Important aspects of canine idiopathic and symptomatic epilepsy
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This dissertation presents an overview of the research performed by the author in examining dogs with seizure disorders. In the first study we summarized the clinical work-up and ictal analysis of 240 dogs with recurrent seizures. The aim was to examine the underlying aetiology and to compare idiopathic epilepsy (IE) with symptomatic epilepsy (SE) regarding signalment, history, ictal patterns and findings of the clinical and neurological examination. The diagnosis of symptomatic epilepsy was based on confirmed pathological changes in haematology, serum biochemistry, cerebrospinal fluid (CSF) analysis and morphological changes in the brain by CT/MRI or histopathological examinations. The seizure aetiologies were classified as idiopathic epilepsy in 115 (48%) dogs and symptomatic epilepsy in 125 (52%). Symptomatic epilepsy was mainly caused by intracranial neoplasia (39 dogs, 16%) and encephalitis (23 dogs, 10%). The following variables showed significant differences between the IE and SE groups: age, body weight, presence of partial seizures, cluster seizures, status epilepticus, ictal vocalization and neurological deficits. Status epilepticus, cluster seizures, partial seizures, vocalization during seizure and impaired neurological status were more readily seen in symptomatic epilepsy. If the first seizure occurred between 1 and 5 years of age or the seizures occurred during the resting condition the diagnosis was more likely to be IE than SE. In the second study we investigated the clinical usefulness of EEG in dogs with seizures in a clinical setting in combination with other advanceddiagnostic tools. We found that the interictal electroencephalographic (EEG) examination of epileptic dogs suffering from IE or SE rarely showed epileptic discharges using chemical restraint with propofol (2-6mg/kg). Only 5 out of 40 (12.5%) dogs showed EEG changes, which were considered as epileptiform discharges (ED). The EEG changes identified were spikes in four cases and periodic epileptiform discharges in one case. We concluded that since epileptic discharges were infrequently detected the diagnostic value of EEG in such a work-up seemed to be rather low. Otherwise, we frequently found transient EEG phenomena (spindles, k-complexes, vertex waves, positive occipital sharp transients of sleep, cyclic alternating patterns), which were non-epileptic but their differentiation from epileptic phenomena was challenging and thus being aware of these patterns could reduce misinterpretation. In the following studies possible therapy of two particularly difficult clinical conditions were evaluated. In the third study we investigated the therapeutic effect of immunosuppressive cyclosporine on granulomatous meningoencephalomyelitis (GME), a condition that can cause seizures and which has a poor long-term prognosis. Fourteen dogs were included in this study and randomly divided into two groups. Seven dogs were treated with corticosteroids and seven dogs with corticosteroids in combination with cyclosporine. The median survival time of the seven dogs on immunosuppressive corticosteroid therapy was 28 days (range 3-63 days) while for the seven dogs with additional cyclosporine treatment it was 620 days (range 8-870). Four dogs were still alive at the time the study was completed. We concluded that cyclosporine combination therapy prolongs survival time in comparison with prednisolone therapy in dogs with granulomatous meningoencephalomyelitis. Total remission can also occur. The fourth study evaluated the effect of gabapentinin the at-home treatment of 15 dogs with idiopathic refractory epilepsy, including cluster seizures (CS). When a CS started, additional gabapentin treatment was initiated PO at a dosage of 20 mg/kg TID for at least 3 days by the owner. In four dogs, a 49-100% reduction was reported in the seizures per cluster. The severity and duration of seizures were reduced in four and two dogs, respectively. The general interictal condition during CS was considerably ameliorated by gabapentin in four dogs. Eight out of fourteen owners considered that their dog’s quality of life during a CS had been improved by the use of gabapentin. We concluded that gabapentin can be considered as an alternative at-home treatment for CS, although only a small proportion of dogs might experience considerable benefits.