Ivanchenko N. Canine epilepsy (etiology, diagnostics, therapy)

The thesis highlights the results of the research regarding the role of such diseases as canine distemper, leptospirosis, herpes types 1 and 2, toxoplasmosis, neosporosis, Lyme borreliosis and brucellosis in pathogenesis of canine «unknown cause epilepsy» (IVETF, 2015). The hypothesis of indirect immunologically caused influence of infectious and invasive agents on epileptogenesis in dogs is expressed, as well as the support of the veracity of the data on the relationship between the immune system and epileptogenesis as an amplifying feedback loop. In the thesis results proving the therapeutic efficacy of such amino acids as leucine, valine, isoleucine, glycine and taurine (cysteine derivative) administrated orally are presented. Also, data on elaborated active scalp electrode for canine electroencephalography are provided. During 2 months above mentioned substances were administrated to eight dogs that were diagnosed as having unknown cause epilepsy in such daily doses per kilogram divided equally in order to be given every 8 h: L-leucine – 150 mg, L-isoleucine – 275 mg; L-valine – 240 mg; glycine – 300 mg; taurine (cysteine derivative) – 240 mg. Performing ion exchange liquid chromatography changes taking place after 1 and 2 months in the dogs’ blood amino acid pool and cerebrospinal fluid in case of exogenous amino acid overload were analyzed. The therapeutic efficacy of mentioned composition was estimated by monitoring seizure frequency, qualitative and quantitative electroencephalography (QEEG) using fast Fourier transformation (FFT) to the frequency range of delta, theta, alpha and beta bands. After one-month treatment the frequency ranges of delta, theta and alpha bands lowered whereas the frequency of beta band became higher comparing with pretreatment data. Clinically antiepileptic effect of amino acid composition was represented by the prolongation of interictal periods per 2 to 3 times in 37.5 % of dogs and by elimination of cluster seizures. The therapeutic efficacy period was short (approximately 35–48 days). To our opinion it was due to compensatory mechanisms of protein metabolism that were represented by partial amino acid molar ratio stabilization in amino acid blood pool.