes, vertex waves, positive occipital sharp transients of sleep, cyclic alternating patterns), which are non-epileptic but their differentiation from epileptic phenomena is challenging.

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In the present study, 240 cases of dogs with seizures were analysed retrospectively. The aim was to examine the underlying aetiology and to compare primary or idiopathic epilepsy (IE) with symptomatic epilepsy (SE) concerning signalment, history, ictal pattern, clinical and neurological findings. The diagnosis of symptomatic epilepsy was based on confirmed pathological changes in haematology, serum biochemistry, cerebrospinal fluid (CSF) analysis and morphological changes of the brain by CT/MRI or histopathological examination. Seizure aetiologies were classified as idiopathic epilepsy (IE, n = 115) and symptomatic epilepsy (SE, n = 125). Symptomatic epilepsy was mainly caused by intracranial neoplasia (39) and encephalitis (23). The following variables showed significant difference between the IE and SE group: age, body weight, presence of partial seizures, cluster seizures, status epilepticus, ictal vocalisation and neurological deficits. In 48% of the cases, seizures were found to be due to IE, while 16% were due to intracranial neoplasia and 10% to encephalitis. Status epilepticus, cluster seizures, partial seizures, vocalisation during seizure and impaired neurological status were more readily seen with symptomatic epilepsy. If the first seizure occurred between one and five years of age or the seizures occurred during resting condition, the diagnosis was more likely IE than SE.

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Authors: Andrea Klang, Sandra Högler, Nora Nedorost, Christiane Weissenbacher-Lang, Ákos Pákozdy, Bethan Lang and Herbert Weissenböck

Hippocampal necrosis and hippocampal sclerosis in cats is a neuropathological entity which is a major concern in feline epilepsy. The aim of our study was to identify associated pathologic brain lesions possibly serving as aetiological triggers in this condition. Therefore, the formalin-fixed and paraffin waxembedded brain tissue of 35 cats diagnosed with hippocampal necrosis or sclerosis was examined retrospectively. In 26 cats inflammatory infiltrates could be found in the hippocampus or adjacent brain regions. Fifteen out of these animals demonstrated mild to moderate infiltrations by lymphocytes and complement deposition in the hippocampus similar to human limbic encephalitis, seven showed unspecific, predominantly non-suppurative inflammation, and two demonstrated suppurative inflammation of the hippocampus or adjacent brain regions. Additionally, one cat was diagnosed with central nervous manifestation of feline infectious peritonitis virus and another one with cerebral Toxoplasma gondii infection. Intracranial neoplasia was present in five cases altogether. Three of them comprised meningioma which was present additionally to lesions resembling limbic encephalitis in two cases, and a dentate gyrus alteration in one case. The other two tumour-associated cases comprised oligodendroglioma. Structural alterations of the dentate gyrus together with hippocampal sclerosis were encountered in three cases in total. Besides the case associated with a meningioma, one case demonstrated lesions resembling limbic encephalitis. A vascular infarct in the temporal lobe was encountered in one cat. In four cases no lesions other than hippocampal necrosis or sclerosis were found. The involvement of feline immunodeficiency virus infections, which may be able to produce hippocampal lesions, was not encountered in the cats examined.

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